what is your favorite probiotix to take for ulcers
Introduction
During the concluding decade of our probiotic yogurt programs in the East-African countries Uganda, Tanzania, and Kenya, we took annotation of the high incidence of self-reported ulcers and accompanying stomach pains, as reported decades ago for in particular Northern Tanzania and South-Western Uganda and some regions in Kenya (Tovey and Tunstall, 1975; Balint, 1998). Interestingly, during our fieldwork aimed at the stimulation of local production and consumption of probiotic yogurt to improve health and wealth in local communities, we observed a decrease of complaints amongst consumers and realized that there might be an effect from the intake of probiotic yogurt containing Lactobacillus rhamnosus yoba 2012 (LRY), the generic variant of Lactobacillus rhamnosus GG (LGG) (Kort and Sybesma, 2012; Sybesma et al., 2013), on the reduction of symptoms associated with ulcers.
Over the terminal years a number of reviews take been published on H. pylori ulcers (Blaser and Atherton, 2004; Comprehend and Blaser, 2009), the prevalence of H. pylori and ulcers in different populations (Kidd et al., 1999b; Roberts et al., 2016), the interaction between H. pylori and LGG (Hamilton-Miller, 2003; Gotteland et al., 2006), and furnishings of LGG administration on ulcers (Lam et al., 2007a,b). The present paper is, however, the first review that summarizes the incidence of H. pylori in Due east-Africa and its pathology afflicted by immune responses, genetic factors and environmental factors, including specific regional diets, emphasizing the importance of this topic for Eastward-Africa. In addition, this article reviews effects of the probiotic bacterium LGG on H. pylori colonization as well as on inflammation and associated injury of gastric mucosa, in either presence or absence of other treatments. Finally, this review provides substantiation for our on-going probiotic yogurt programs in East-Africa, as reported in this Research Topic in Frontiers in Microbiology in another contribution past Westerik et al. (2018), to likely reduce H. pylori-associated pathology.
Previous studies also suggested that LGG prevented H. pylori colonization, which often occurs in early childhood (Misiewicz et al., 1995; Peña and Versalovic, 2003; Myllyluoma et al., 2008). Information technology is therefore expected that assistants of probiotic yogurt containing LGG to children in resource-poor countries from early on childhood, can reduce the incidence of H. pylori colonization in the general population. Besides prevention of H. pylori, LGG may present an approach to establish and manage a harmless relationship betwixt the host and H. pylori when the latter 1 is already present, counteracting the need for H. pylori eradication therapy. Kort et al. (2015) and Sybesma et al. (2015) take shown that yogurt containing LRY could exist made accessible for people in resource-poor countries in a sustainable way. This is done through providing freeze-dried yogurt starter cultures containing LRY at cost cost, in combination with a training programme for the local population on standardized and rubber yogurt production with locally available equipment.
Prevalence of H. pylori in Due east Africa
Helicobacter pylori is a Gram-negative screw bacterium that inhabits the surface of the mucous layer of the human tummy and duodenum (upper intestine), usually in a chronic style, though H. pylori colonization tin also be temporarily (Hestvik et al., 2010). The majority of carriers take acquired this bacterium through contact with other human beings before the age of 10 years old, more and so in cramped housing areas with poor sanitation practices. When nowadays, H. pylori is the dominant microorganism, as very few other leaner tin can survive in the stomach.
Helicobacter pylori is constitute in more than l% of world's population, spread all effectually the globe (Kodaman et al., 2014). In x–20% of the carriers, H. pylori is believed to be a gene in the development of gastric pathology (Fernando et al., 2001; Gotteland et al., 2006; Kate et al., 2013). Gastric pathology often starts with gastritis (inflammation of the tummy lining), which can go atrophic (degenerating cells) and via gastric metaplasia (abnormal modify in tissue) can pb to peptic ulcers and in rare cases to gastric cancer. Duodenal ulcers are much more mutual than gastric (tum) ulcers. Over the grade of the 20th century, H. pylori colonization has go less common in Westernized populations, and in some countries the incidence has dropped below twenty% (Get, 2002; Roberts et al., 2016). This is probably associated with improved sanitation, smaller family sizes, and frequent use of antibiotics from babyhood (Cover and Blaser, 2009). In contrast, general estimates on the prevalence of H. pylori nonetheless indicate that over 51% of people living in developing countries, and even 57% of people living on the African continent, are H. pylori positive. When taking into business relationship the historic period of subjects, 52% of African children less than ten years of historic period, and over 64% of the African adults are H. pylori positive (Zamani et al., 2018). Hence, the high incidence of H. pylori in Eastward-Africa might be a chance cistron in the development of gastric pathology amongst the local population. A summary of studies on the incidence of H. pylori and gastric pathology in East-Africa tin can exist found in Table 1. Table i shows great diverseness in the incidence rate between 25 and 87%. This may be due to customs-specific differences, only likewise unlike diagnostic methods used to determine the presence of H. pylori (Ricci et al., 2007; Zamani et al., 2018). Notwithstanding, nosotros tin conclude that H. pylori is a significant hazard factor in the development of gastric pathology in East-Africa.
