AUP de los Sectores Populares: Una Práctica Incompatible con el

Lactic acid bacteria (LAB) ar

beverages and contribute both to the sensory qualities

e. Moreover, they are present in large numbers in the normal human and animal gastrointestinal flora (Sgouras et al., 2004).

Prebiotics have been used in conjunction with probiotics to aid their survival and action. Several carbohydrate derivatives such as oli

eral have ‘bifidogenic’ activity when tested under in vitro conditions in a gut model. Oligosaccharides can be designed with specific linkages and different degrees of polymerization which are resistant to digestion by human luminal enzymes (Olano-martin et al., 2000). Presently there is an attempt to develop ‘synbiotics’, i.e. products containing both probiotics and targeted prebiotics as a therapeutic agent for treatment of several gastrointestinal diseases. Although prebiotics have not been speciafically designed for treating H. pylori, they are useful in enhancing the chances of survival and the viability of probiotic organisms. There is a possibility to design oligosaccharides that mimic H. pylori attachment to the gastric cells, and thus may be used to compete for attachment sites on the gastric membrane.

Health benefits of probiotic organisms include their ability to relieve symptoms of lactose intolerance (De verse et al., 1992), immunomodulation, chole

Chapter 1 ______________________________________________________________________________ 81 treatme

erapy. Wang et al., ctobacillus- and Bifidobacterium-containing nt of diarrhoea (Guandilini et al., 2000) to name a few. Many mechanisms have been postulated to explain how probiotics enhance intestinal health, including competition for limited nutrients, inhibition of epithelial and mucosal adherence of pathogens, inhibition of epithelial invasion by pathogens, the production of antimicrobial substances and/or stimulation of mucosal immunity (Servin and Coconnier, 2003). Although probiotics have proven to be a promising treatment, controlled clinical trials are necessary to validate the benefit of probiotics (O’sullivan et al., 2005). Probiotics are known to adhere to the intestinal cells and even gastric cells, but often it is not clear whether the probiotic organisms actually colonize the gastrointestinal tract, as they are not recovered from the faeces once the probiotic therapy is discontinued.

1.8.2.1 Effect of probiotics organisms on H. pylori

Several authors have studied the inhibitory effect of probiotic organisms on H. pylori, with the aim to develop an alternative treatment to the current antibiotic th

(2004) studied the effect of consumption of La

yoghurt in subjects positive for H. pylori infection and concluded that regular intake of yoghurt containing these organisms can effectively suppress H. pylori infection in humans. Lactobacillus acidophilus (johnsonii) La1 culture supernatant was shown to be inhibitory in vitro and in vivo against H. pylori infection in humans (Michetti at al., 1999). In vitro inhibitory activity against several strains of H. pylori was observed in the presence of viable L. casei strain Shirota cells, and a significant reduction in the levels of H. pylori colonization was observed in the antrum and body mucosa in vivo when treated with L. casei strain Shirota (Sgouras et al., 2004). L. gasseri OLL2716 in ingested yogurt was determined to be effective in both suppressing H. pylori infection in human subjects, as well as reducing gastric mucosal inflammation (Sakamoto et al., 2001). Treatment of H. pylori by the oral administration of L. salivarius in a gnotobiotic murine model was attributed to the high levels of lactic acid produced by the probiotic which mediated

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that probiotic supplementation reduced the side-effects and permitted a slight improv

the suppression of colonization (Aiba et al., 1998). Armuzzi et al., (2001) investigated the effect of administering L. GG in conjunction with the standard triple therapy to minimize the associated gastrointestinal side effects, and observed improved treatment tolerability as well as a significant reduction in the side effects experienced. It has been reported that L. reuteri strains share glycolipid specificity with H. pylori and can therefore inhibit binding of the pathogen to the glycolipid receptors (Mukai et al., 2002). The MUC5AC glycoprotein has been identified as the primary receptor for H. pylori in the human stomach (Van de bovenkamp et al., 2003). L. reuteri and L. paracasei demonstrated probiotic properties by direct modulation of the mucosal inflammatory response in a H. hepaticus- challenged IL-10 deficient murine colitis model (Pena et al., 2005).

