Total Load of the Intestinal Bacteria

According to Madsen et al. (72), when IL-10 gene-deficient mice are raised under germ-free conditions the mucosal production of IFN-y and TNF-a is within normal range, while both cytokines are up-regulated under normal conditions. This observation suggests that colitis in I L -10 gene-deficient mice occurs as a consequence of Th1-driven response to normal mucosal microflora. Treatment of both control and I L -10 gene-deficient mice with VSL3 decreased IFN-y and TNF-a secretion and substantially increased the total load of probiotics in the colon in both groups. The observed reduction in proinflammatory cytokine secretion indicates that the intestine is able to discriminate and define selective responses to different nonpathogenic strains of bacteria.

These findings are similar to those by Haller et al. (73), who showed that intestinal epithelial cells are able to differentiate between commensal nonpathogenic bacteria and deliver distinct cytokine responses to underlying immune cells in vitro. In their study they co-cultured enterocyte-like CaCO-2 cells with human blood leukocytes in separate compartments of transwell cultures to determine whether nonpathogenic bacteria can modify the immune response of the intestinal epithelium. Haller et al. (73) stimulated CaCO-2 and peripheral blood mononuclear cells in (PBMC) co-cultures with nonpathogenic bacteria and enteropathogenic E. coli. TNF-a, IL-1~, IL-8, monocyte chemoattracting protein 1 (MCP-1), and IL-10 were studied by enzyme-linked immunosor­bent assays (cytokine secretion) and by semiquan­titative reverse transcription-polymerase chain re­action.

The results showed that the challenge of CaCO-2 cells with nonpathogenic E. coli and Lactobacillus sakei induced the expression of IL-8, monocyte chemoattractant protein-1 (MCP-1), IL­1~, and TNF-a mRNA in the presence of underlying leukocytes. Leukocyte sensitized CaCO-2 cells produced TNF-a and IL-1~, whereas IL-10 was ex­clusively secreted by human peripheral blood mononuclear cells. CaCO-2 cells alone remained hypo responsive to the bacterial challenge. Lacto­bacillus johnsonii, an intestinal isolate, showed reduced potential to induce proinflammatory cytokines but increased TGF-~ mRNA in leukocyte sensitized CaCO-2 cells. TNF-a was identified as one of the early mediators involved in cellular crosstalk. In the presence of leukocytes, discriminative activation of CaCO-2 cells was observed between enteropathogenic E. coli and nonpathogenic bacteria.

It was concluded that the differential recognition of nonpathogenic bacteria by CaCO-2 cells required the presence of underlying leukocytes. These results strengthened the hypothesis that bacterial signaling at the mucosal surface depends on a network of cellular interactions (73).

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