Article

The Key Role of Segmented Filamentous Bacteria in the Coordinated Maturation of Gut Helper T Cell Responses

INRA, U910, Unité Ecologie et Physiologie du Système Digestif, Domaine de Vilvert, 78350 Jouy-en-Josas, France.
Immunity (Impact Factor: 21.56). 10/2009; 31(4):677-89. DOI: 10.1016/j.immuni.2009.08.020
Source: PubMed

ABSTRACT

Microbiota-induced cytokine responses participate in gut homeostasis, but the cytokine balance at steady-state and the role of individual bacterial species in setting the balance remain elusive. Herein, systematic analysis of gnotobiotic mice indicated that colonization by a whole mouse microbiota orchestrated a broad spectrum of proinflammatory T helper 1 (Th1), Th17, and regulatory T cell responses whereas most tested complex microbiota and individual bacteria failed to efficiently stimulate intestinal T cell responses. This function appeared the prerogative of a restricted number of bacteria, the prototype of which is the segmented filamentous bacterium, a nonculturable Clostridia-related species, which could largely recapitulate the coordinated maturation of T cell responses induced by the whole mouse microbiota. This bacterium, already known as a potent inducer of mucosal IgA, likely plays a unique role in the postnatal maturation of gut immune functions. Changes in the infant flora may thus influence the development of host immune responses.

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    • "It is identified that segmented filamentous bacteria (SFB), a nonculturable Clostridia-related species , is showed the biggest difference between Th17 celldeficient and Th17 cell-sufficient mice, which is capable of specifically inducing Th17 cells in the gut [99] [100]. This bacterium is also known as a potent inducer of mucosal IgA, which plays a unique role during the postnatal maturation of gut immune functions [101] "

    Full-text · Dataset · Aug 2015
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    • "Data from GF mouse studies must also be interpreted in context as several normal host physiologic parameters are altered in these mice. For example, GF mice have underdeveloped immune systems (Atarashi et al. 2011; Gaboriau-Routhiau et al. 2009; Helgeland et al. 1996; Ivanov et al. 2009; Macpherson and Harris 2004; Umesaki et al. 1993), slower intestinal epithelial turnover (Savage et al. 1981), differences in epithelial gene expression (Chowdhury et al. 2007; Hooper et al. 2001), differing nutritional requirements, less body fat despite increased consumption (Backhed et al. 2004), and markedly enlarged ceca. The latter may lead to death from volvulus or may indirectly lower reproductive performance, presumably due to competition for space with the gravid uterus. "
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    • "mechanism by which CD103 + CD11b + DCs may support intestinal Th17 cell development is through their enhanced ability to produce IL- 6 in response to microbial signals (Fig. 2a,b). Indeed, a commensal microbe that is unique in its ability to preferentially induce Th17 cells is segmented filamentous bacteria (SFB; Fig. 3) (Ivanov et al., 2009; Gaboriau-Routhiau et al., 2009). This SFB-driven Th17 development in the intestine is dependent on MHC class II expression on CD11c + cells but independent of SLOs—suggesting that intestinal DCs may provide antigenic stimulation of naïve CD4+ T cells directly in situ (Goto et al., 2014; Geem et al., 2014; Lecuyer et al., 2014). "
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