Tursi et al. (2004) studied the effect of 1- day quadruple therapy with L. casei subsp. casei DG, administered to patients who had failed the first attempt at eradication of H. pylori. They reported

ement in eradicating H. pylori. Pretreatment of mice with L. rhamnosus (R0011) and L. acidophilus (R0052) helped reduce the numbers of colonizing H. pylori as well as the bacterial- induced inflammation in mice, but did not prevent H. pylori induced apoptosis in the gastric mucosa (Johnson-Henry et al., 2004). High oral doses of L. brevis proved to be ineffective in eradicating H. pylori from the stomach of H. pylori-positive patients, but did reduce the intragastric bacterial load. The authors concluded that L. brevis has an enzyme, arginine deiminase, which may alter the polyamine metabolism leading to a reduction in colonization by H. pylori (Linsalata et al., 2004). A lyophilized and inactivated culture supplement of L. acidophilus increased the eradication rates of a standard triple anti-H. pylori therapy in a randomized human trial (Canducci et al., 2000). In another study, patients positive for H. pylori were fed yogurt containing lactobacilli and bifidobacteria, in conjunction with the regular triple

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omi et al. (2000) elucidated the mechanism of lactic acid on

therapy. Not only were higher eradication rates seen, but there was a restoration of depletion of the bifidobacteria after triple therapy (Sheu et al., 2002). Similarly, L. casei Shirota, and L. acidophilus are able to inhibit the growth of H. pylori. In an intervention study, 14 patients infected with H. pylori received L. casei Shirota (2 × 1010 cfu/day) fermented milk for 6 weeks. H. pylori bacterial load was assessed by the breath urea test. Ureolytic activity was reduced in 64% of the patients that consumed fermented products, compared to 33% of the control group (Cats et al., 2003). Recently there has been an attempt to characterize the substance(s) produced by probiotics that is inhibitory to H. pylori.

Lactic acid is a well known antimicrobial agent, and works by lowering the pH to a value inhibitory to most microorganisms. It is produced by several lactic acid bacteria and that may account for the inhibitory activity seen. Alak

Gram negative organisms, and found that lactic acid disrupts the outer membrane (lipopolysaccharide layer) in these organisms, thus making it susceptible to detergents or lysozyme. Suppression of H. pylori by L. salivarius has been attributed to high levels of lactic acid produced by the lactobacilli (Sakamoto et al., 2001). Other metabolites produced by probiotics, which are known to kill H. pylori in vitro include formate and sodium acetate, along with lactic acid (Oh et al., 2002). Midolo et al. (1995) concluded that the effect of lactic acid on H. pylori is dependent on both pH and concentration. They also found other acids such as hydrochloric and acetic acids to be significantly less inhibitory. A very interesting study involving screening 17 strains of lactobacilli against 10 strains of H. pylori revealed that the inhibition was related to acid production and lowering of the pH. A specific strain, L. acidophilus CRL 639, showed autolytic behaviour and the bactericidal effect was attributed to a proteinaceous substance released by the lysed cells (Lorca et al., 2001). L. salivarius WB 1004

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a nonamicoumacin antibio

inhibited the attachment of H. pylori to murine and gastric epithelial cells and reduced interleukin-8 (IL-8) release in vitro. Interestingly, the ingestion of the probiotics helped eliminate colonization by H. pylori in the infected murine model (Kabir et al., 1997).

Some probiotic, non-lactic strains such as Weissella confusa produce a class II, nonproteinaceous material which is active against H. pylori (Nam et al., 2002). Similarly, Bacillus subtilis produces antibiotics, identified as amicoumacin A and

tic against H. pylori in vitro (Pinchuk et al., 2001). Probiotics also compete for adhesive or binding sites on the gastric membrane, thus preventing mucosal adhesion by Helicobacter. L. reuteri, W. confusa, L. casei rhamnosus and many other bacteria have competitively inhibited binding of H. pylori thus displaying antimicrobial behaviour. Bacillus clausii was administered to symptom-free H. pylori positive patients, in a randomized, double-blind, placebo controlled trial. B. clausii reduced the common side-effects associated with anti- H. pylori antibiotic therapy (Nista et al., 2004). Presented in Table 1.21 is a listing of strains of probiotic bacteria used in treatment of Helicobacter pylori infection.

Chapter 1 ______________________________________________________________________________ 85 Table 1.21 Probiotic cultures used to treat Helicobacter pylori infection

Strains Author and Year