TABLE i. Summary of studies on the incidence of H. pylori and gastric pathology in Due east Africa.
Pathogenesis and Other Consequences of H. pylori Colonization
The high incidence of H. pylori among East African populations per se does not necessarily cause increased levels of gastric pathology, as H. pylori induced gastric pathology is influenced by genetic factors of the H. pylori strain as well equally past specific allowed responses of the host. At the same fourth dimension, it has been reported that H. pylori might exert benign functions in African populations (Blaser and Atherton, 2004; Cover and Blaser, 2009).
In the context of pathology, Blaser and Atherton (2004) distinguish two topographic distributions of H. pylori induced gastric inflammation, both having unlike outcomes. Firstly, inflammation could be in the lower office of the stomach simply (antral-gastritis), which via a pour of cell signaling leads to increased gastric acid output and later on increases the take chances for duodenal ulcers. Secondly, inflammation of the whole stomach (pan-gastritis) could induce cascades of signaling that lead to reduced acrid output and associated increased take a chance for gastric ulcers. This topographic distribution might be determined past genetic factors of H. pylori strains every bit well as environmental factors.
Helicobacter pylori strains exhibit a loftier level of genetic diversity. Certain genetic characteristics of this bacterium have been associated with increased interactions with the host cells. One of the best documented characteristics is the presence of the pathogenicity island cagA, which expresses the effector protein CagA that can be injected into epithelial cells (Crabtree et al., 1991; Bravo et al., 2002). Connected to the presence of cagA is the presence of an active VacA protein (Kidd et al., 1999a). All H. pylori strains comprise the vacA gene just with a nifty variance in nucleotide sequence, and not all expressed VacA proteins have the same functional activities. Active VacA causes alterations in epithelial cells and immune cells due to massive vacuolation (Cover and Blanke, 2005). Strains that both express CagA and active VacA are more likely to crusade gastric inflammations and subsequent pathology including peptic ulcers and gastric cancer (Cover and Blaser, 2009). Other authors identified the dupA gene as a virulence gene in H. pylori strains that is associated with duodenal ulcers (Kate et al., 2013). Immune responses confronting these virulent factors involve Th1 cells, which paradoxically play a major role in H. pylori associated pathogenesis by enhancing inflammation (Blaser and Atherton, 2004).
With regards to the virulence factors, people in adult countries are institute to be colonized by nearly equal proportions of cagA+ and cagA- strains (fifty% cagA+), whereas people in developing countries are predominantly colonized by cagA+ strains (79% cagA+) (Parsonnet et al., 1997). However, it has been suggested that people in developing countries respond to H. pylori in a way that is associated with a relatively low risk for pathogenesis (Holcombe, 1992; Mitchell et al., 2009). For example, Segal et al. (2001) plant that amongst people in several African countries, gastric cancer accounts only for 2–3% of all cancers, whereas the international boilerplate is 9% (Parkin, 2004). This might be due to modulated immune responses to H. pylori as a consequence of infections with a myriad of gastrointestinal pathogens from early on life, which primarily occur in developing countries. Mitchell et al. (2009) quantified the immune response by measuring the IgG1/IgG2 ratio (a marker of the T helper prison cell response) in Sowetan (South-African), German and Australian symptomatic H. pylori-positive subjects. A less pro-inflammatory, IgGI predominant response (IgG1/IgG2 ratio > ane) was observed in 81% of Sowetans, only only in 4.7% of Australians and four.four% of Germans.
The realization that H. pylori has colonized in the gut of mankind for thousands of years (Ghose et al., 2002), creating long-continuing dynamic equilibriums, led to the assumption that there must be a common beneficial relationship (Blaser and Atherton, 2004; Cover and Blaser, 2009). Kodaman et al. (2014) postulate that H. pylori co-evolves with host populations and every bit a outcome, H. pylori is less virulent upon colonization in its 'natural host' compared to its colonization in populations from other ethnic origins. The authors reported a potent correlation betwixt H. pylori virulence in people of Amerindian origin and the presence of H. pylori of African origin and concluded that members of multicultural societies were at higher risk of H. pylori associated pathology (Kodaman et al., 2014).
