Tolerogenic Dendritic Cells Shape a Transmissible Gut Microbiota That Protects From Metabolic Diseases.

Excess chronic contact between microbial motifs and intestinal immune cells is known to trigger a low-grade inflammation involved in many pathologies such as obesity and diabetes. The important skewing of intestinal adaptive immunity in the context of diet-induced obesity (DIO) is well described, but how dendritic cells (DCs) participate in these changes is still poorly documented. To address this question, we challenged transgenic mice with enhanced DC life span and immunogenicity (DC mice) with a high-fat diet.

Host/microbiota interactions in health and diseases-Time for mucosal microbiology!

During the last 20 years, a new field of research delineating the importance of the microbiota in health and diseases has emerged. Inappropriate host-microbiota interactions have been shown to trigger a wide range of chronic inflammatory diseases, and defining the exact mechanisms behind perturbations of such relationship, as well as ways by which these disturbances can lead to disease states, both remain to be fully elucidated. The mucosa-associated microbiota constitutes a recently studied microbial population closely linked with the promotion of chronic intestinal inflammation and associated disease states.

Publisher Correction: Excess calorie intake early in life increases susceptibility to colitis in adulthood.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Excess calorie intake early in life increases susceptibility to colitis in adulthood.

Epidemiological data reveal an association between obesity and inflammatory bowel disease (IBD). Furthermore, animal models demonstrate that maternal high-fat diet (HFD) and maternal obesity increase susceptibility to IBD in offspring. Here we report that excess calorie intake by neonatal mice, as a consequence of maternal HFD, forced feeding of neonates or low litter competition, leads to an increase during weaning in intestinal permeability, expression of pro-inflammatory cytokines and hydrogen sulfide production by the microbiota.

The intestinal microbiota regulates host cholesterol homeostasis.

Background: Management of blood cholesterol is a major focus of efforts to prevent cardiovascular diseases. The objective of this study was to investigate how the gut microbiota affects host cholesterol homeostasis at the organism scale.

Results: We depleted the intestinal microbiota of hypercholesterolemic female Apoe mice using broad-spectrum antibiotics.

Mouse models for the study of fate and function of innate lymphoid cells.

Natural killer (NK) cells and lymphoid tissue inducer (LTi) cells were discovered more than 40 and 20 years ago, respectively. These two cell types were initially studied for their unique functions in the elimination of infected or transformed cells, and in the development of lymphoid tissues. It took an additional 10 years to realize that NK cells and LTi cells were members of a larger family of innate lymphoid cells (ILCs), whose phenotypes and functions mirror those of T cells.

Control of pathogens and microbiota by innate lymphoid cells.

Innate lymphoid cells (ILCs) are the innate counterpart of T cells. Upon infection or injury, ILCs react promptly to direct the developing immune response to the one most adapted to the threat facing the organism. Therefore, ILCs play an important role early in resistance to infection, but also to maintain homeostasis with the symbiotic microbiota following perturbations induced by diet and pathogens.

Segmented filamentous bacterium uses secondary and tertiary lymphoid tissues to induce gut IgA and specific T helper 17 cell responses.

Segmented filamentous bacterium (SFB) is a symbiont that drives postnatal maturation of gut adaptive immune responses. In contrast to nonpathogenic E. coli, SFB stimulated vigorous development of Peyer's patches germinal centers but paradoxically induced only a low frequency of specific immunoglobulin A (IgA)-secreting cells with delayed accumulation of somatic mutations.

Role of microbiota in postnatal maturation of intestinal T-cell responses.

Purpose Of Review: Taking advantage of their rapid growth and capacity for continuous genetic adaptation, prokaryotes have colonized all possible ecological environments on earth, including the body surfaces of eukaryotes and their gastrointestinal tract. The mammalian gut contains a complex community of 10 bacteria with a meta-genome containing 1500-fold more genes than the human genome. The forces that control the relationships between eukaryotic hosts and their intestinal bacterial symbionts have, thus, become a major focus of interest.

The key role of segmented filamentous bacteria in the coordinated maturation of gut helper T cell responses.

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.