Induction of Intestinal Th17 Cells by Segmented Filamentous Bacteria

http://envismadrasuniv.org/Physiology/pdf/Gut%20flora%20in%20health%20and%20disease.pdf

Gut flora in health and disease

Microbial colonization of mucosal tissues during infancy plays an instrumental role in the development and education of the host mammalian immune system. These early-life events can have long-standing consequences: facilitating tolerance to environmental exposures or contributing to the development of disease in later life, including inflammatory bowel disease, allergy, and asthma. Recent studies have begun to define a critical period during early development in which disruption of optimal host-commensal interactions can lead to persistent and in some cases irreversible defects in the development and training of specific immune subsets. Here, we discuss the role of early-life education of the immune system during this “window of opportunity,” when microbial colonization has a potentially critical impact on human health and disease.

/pdf/how-colonization-by-microbiota-in-early-life-shapes-the-3mzuzrq71a.pdf

How colonization by microbiota in early life shapes the immune system

Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells

http://www.hmphanmi.com.cn/hmp/upload/event/study_4/3.pdf

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

Segmented filamentous bacteria (SFBs) are apathogenic autochthonous bacteria in the murine small intestine that preferentially attach to Peyer9s patch epithelium. SFBs have never been cultured in vitro. We have studied the effects of SFBs on the immune system of the host. Mice monoassociated with SFBs were compared with germ-free mice and with mice without SFBs but with a specific-pathogen-free (SPF) gut flora. SFBs versus no microbial flora raised the number of lymphoid cells in the lamina propria of the ileal and cecal mucosa, raised the number of immunoglobulin A (IgA)-secreting cells in the intestinal mucosa, produced elevated IgA titers in serum and intestinal secretions, and enhanced the concanavalin A-induced proliferative responses of mesenteric lymph node cells. The SPF flora had effects similar to but less pronounced than those mediated by SFBs. The results indicate that SFBs stimulate the mucosal immune system to a greater extent than do other autochthonous gut bacteria.

Apathogenic, intestinal, segmented, filamentous bacteria stimulate the mucosal immune system of mice.

Improved procedure for the isolation of functionally active lymphoid cells from the murine intestine

In this study we investigated the contribution of the small intestine of C3H/He mice to the spontaneous ('background') immunoglobulin (Ig) production in terms of the number of Ig-secreting cells (Ig-SC), and compared the results with the numbers of Ig-SC found in various lymphoid organs (spleen, bone marrow, mesenteric lymph nodes and Peyer's patches). The results show that in C3H/He mice of 20 weeks of age, on average 16 x 10(6) Ig-SC can be isolated from the small intestine. Almost all of these Ig-SC produce IgA. Compared to the other lymphoid organs, the small intestine contains more than 80% of all Ig-SC present in adult C3H/He mice. These results are in agreement with the need to maintain relatively high levels of Ig at the mucosal surfaces, especially of secretory IgA, for the prevention of penetration of these surfaces by micro-organisms. In man and mouse most of these Ig are supposed to be produced locally in the underlying mucosal tissues and subsequently transported across the epithelium. Although the IgM and IgG levels in serum are predominantly maintained by non-mucosae associated lymphoid organs, the results of this study clearly indicate that the mucosal tissues are the major site of 'background' Ig-production.

Contribution of immunoglobulin-secreting cells in the murine small intestine to the total 'background' immunoglobulin production.

We studied the effect of mucosal presentation of ovalbumin (OVA) conjugated to cholera toxin (CT) or cholera toxin B subunit (CTB) on the intestinal immune responses against OVA. Mice were primed intraperitoneally (i.p.) with OVA in a water-in-oil emulsion and boosted intraduodenally (i.d.) with OVA conjugated to CT or CTB in various molar ratios. Responses were evaluated by testing intestinal secretions for OVA-specific antibodies and by quantifying the OVA-specific antibody secreting cells (ASC) in the lamina propria of the small intestine. OVA-CT conjugates were tested in a molar ratio ranging from 1.8:1 to 4500:1. OVA-CTB conjugates were tested in a molar ratio ranging from 0.25:1 to 500:1. The optimum intestinal immune response was reached at a molar ratio of 1.8:1 for OVA-CT and 5:1 for OVA-CTB. The binding capacity of OVA-CTB, but not of OVA-CT, to GM1 ganglioside corresponded with the capacity to enhance the intestinal immune response. The effect of conjugating CTB or CT to OVA on the immune response against OVA was more striking when mice were not only boosted i.d., but also primed i.d. Both OVA-CT and OVA-CTB induced detectable immune responses, whereas free OVA did not. Therefore, the carrier effect of CT or CTB is essential to trigger a mucosal immune response against OVA when presented mucosally only. We conclude that enhancing antigen uptake greatly facilitates mucosal immune responses.

Manipulation of intestinal immune responses against ovalbumin by cholera toxin and its B subunit in mice.

Conversion of orally induced suppression of the mucosal immune response to ovalbumin into stimulation by conjugating ovalbumin to cholera toxin or its B subunit

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