In improver to beingness harmless in many cases, information technology has even been proposed that cagA+ H. pylori could exert beneficial functions in the torso. Over the past decennia, gastroesophageal reflux illness (Vicari et al., 1998), Barrett'due south esophagus (Vaezi et al., 2000), esophageal adenocarcinoma (Ye et al., 2004) and dysfunctional responses to common allergens leading to subsequent childhood asthma and allergic disorders (Cover and Blaser, 2009) have get more common in the developed world. Recent research has associated the increase of those diseases with the subtract of cagA+ H. pylori colonized persons. Mechanisms have been proposed on how the absenteeism of cagA+ H. pylori induced pan-gastritis could lead to an increment in acrid production (Blaser and Atherton, 2004), which in plough could lead to an increased take chances of the above mentioned diseases. Indeed, Segal et al. (2001) found that incidence of gastro-oesophageal reflux and its complications were low in blackness populations where the incidence of cagA+ H. pylori is high. However, in that location was no uniform understanding on the topic, as for example Moon et al. (2009) establish that there is an increment in reflux illness among H. pylori positive children in America. Nevertheless, considering the differences in topographic distribution of gastritis and subsequent different pathologies (Blaser and Atherton, 2004), the report by Moon et al. (2009) did not necessarily contradict those of others.
Another possible benign consequence of H. pylori is protection against tuberculosis, as a study in W Africa indicated that persons with latent tubercular infections accept lower chances of re-activating their infections when they are H. pylori positive. This is attributed to the fact that H. pylori induces the release of IFN-y, an interferon that activates defenses against different types of infections including tuberculosis (Perry et al., 2010). Finally, H. pylori is proposed to play a positive role in trunk weight regulation: H. pylori positive persons produce reduced levels of ghrelin, a weight-regulating hormone that is produced for 60–lxxx% in the stomach. H. pylori eradication leads to an increased production of ghrelin and a subsequent increase in body weight (Nwokolo et al., 2003).
Correlation Between Nutrition and Lifestyle, and H. pylori Associated Pathology
There is evidence for a connection between H. pylori and dyspeptic symptoms (suffering from indigestion), equally it has been shown that the odds ratio of a person with dyspeptic symptoms being a carrier of H. pylori is higher than the H. pylori incidence in the full general population (Kidd et al., 1999b). Furthermore, H. pylori eradication leads to long-term cure in the majority of peptic ulcer patients, whereas the natural relapse charge per unit is 70% (Kate et al., 2013).
However, this statement is non a definite proof for a causal relationship between H. pylori and dyspepsia. It has been suggested that genetic predisposition and ecology factors such equally diet, smoking, age and the use of non-steroidal anti-inflammatory drugs (NSAIDs) can lead to high gastric acid production, which in turn can lead to gastric metaplasia and subsequent development of duodenal ulcers (Tovey, 2009; Kate et al., 2013). Similarly, the intake of iron supplements has been associated with gastric pathology through the consecration of oxidative stress (Naito et al., 1995; Fisher and Naughton, 2004). The positive correlation between H. pylori and dyspeptic symptoms is attributed to the fact that treatment of duodenal ulcer with acid-reducing medicine facilitates H. pylori colonization in the stomach. Hence, the cocky-reported high incidence of ulcers in Uganda might be partly a result of lifestyle and dietary habits of the local population.
The hypothesis that H. pylori colonization is a result rather than a crusade of ulcers, is supported by a retrospective case review of 208 persons, of which 37 were diagnosed with duodenal ulcers. A total number of 32 of the ulcer patients had been suffering from the ulcer for more vi months, and all 32 were found to be H. pylori positive. Just v patients suffered from ulcers less than half dozen months, but all five were found to be H. pylori negative (Boulos et al., 2002). Upon colonization, H. pylori might produce toxic substances that inhibit the natural healing of the ulcers, which explains why H. pylori eradication leads to highly increased chances of long-term cure of ulcers (Tovey, 2009; Kate et al., 2013).
Tovey (2009) emphasizes the role of dietary protective factors. Dietary fiber intake was one of the kickoff factors that was suspected to exist negatively associated with the incidence of ulcers. In an intervention study amid 42 culturally rice-eating subjects with a history of duodenal ulcers, 21 were changed to a predominantly unrefined wheat diet, whereas the remaining 21 continued the rice diet. Over a period of 5 years, 81% of the subjects in the rice-eating group reported ulcers, versus simply 14% in the wheat-eating group (Malhotra, 1978). In a Norwegian study, 73 subjects who recently healed from an ulcer (but by whom H. pylori was non necessarily eradicated) were assigned to either a high-fiber diet or a depression-fiber diet. After 6 months, ulcers had reoccurred in fourscore% of the subjects on the low-fiber diet, versus only in 45% of the subjects on high-fiber diet (Rydning et al., 1982).
