Commensalism

Commensalism is a long-term biological interaction (symbiosis) in which members of one species gain benefits while those of the other species neither benefit nor are harmed. This is in contrast with mutualism, in which both organisms benefit from each other; amensalism, where one is harmed while the other is unaffected; parasitism, where one is harmed and the other benefits, and parasitoidism, which is similar to parasitism but the parasitoid has a free-living state and instead of just harming its host, it eventually ends up killing it. The commensal (the species that benefits from the association) may obtain nutrients, shelter, support, or locomotion from the host species, which is substantially unaffected. The commensal relation is often between a larger host and a smaller commensal; the host organism is unmodified, whereas the commensal species may show great structural adaptation consistent with its habits, as in the remoras that ride attached to sharks and

Dysregulation of Allergic Airway Inflammation in the Absence of Microbial Colonization

Nicola Harris, Tina Herbst, Benjamin John Marsland

RATIONALE: The incidence of allergic disorders is increasing in developed countries and has been associated with reduced exposure to microbes and alterations in the commensal bacterial flora. OBJECTIVES: To ascertain the relevance of commensal bacteria upon the development of an allergic response, we utilized a model of allergic airway inflammation in germ-free (GF) mice that lack any exposure to pathogenic or non-pathogenic microorganisms. METHODS: Allergic airway inflammation was induced in GF, specific pathogen free (SPF) or recolonized mice by sensitization and challenge with ovalbumin (OVA). The resulting cellular infiltrate and cytokine production were measured. MEASUREMENTS AND MAIN RESULTS: Our results show that the total number of infiltrating lymphocytes and eosinophils were elevated in the airways of allergic GF mice as compared to control SPF mice, and that this increase could be reversed by re-colonization of GF mice with the complex commensal flora of SPF mice. Exaggerated airway eosinophilia correlated with increased local production of Th2 associated cytokines, elevated IgE production and an altered number and phenotype of conventional dendritic cells (cDC). Regulatory T cell populations and regulatory cytokine levels were unaltered but GF mice exhibited an increased number of basophils and decreased numbers of alveolar macrophages (AM) and plasmacytoid dendritic cells (pDC). CONCLUSIONS: These data demonstrate that the presence of commensal bacteria is critical for ensuring normal cellular maturation, recruitment and control of allergic airway inflammation.

2011

Functional intestinal bile acid 7-alpha-dehydroxylation by Clostridium scindens associated with protection from C. difficile infection in a gnotobiotic mouse model

Rizlan Bernier-Latmani, Lyne Desharnais, Laure Menin

Bile acids, important mediators of lipid absorption, also act as hormone-like regulators and as antimicrobial molecules. In all these functions their potency is modulated by a variety of chemical modifications catalyzed by bacteria of the healthy gut microbiota, generating a complex variety of secondary bile acids. Intestinal commensal organisms are well adapted to normal concentrations of bile acids in the gut. In contrast, physiological concentrations of the various intestinal bile acid species play an important role in the resistance to intestinal colonization by pathogens such as Clostridium difficile. Antibiotic therapy can perturb the gut microbiota and thereby impair the production of protective secondary bile acids. The most important bile acid transformation is 7 alpha-dehydroxylation, producing deoxycholic acid (DCA) and lithocholic acid (LCA). The enzymatic pathway carrying out 7 alpha-dehydroxylation is restricted to a narrow phylogenetic group of commensal bacteria, the best-characterized of which is Clostridium scindens. Like many other intestinal commensal species, 7 alpha-dehydroxylating bacteria are understudied in vivo. Conventional animals contain variable and uncharacterized indigenous 7 alpha-dehydroxylating organisms that cannot be selectively removed, making controlled colonization with a specific strain in the context of an undisturbed microbiota unfeasible. In the present study, we used a recently established, standardized gnotobiotic mouse model that is stably associated with a simplified murine 12-species "oligo-mouse microbiota" (Oligo-MM12). It is representative of the major murine intestinal bacterial phyla, but is deficient for 7 alpha-dehydroxylation. We find that the Oligo-MM12 consortium carries out bile acid deconjugation, a prerequisite for 7 alpha-dehydroxylation, and confers no resistance to C. difficile infection (CDI). Amendment of Oligo-MM12 with C. scindens normalized the large intestinal bile acid composition by reconstituting Ty-dehydroxylation. These changes had only minor effects on the composition of the native Oligo-MM12, but significantly decreased early large intestinal C. difficile colonization and pathogenesis. The delayed pathogenesis of C. difficile in C. scindens-colonized mice was associated with breakdown of cecal microbial bile acid transformation.

Frontiers Media Sa2016

Functional intestinal bile acid 7-alpha-dehydroxylation by Clostridium scindens associated with protection from C. difficile infection in a gnotobiotic mouse model

Rizlan Bernier-Latmani, Lyne Desharnais, Laure Menin

Frontiers Media Sa2016

Modulation of immune responses by commensal bacteria and intestinal helminth

Dysregulation of Allergic Airway Inflammation in the Absence of Microbial Colonization

Functional intestinal bile acid 7-alpha-dehydroxylation by Clostridium scindens associated with protection from C. difficile infection in a gnotobiotic mouse model

Modulation of immune responses by commensal bacteria and intestinal helminth

Functional intestinal bile acid 7-alpha-dehydroxylation by Clostridium scindens associated with protection from C. difficile infection in a gnotobiotic mouse model

Dysregulation of Allergic Airway Inflammation in the Absence of Microbial Colonization