A proposal model: mechanisms of immunomodulation induced by probiotic bacteria. Review.

GALDEANO, C.; DE MORENO DE LEBLANC, A.; VINDEROLA, G.; BIBAS BONET, M.E.; PERDIGÓN, G.

CLINICAL AND VACCINE IMMUNOLOGY

American Society for Microbiology

Año: 2007 vol. 14 p. 485 - 492

1556-6811

The mammalian microbiota comprises several hundred differentbacterial species, many of which have a beneficial effecton the host. For example, they are involved in preventingcolonization of the gut by pathogens and maintaining the gutmucosal immunity (85). The gut microbiota is more abundantin the large intestine of mammals, with densities rising to over1011 organisms/g intestinal content (84, 86). The number ofbacterial cells in the entire gut exceeds the number of eukaryoticcells in the host, but under normal circumstance theycoexist without any adverse effect on the host. The influence ofthe resident microflora on mucosal immune function and guthealth has become an area of scientific and clinical importance(22, 26). There is an active dialogue between the commensalmicroorganisms and the host mucosal immune system (21, 48).This cross talk elicits different host responses to commensaland pathogenic bacteria. Commensal bacteria may even sharemolecular patterns recognized by toll-like receptors (TLRs),which can recognize patterns associated mainly with pathogens.However, the mucosal immune system of the healthyintestine allows the persistence of this microbiota associatedwith the intestine and avoids immunological tolerance, maintainingthe intestinal homeostasis. Now, there is acceptance ofthe concept that oral tolerance is not generated by commensalintestinal bacteria; the host would ignore or fail to recognizethe presence of indigenous microorganisms (49). The healthyhost is able to elicit a good mucosal immune response againstluminal antigens and to maintain a “physiological state of inflammation”in the gut, but it is also capable of responding toinvading commensal organisms or pathogens. In the healthyhost the penetration of the commensal bacteria is usually preventedby the barrier afforded by the intestinal epithelium andthe immune cells associated with the mucosa, which are highlyadapted to the presence of the normal microbiota (71). Thesignals sent by these microorganisms prevent their penetrationand keep them outside the intestinal tissue. If the commensalmicroorganisms invade the host tissues, the innate immunemechanisms contribute to their rapid clearance, but whenpathogens enter the intestine, innate and adaptive mechanismsare coordinately stimulated to respond to the danger signals(38, 60). Although mucosal epithelial tissues form an efficientbarrier that prevents the entrance of the environmental pathogensand the external antigens into the host internal milieu,mucosal tissues represent the main sites of infection by pathogens.Many attempts have been made to understand the gutimmunomodulation by pathogenic bacteria but not the mechanismsinvolved in the modulation of the gut immune systemby commensal bacteria and by nonpathogenic microorganismspresent in many foods included in the daily diet.