A case–control written report in the Britain compared 78 subjects with duodenal ulcer with 156 matching control subjects (two matches for every ulcer subject). After decision-making for total calorie intake, it was constitute that sugar intake correlated positively and high vegetable fiber intake negatively with ulcers, whereas cereal fibers did not prove a specific correlation. After further controlling for smoking, social class and body weight, only the intake of refined sugar remained a significant factor that correlated with ulcer incidence (Katschinski et al., 1990).
From an anecdotal study on the incidence of peptic ulcers in sub-Saharan Africa, a correlation between areas with a high incidence of ulcers and high intake of starchy foods, such as bananas, cassava, sweetness potato, white wheat flour, white maize flour, and white rice has been suggested. This was opposed to regions with loftier intake of millet and home-pounded (unrefined) maize, where the incidence of ulcers was depression (Tovey, 2009). However, Tovey (2009) suggests that it is not the fiber from the unrefined cereal in itself, but rather the phospholipids, sterol esters, and sterol fractions of the lipid components from the cereal fiber fraction that exercises the protective action.
Other studies identified the plant-derived polyunsaturated fat acids lipid fraction, such as linoleic and linolenic acrid, to have inhibitory effects on H. pylori. In vitro studies with these components showed to cause cell decease to H. pylori past damaging the bacterial outer lipid membrane (Thompson et al., 1994). Besides, sure fat acids are precursors for prostaglandins which protect the gastric mucosa against injury through increased mucus secretion. Furthermore, arachidonic acrid has been shown to improve gastric claret vessel synthesis, thereby speeding up gastric healing processes (Hollander and Tarnawski, 1990).
Also in more dated review studies on the relationship between diet and duodenal ulcers Misciagna et al. (2000) concluded that there were potent indications for a negative correlation between duodenal ulcers and the intake of fiber, mainly soluble fiber from fruit and vegetables, and mayhap polyunsaturated fat-acids, vitamin A, and vitamin C. However, the study fabricated note of the overall poor quality from the studies that led to this determination.
Other studies suggest a correlation between intake of salt and gastric pathology, partly modulated through H. pylori, nigh commonly in the form of gastric cancer (Wang et al., 2009). Ulceration has also been mentioned as an consequence of high common salt intake (Kato et al., 1992), though another written report found no effect of common salt intake on gastric inflammation (Lee et al., 2014). An in vitro study suggested that salt induces expression of virulence factors in H. pylori (Xu et al., 2011), which provides a possible explanation for increased gastric pathology upon high salt intake.
The Probiotic LGG in H. pylori Eradication Therapy
One of the few other bacteria that can bide under the same gastric circumstances as H. pylori (Bezkorovainy, 2001), being resistant to acid and bile (Fernandez et al., 2003), is LGG and its generic variant LRY. The probiotic bacterium LGG is world's best documented probiotic bacterium, with many unique characteristics and reported health benefits (Segers and Lebeer, 2014). Especially to provide access to this bacterium for people in developing countries, the LRY has been incorporated in an affordable probiotic starter culture that enables local communities to make their own probiotic fermented food (Kort et al., 2015; Westerik et al., 2016). H. pylori can be inhibited in a dose dependent manner by LRY through several pathways, as discussed below, and hence may play a role in the reduction of H. pylori related gastric pathology in East Africa (Angol et al., 2017).
Currently, the standard method to eradicate H. pylori is a iii-component therapy treatment that combines acid suppression with two antibiotics for 1 calendar week. This method is also used in East Africa for those who tin afford it (Angol et al., 2017). However, H. pylori becomes increasingly resistant against this therapy, and the success rates are dropping below seventy% (Malfertheiner et al., 2012). Furthermore, the therapy typically has low patient compliance due to many side effects such equally diarrhea, nausea, vomiting, bloating, and abdominal hurting (Armuzzi et al., 2001a). The European Helicobacter Written report Grouping recently acknowledged that sure probiotics show promising results every bit an adjuvant handling in reducing side effects of the antibody therapy (Malfertheiner et al., 2012).
A summary of studies on the role of LGG in H. pylori eradication therapy can be plant in Table 2. All studies confirmed a beneficial outcome of LGG in reducing side effects of eradication therapy. Five studies with an average sample size of 70, showed no significant consequence on the H. pylori eradication rate. All the same, the sixth study with a sample size of 650 showed H. pylori eradication rates of 87% and 73% in the LGG-supplemented grouping and the control grouping, respectively.
Table 2. Summary of studies on the role of LGG in H. pylori eradication therapy.
