Lactobacillus plantarum inhibits the intestinal epithelial migration of neutrophils induced by enteropathogenic Escherichia coli
ABSTRACT Lactobacillus plantarum is a Gram-positive bacillus known for its effect as a probiotic agent. The goal of the study was to determine whether L. plantarum is capable of inhibiting the transepithelial neutrophil migration induced by enteropathogenic Escherichia coli (EPEC).
Cultured intestinal epithelial T-84 cell monolayers were rapidly infected with EPEC. L. plantarum or culture supernatants were added to the monolayers before and after the infection. Indium-labeled neutrophils were added to the basolateral side of inverted monolayers. After 150-minute incubation, radioactivity of the neutrophils that migrated in the physiologic direction was assayed, and the number of migrating neutrophils was calculated. L. plantarum was also added to the monolayers before and after EPEC infection, and the number of adherent EPEC was determined by plate counting.
EPEC-induced neutrophil migration and EPEC binding to monolayers were inhibited by viable L. plantarum but only when added to the monolayers before EPEC. Culture supernatants failed to inhibit the neutrophil migration.
These results suggest that L. plantarum is beneficial in inhibiting neutrophil migration induced by EPEC, but only when preincubated with host epithelia. Rather than an indirect effect through a secreted substance produced by the probiotic agent, its effect is direct and requires the presence of the bacterium.
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- "Thus, the prevention of excessive neutrophil recruitment may represent a tool to counteract the development of pathogen-induced inflammatory reactions. A reduction of inflammatory cell infiltration by certain lactobacilli and bifidobacteria in chemically or pathogen-induced intestinal inflammation has been reported (Hidemura et al. 2003; Michail & Abernathy, 2003; Peran et al. 2005). However, it is not clear whether the regulation of inflammatory cell migration is a common effect of probiotics . "
ABSTRACT: Probiotic bacteria may provide protection against intestinal damage induced by pathogens, but the underlying mechanisms are still largely unknown. We investigated whether Bifidobacterium animalis MB5 and Lactobacillus rhamnosus GG (LGG) protected intestinal Caco-2 cells from the inflammation-associated response induced by enterotoxigenic Escherichia coli (ETEC) K88, by inhibiting pathogen attachment to the cells, which is the first step of ETEC pathogenicity, and regulating neutrophil recruitment, a crucial component of inflammation. A partial reduction of ETEC adhesion was exerted by probiotics and their culture supernatant fractions either undigested or digested with proteases. ETEC viability was unaffected by the presence of B. animalis, LGG or their supernatant fractions in the culture medium, indicating an absence of probiotic bactericidal activity. Probiotics and their supernatant fractions, either undigested or digested with proteases, strongly inhibited the neutrophil transmigration caused by ETEC. Both B. animalis and LGG counteracted the pathogen-induced up regulation of IL-8, growth-related oncogene-alpha and epithelial neutrophil-activating peptide-78 gene expression, which are chemokines essential for neutrophil migration. Moreover, the probiotics prevented the ETEC-induced increased expression of IL-1beta and TNF-alpha and decrease of transforming growth factor-alpha, which are regulators of chemokine expression. These results indicate that B. animalis MB5 and LGG protect intestinal cells from the inflammation-associated response caused by ETEC K88 by partly reducing pathogen adhesion and by counteracting neutrophil migration, probably through the regulation of chemokine and cytokine expression.British Journal Of Nutrition 07/2006; 95(6):1177-84. DOI:10.1079/BJN20051681 · 3.34 Impact Factor
Article: Antibioticoterapia con probióticos
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ABSTRACT: Using microorganisms to influence positively the course of an illness caused by injurious microorganisms is an approach with mounting clinical evidence showing efficacy. Whereas antibiotics will remain an important therapeutic option, there are limitations and problems to their increasing and chronic usage, and probiotics offer a strategy to reduce antibiotic usage. Increasingly, it has become clear that the mechanisms whereby probiotics can impact in intestinal diseases involve a large repertoire of responses. This review summarizes recent findings on how probiotics may effect benefit through interactions with host eukaryotic cells. Limiting the access of microbes associated with the development of disease to host mucosal surfaces and altering the responses of host to microbial insults are potential mechanisms whereby probiotics can influence the pathogenesis of disease. Evidence is accumulating that live, viable probiotic organisms diminish accessibility to intestinal epithelial cell; however, the mucosal exclusion is not through direct blockage of shared epithelial receptors between probiotic microbes and pathogenic organisms. Modulation of mucosal defenses such as innate protective mechanisms, enhanced epithelial cell survival, and immune responses have all been shown to have potential in aiding in these actions. Intestinal epithelial cell adherence influences response and, as such, appears to be necessary but may not be wholly sufficient, because soluble bacterial factors have been reported to effect modulation of immune and nonimmune responses of eukaryotic cells. There is a considerable repertoire of responses potentially responsible for the effects of probiotics, and these responses appear to involve a complex interplay between the microbes of the intestinal tract and the cells of the host. Continued work can be expected to further the understanding of the mechanisms involved, and more work is needed to determine the relative clinical importance of each of the phenomena. These studies are expected to help direct the most efficacious use of probiotics for inflammatory conditions arising from the intestinal tract.Current Opinion in Gastroenterology 02/2004; 20(1):22-6. DOI:10.1097/00001574-200401000-00006 · 3.66 Impact Factor