Microbial Colonization Drives Lymphocyte Accumulation and Differentiation in the Follicle-Associated Epithelium of Peyer’s Patches

Abstract

Peyer’s patches (PPs) are lined by follicle-associated epithelium (FAE) with Ag-transporting M cells. To investigate the spatial relationships of B cells, T cells, and dendritic cells (DCs) in PPs during microbial colonization, their in situ redistribution was examined in germfree (GF) rats exposed to a conventional pathogen-free microflora (conventionalized, CV). Although occasional B and T cells occurred in the FAE of GF rats, it contained mainly immature DCs (CD4+CD86−), whereas mature DCs (CD86high) were seen in the interfollicular zones even under GF conditions. In CV rats, DCs had disappeared from the FAE, which instead contained clusters by B and T cells associated with induction of putative M cell pockets. CD86 was seen neither in the FAE nor in the follicles under GF conditions, but it became apparent on intraepithelial B cells 5 wk after colonization. The level of CD86 on these B cells was comparable to that on germinal center B cells, although the B cell follicles did not show direct contact with the M cell areas. B cells in the follicular mantles acquired Bcl-2 after 12 wk in CV rats, whereas B cells in the FAE did not express Bcl-2 at a substantial level throughout the experimental period. The cellular redistribution patterns and phenotypic characteristics observed after colonization suggested that immature DCs, but not B cells, are involved in Ag presentation during primary immune responses against intestinal bacteria. However, the spatial cellular relationships sequentially being established among DCs, B cells, and T cells in PPs, are most likely important for the induction of post-germinal center B cells subsequently residing within the M cell pockets.

Salmonella enterica serovar Choleraesuis infection of the porcine jejunal Peyer's patch rapidly induces IL-1β and IL-8 expression

“…Intestinal tissues were obtained from pigs conventionally colonized with commensal microflora, as a competent intestinal immune system was necessary in these studies. Enteric commensal bacteria are critical to the development of Peyer's patches (Pabst and Rothkotter, 1999), production of antibodies (Butler et al, 2002;Cukrowska et al, 2001), and migration of B and T lymphocytes to the Peyer's patches (Yamanaka et al, 2003). Our findings indicate that intact JPP respond rapidly to Salmonella infection by increased expression of IL-1β and IL-8 mRNAs, and efficient Salmonella adhesion and internalization are required to induce these changes in mRNA expression.…”

Le dialogue microbiote-cellules souches

“…La stimulation par le MDP de cryptes intestinales murines avant leur mise en culture, entraîne une forte hausse du nombre d'organoïdes formés. Nous avons montré que ce phéno- 4 Ne touchant pas toutes les cellules. .…”

“…Enfin, le microbiote structure la barrière intestinale en régulant ses propriétés physiques, telles que la composition et l'épaisseur des couches de mucus qui tapissent l'épithélium [2], ou les jonctions serrées des cellules épithéliales [3]. Il régule également le développement du système immunitaire muqueux [4,47] (➜). L'impact du microbiote intestinal n'est pas limité à l'intestin, il s'exerce également à l'échelle systémique des organismes hôtes.…”

The developing intestinal microbiome and its relationship to health and disease in the neonate

“…20 Bacteria stimulate the gut-associated lymphoid tissue to produce antibodies to pathogens. 11,12,14,21 The immune system recognizes and fights harmful bacteria, but does not react against helpful species (as well as the host's own organs)Fa tolerance developed in infancy, and sometimes termed the 'old friends' hypothesis. 22 This hypothesis appears to be a synthesis of the hygiene hypothesis that proposes that these microorganisms that have evolved with humans have an essential role in the establishment of the immune system wherein the microorganisms and the host have evolved a co-dependence.…”

“…[9][10][11][12] Previous studies have demonstrated that germ-free animals do not develop normal lymph node architecture, with extensive defects in the development of gut-associated lymphoid tissue, arrested capillary network development in the gut and reduced antibody production. [11][12][13][14] It is becoming increasingly evident that the microbes of the intestine may be involved in the so-called 'hygiene hypothesis' wherein a lack of exposure to a variety of microorganisms, especially during early life, may result in the development of diseases such as type 1 diabetes, asthma, allergies, celiac disease, inflammatory bowel disease and obesity. [15][16][17][18] In the case of allergies, a lack of stimulation of Th1-cell responses predisposes to the development of Th2 cell responses and to Th17 cells that induce production of IL-17.…”