Ulcer Prevention and Suppression by LGG
Apart from its role equally co-supplement during H. pylori eradication therapy, LGG has a direct inhibitory consequence on H. pylori and has the potential to directly preclude and reverse gastric pathology in Due east African populations. Accordingly, in a review of 13 clinical trials reporting on the activity of probiotics on H. pylori, Hamilton-Miller (2003) concludes that probiotics can reduce the severity of H. pylori induced pathology, just are not able to eradicate H. pylori completely. Three singled-out pathways in which LGG counteracts H. pylori-induced gastric pathology in the stomach and duodenum tin can be discriminated: (i) competition for bounden sites between LGG and H. pylori, (ii) attenuation of the host's H. pylori-induced apoptosis, inflammation responses and stimulation of angiogenesis, and (iii) production of anti-microbial substances such every bit lactic acid.
Competition for Binding Sites
In vitro pre-treatment of epithelial glandular cells (coca-2 cell culture) with 10seven cfu/ml LGG was found to inhibit subsequent adhesion past H. pylori with 53%, and at 109 cfu/ml LGG inhibited H. pylori with 66%. Competition for binding sites on the epithelial cells was cited every bit a probable crusade (Myllyluoma et al., 2008) (Figure 1), which appeared to be unrelated to adhesion capacity or organic acrid production. Note that binding alone is not a marking for anti-H. pylori activity (Peña and Versalovic, 2003; Myllyluoma et al., 2008).
Figure 1. Interactions of Lactobacillus rhamnosus GG or LRY (green) with Helicobacter pylori (carmine) and damaged epithelial cells at the gastric mucosal surface. (A) H. pylori upregulates TNF-α (Peña and Versalovic, 2003) and IL-8 (Myllyluoma et al., 2008; Rokka et al., 2008), which in plow upregulate gastrin-17 (Myllyluoma et al., 2007). H. pylori produces urease to reduce the pH in its immediate environment as means of survival (Chen et al., 2010). (B) Interactions under A are causing inflammation and apoptosis. (C) Gastric inflammation and apoptosis pb to ulceration. (D) LRY binds specifically at affected (mucosal) tissue due to change in microbiota and inflammatory markers (immunoglobulins and cytokines) and qualitative and quantitative changes in the fungus (Lam et al., 2007b). LRY upregulates COX-2 protein expression in damaged (ulcerated) stomachs (Jackson et al., 2000), which induces PGE2 modulated vascular endothelial growth factor (VEGF) expression, causing angiogenesis (Korhonen et al., 2004; Tamura et al., 2006; Lam et al., 2007b). LRY inhibits H pylori induced IL-eight (interleukin-8) release (Myllyluoma et al., 2008; Rokka et al., 2008) and TNF-α release (Peña and Versalovic, 2003; Kim et al., 2006). Through suppression of TNF-α and IL-8, H pylori induced elevated gastrin-17 levels are attenuated (Myllyluoma et al., 2007). (E) LRY inhibits H pylori adhesion (Myllyluoma et al., 2008), which appears to exist related to competition for binding sites (Peña and Versalovic, 2003; Myllyluoma et al., 2008). LRY activates Akt/protein kinase B, which is an anti-apoptotic signaling pathway (Yan and Polk, 2002). LRY blocks p38 MAP, which is a pro-apoptosis (cell survival) signaling pathway (Yan and Polk, 2002). LRY induces upregulation of ornithine decarboxylase (ODC) (enzyme essential in DNA stabilization and thus cell growth) and B-jail cell lymphoma two (Bcl-two) causing attenuation of apoptosis (Lam et al., 2007b). LRY shows antagonistic activity against H. pylori in vitro, possibly associated with lactic acid product (De Keersmaecker et al., 2006; Hütt et al., 2006). Lactic acid increases the cell wand permeability of H. pylori. As well, product of exopolysaccharide (Allonsius et al., 2017), lectin (Petrova et al., 2016), and/or peptides with antimicrobial activity (Lu et al., 2009) by LRY has been shown to inhibit other pathogenic bacteria, however, this result has not been shown for H. pylori specifically. LRY inhibits urease activeness of H. pylori (Chen et al., 2010). (F) LRY upregulates COX-1 (cyclooxygenase-1) poly peptide expression (Jackson et al., 2000; Lam et al., 2007a) in normal stomachs (ulcer prevention), which increases PGE2, which in turn protects mucus cells and increases trans mucosal resistance, thereby protecting mucosal cells from apoptosis (Jackson et al., 2000; Lam et al., 2007a). LRY upregulates the expression of MUC3 and MUC6 mucin gene, causing meaning increase in thickness of the basal mucus layer (Mack et al., 2003; Lam et al., 2007a). (G) LRY causes upregulation of phosphorylation level of epidermal growth factor receptor (EGF receptor), leading to cell proliferation and angiogenesis and suppresses cell apoptosis (Lam et al., 2007b). LRY initially improves epithelial (mucosal) barrier function (Gotteland et al., 2001; Myllyluoma et al., 2008) but increases H. pylori induced bulwark deterioration after incubation for 24–42 h, hence causes delayed cell membrane impairment and leakage (Myllyluoma et al., 2008).
Secondly, a written report on mice found that during a pre-treatment with a combination of the probiotic leaner L. acidophilus R0052 and 50. rhamnosus R0011 and subsequent administration of H. pylori, colonization was reduced from 100% in the control group to 50% in the probiotic pre-treated group (Johnson-Henry et al., 2004). Note that this effect has non been proven for LGG specifically.
In a 3rd study, a decrease in H. pylori of 27% was measured in a probiotic intervention amidst 13 Finnish H. pylori positive subjects, based on the well accepted 13C-Urea Breath Examination, which values were an indirect indicator of H. pylori density in gastric mucosa. The subjects daily consumed a drink with 4 probiotic strains, including LGG, with each of the strains in a concentration of 2.five × 109 cfu, for the duration of 56 days, for the duration of 56 days (Myllyluoma et al., 2007).
Upon the formation of an ulcer, probably regardless of the causative factor of the ulceration, a spectrum of bacteria other than H. pylori has been institute to colonize the ulcer surface and to subsequently impair ulcer healing (Elliott et al., 1998). This has been attributed to a local increase of the pH around the ulcer surface, assuasive for strongly increased bacterial growth equally compared to normal stomach tissue. The aforementioned study institute that antibiotic treatment, preferably with a mixture of different antibiotics, increased ulcer healing. Secondly, promotion of lactic acid bacteria (not-specified) in the breadbasket competed with outgrowth of other possibly harmful leaner, and increased the rate of ulcer healing. Other studies have indicated specifically the suppressing effect of LGG on several pathogens (Rinkinen et al., 2003; Hütt et al., 2006) and its site-specific binding to damaged tissue (Ouwehand et al., 2003).
Modulation of Immune Responses
LGG has shown to modulate local allowed responses upon colonization with H. pylori or ulceration through the pathways every bit summarized in Figure 1.
In vitro pre-handling of epithelial glandular cells (coca-2 cell culture) with x7 cfu/ml LGG was shown to annul acute H. pylori jail cell membrane leakage by initially tightening the barrier function (Gotteland et al., 2001; Myllyluoma et al., 2008). Even so, over time H. pylori induced barrier deterioration after incubation for 24–42 h, causing delayed cell membrane impairment and leakage (Myllyluoma et al., 2008).
H. pylori upregulates TNF-α (Peña and Versalovic, 2003) and IL-8 (Myllyluoma et al., 2008; Rokka et al., 2008), which in turn upregulate gastrin-17. IL-8 is a chemokine which induces inflammation (Rokka et al., 2008) and TNF-α is a cytokine which induces apoptosis (Peña and Versalovic, 2003). Gastric inflammation and apoptosis lead to ulceration. Gastrin-17 has been associated with gastric cancer (Myllyluoma et al., 2007). LGG inhibits H pylori induced IL-8 (interleukin-viii) release (Myllyluoma et al., 2008; Rokka et al., 2008) and TNF-α release (Peña and Versalovic, 2003; Kim et al., 2006), although information technology must be noted that another in vitro report (Zhang et al., 2005) showed that high doses of LGG (1010 cfu) tin increment IL-8 production in the absence of H. pylori. Through suppression of TNF-α and IL-8, H pylori induced elevated gastrin-17 levels were attenuated (Myllyluoma et al., 2007). A decrease in the hormone gastrin-17 levels was measured in subjects who daily consumed a drink with iv probiotic strains including LGG. This report concluded that gastrin-17 could exist seen as a maker for non-atrophic gastritis, that probiotics tin have a moderate positive influence on non-atrophic gastritis (Myllyluoma et al., 2007).
Autonomously from H. pylori, alcohol has been associated with gastric mucosal damage, and alcoholism tin exist another cause of peptic ulcers. Rats pre-treated with LGG for 3 days responded to the assistants of ethanol in a dose-dependent manner: ane h after administering ten ml/kg bodyweight of 60% 5/5 ethanol, the ii × 108 cfu/24-hour interval pre-treated group did not show any difference, while in the 2 × x9 cfu/day grouping showed 45% smaller gastric lesions as compared to the control group (Lam et al., 2007a). The study concluded that LGG significantly increases the mucosal layer and mucosal integrity (trans mucosal resistance) through upregulated expression of MUC3 (Mack et al., 2003) and MUC6 mucin genes, thereby counteracting the effects that ethanol normally has on the mucus layer (Lam et al., 2007a). Nevertheless, LGG regulates COX-ane (cyclooxygenase-1) protein expression (Jackson et al., 2000; Lam et al., 2007a) in normal stomachs, which increases PGE2, which protects mucus cells and increases trans mucosal resistance, thereby protecting mucosal cells from apoptosis (Jackson et al., 2000; Lam et al., 2007a) and reducing chances of ulceration.
In a subsequent report of Lam et al. (2007b), ulcers were induced by luminal application of acetic acid solution, and LGG was administered in the same manner as described for the previous study, but this time after the ulcer-induction. LGG supplementation had no obvious effects in the control grouping, but for the ulcer-induced group the larger dose at 109 cfu/day induced enhanced cell proliferation of 54%, increased blood vessels generation (angiogenesis) past 41% at the ulcer margins and reduced cell expiry (apoptosis) by 33%, thereby obtaining significantly reduction of gastric ulcer area past 32% after 3 days of LGG administration. These furnishings were found to be modulated firstly past the upregulation of phosphorylation level of epidermal growth factor receptor (EGF receptor) causing angiogenesis, cell proliferation and attenuation of apoptosis. Secondly, COX-ii protein expression was upregulated, which induces PGE2 modulated vascular endothelial growth factor (VEGF) expression, causing angiogenesis (Korhonen et al., 2004; Tamura et al., 2006; Lam et al., 2007b). Thirdly, LGG upregulates ornithine decarboxylase (ODC) (enzyme essential in Deoxyribonucleic acid stabilization and thus cell growth) and B-cell lymphoma 2 (Bcl-ii), thereby causing attenuation of apoptosis (Lam et al., 2007b). The healing continued upon administration of LRY for more days. The report concludes that LGG does not affect the normal gastric mucosa, only normalizes gastric mucosa that is contradistinct by events such as ulcers. LGG has shown to bind specifically at affected (mucosal) tissue due to a alter in microbiota and inflammatory markers (immunoglobulins and cytokines) and qualitative and quantitative changes in the mucus. The study has not shown whether it is the live LGG, its metabolites, its cell wall components or other results of gene expression that exert the healing properties of the organism (Lam et al., 2007b).
Similarly, in an intervention among 16 human subjects, a 5-day pre-handling with a probiotic dairy product containing among others ii.iv × 109 cfu LGG per twenty-four hours, has been proven to stabilize the abdominal barrier part against increased permeability normally induced by NSAIDs past 77%, thereby preventing the alterations from futurity pathology such as ulcers (Gotteland et al., 2001). Heat-killed LGG did not bear witness protective effects. Interestingly, a study past Kamil et al. (2007) on ulceration in the small intestine of rats every bit induced by NSAIDs, found that although LGG increased cell proliferation and reduced jail cell apoptosis, it all the same aggravated the NSAID induced ulcer size, maybe through increased inflammation.
Other pathways include the activation of Akt/protein kinase B by LGG, which is an anti-apoptotic signaling pathway (Yan and Polk, 2002). Secondly, LGG blocks p38 MAP, which is a pro-apoptosis (cell survival) signaling pathway (Yan and Polk, 2002). Lastly, H. pylori produces urease to reduce the pH in its immediate environment as means of survival, which is inhibited past LGG (Chen et al., 2010), thereby reducing its chances for survival.
The Probiotic LGG Produces Antimicrobial Substances Against H. pylori
Antagonistic activity against H. pylori in vitro has been associated with lactic acid product (De Keersmaecker et al., 2006; Hütt et al., 2006; Segers and Lebeer, 2014) and to a bottom extent with the production of other short-chain fatty acids (SCFAs) (Gotteland et al., 2006). Lactic acrid increases the cell wall permeability of H. pylori (Effigy 1). Besides, production of exopolysaccharide (Allonsius et al., 2017), lectin (Petrova et al., 2016), and/or peptides with antimicrobial activity (Lu et al., 2009) by LGG has been shown to inhibit other pathogenic leaner, however, this effect has not been shown for H. pylori specifically. A summary of studies on the effect of LGG on H. pylori and gastric pathology can exist institute in Table 3.
Tabular array 3. Summary of studies on the issue of LGG on H. pylori and gastric pathology.
A Sustainable Nutritional Intervention in East Africa – the Case Written report of Uganda
The absence of dietary protective factors in the traditional starch-based nutrition in Uganda which mainly consists of bananas, roots and refined cereals, might exist a major cistron causing the high incidence of ulcers in this land. In rural Uganda, when 1 experiences deadening, precipitous or burning pain in the upper abdomen that might indicates dyspepsia, subsequent self-medication with unproblematic and cheap acid suppressors (magnesium trisilicate) is the common practice. Many clinics lack whatsoever form of diagnostic equipment and volition diagnose ulcers based on description of symptoms only, and subsequently mainly prescribe acid suppressors, though other medicine like histamine antagonists (H2 blockers) and proton-pump inhibitors that suppress acrid secretion are also common. The frequent advice is to not utilize NSAIDs, spices, cigarettes, alcohol or carbonated drinks. Some clinics can perform serum-claret examination to observe the presence of H. pylori antibodies. Only the minority of the population that enjoys a better economical status might visit individual clinics that tin can perform endoscopy, and might opt for the more expensive eradication therapy. In its clinical guidelines, the Uganda ministry of wellness advises to primarily treat ulcers with acid suppressors and encourages regular, minor and frequent meals, likewise as the consumption of milk (Ministry of Health, 2010).
Kort and Sybesma (2012) and Kort et al. (2015) described an intervention with the generic variant of LGG, in grade of an LRY containing yogurt potable, which is locally produced (Westerik et al., 2016) and subsequently consumed past resources-poor communities in rural Uganda. We propose such an intervention as a preferred selection to convalesce the burden of H. pylori induced pathology in resource poor communities. Blaser and Atherton (2004) mentioned that a beneficial function of H. pylori colonization is the reduction of childhood diarrhea. However, when H. pylori is in part replaced by LRY, this beneficial function of H. pylori might not be lost: LRY has the proven power to reduce certain types diarrhea (De Roos and Katan, 2000; Szajewska et al., 2007; Allen et al., 2010; Guandalini, 2011; Guarino et al., 2015), but without the adverse risks that are associated with H. pylori colonization. The local product of probiotic fermented foods tin can be extended to cereal fermentations, most chiefly as a variation on the already popular fermented millet beverage (obushera) for the case of Uganda (Westerik et al., 2016). As it has been suggested that cereal fibers provide boosted protection confronting gastric pathology (Malhotra, 1978; Tovey, 2009), this high-fiber drink may exhibit dual protective activity against ulcer formation.
Conclusion
Studies on the incidence of H pylori in East Africa showed widely varying outcomes, ranging between 25 and 87% in various population groups, perchance due to dissimilar detection methods used, or differences in study population. Pathology upon H. pylori colonization is modulated by several factors including the presence of virulence factors in the H. pylori strain, the 'ethnic' origin of the strain, and the specific immune responses of the host. Autonomously from H. pylori colonization, gastric pathology including ulceration is also affected by lifestyle factors, including nutrition. The right dietary factors have been shown to straight inhibit H. pylori too equally reduce H. pylori induced pathology.
It is expected that administering probiotic yogurt to children in developing countries from early on childhood can reduce the incidence of H. pylori colonization in the general population. Besides prevention of H. pylori, LGG or its generic variant LRY may present an approach to establish and manage a harmless relationship between the host and H. pylori when the latter one is already present, counteracting the need for H. pylori eradication therapy. This alternative arroyo is cheaper and does not carry the gamble of extensive antibody resistance (Michetti, 2001), and is feasible to be implemented sustainably through locally produced yogurt containing LRY.
Information technology should be noted that major changes in diet might play an equally of import role in the prevention and save of gastric pathology. In Uganda, locally available foods with protective factors include unrefined wheat, unrefined maize, unrefined rice, millet, soy beans, total-cream milk, spinach, and cabbage (Tovey, 2009). However, consumption of these products would require education of the population and a modify in mental attitude, since even the rural population as a rule brings produced cereals to an electric manufacturing plant, in which the bran is separated from the cereal and subsequently the bran fraction is being used solely for animate being feeds. An intervention with the mentioned locally produced yogurt could capture the dietary protective benefits of milk as well equally the those of LRY.
Writer Contributions
NW reviewed the cited literature and drafted the manuscript under guidance of RK. WS, GR, and RK critically read and corrected the draft versions of the commodity.
Funding
Funding for this written report was provided by the Yoba for Life Foundation, Amsterdam, Netherlands.
Conflict of Interest Statement
RK and WS are co-founders of the Yoba for Life Foundation (2009), a non-profit organization, accredited past the Dutch Taxation Authorities as a Public Benevolent Institution (PBI), which aims to promote local production and consumption of fermented products in Africa. NW is the Land Coordinator of the Yoba for Life Foundation in Uganda. African fermented products fabricated with the Yoba starter civilisation, are non marketed by the foundation as such, but the Yoba for Life Foundation stimulates local production and ownership, allowing income-generating activities for African small entrepreneurs in the nutrient sector. The Yoba for Life Foundation distributes and sells ready-to-use sachets with dried bacterial starter cultures at cost cost, through a network of partners and volunteers to facilitate the local production of dairy and cereal-based products past controlled bacterial fermentation. The Yoba starter culture contains Lactobacillus rhamnosus yoba 2012, which is a generic variant of Lactobacillus rhamnosus GG.
The remaining author declares that the research was conducted in the absence of whatsoever commercial or fiscal relationships that could be construed equally a potential conflict of interest.
Acknowledgments
We acknowledge all the minor probiotic yogurt producers who may contribute to the consolation of Helicobacter pylori-associated gastric pathology in East Africa.
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