Abstract:Escalante et al. show that a highly prevalent mouse intestinal protozoa, Tritrichomonas muris, was found to be a confounding factor in murine colitis. Mice infected with this parasite had elevated baseline levels of Th1 cytokines and developed exacerbated Th1-mediated disease.
“…This effect of T. musculis was also observed in an independent study of murine colitis (92). Combined, these studies revealed novel host-protozoan interactions that led to increased mucosal host defenses while also increasing the risk of inflammatory disease.…”
Section: Role Of the Protozoan Microbiota In Infection And Inflammationsupporting
Parasitic protozoan infections represent a major health burden in the developing world and contribute significantly to morbidity and mortality. These infections are often associated with considerable variability in clinical presentation. An emerging body of work suggests that the intestinal microbiota may help to explain some of these differences in disease expression. The objective of this minireview is to synthesize recent progress in this rapidly advancing field. Studies of humans and animals and in vitro studies of the contribution of the intestinal microbiota to infectious disease are discussed. We hope to provide an understanding of the human-protozoal pathogen-microbiome interaction and to speculate on how that might be leveraged for treatment.
“…This effect of T. musculis was also observed in an independent study of murine colitis (92). Combined, these studies revealed novel host-protozoan interactions that led to increased mucosal host defenses while also increasing the risk of inflammatory disease.…”
Section: Role Of the Protozoan Microbiota In Infection And Inflammationsupporting
Parasitic protozoan infections represent a major health burden in the developing world and contribute significantly to morbidity and mortality. These infections are often associated with considerable variability in clinical presentation. An emerging body of work suggests that the intestinal microbiota may help to explain some of these differences in disease expression. The objective of this minireview is to synthesize recent progress in this rapidly advancing field. Studies of humans and animals and in vitro studies of the contribution of the intestinal microbiota to infectious disease are discussed. We hope to provide an understanding of the human-protozoal pathogen-microbiome interaction and to speculate on how that might be leveraged for treatment.
“…Bacteroidetes thetaiotamicron , which induces the production of the antimicrobial peptide CRAMP by the transcription factor HIF-1α, prevents Candida albicans gut colonization 52 . In addition to fungi, the common mouse protozoan Tritrichomonas musculis is a transmissible microorganism in mice that increases susceptibility to T cell–dependent intestinal inflammation while providing protection from intestinal infections through inflammasome activation and production of the cytokine IL-18 by intestinal epithelial cells 53,54 .…”
Section: Interaction With Symbiotic Fungi Protozoa Worms and Virusesmentioning
The study of the intestinal microbiota has begun to shift from cataloging individual members of the commensal community to understanding their contributions to the physiology of the host organism in health and disease. Here, we review the effects of the microbiome on innate and adaptive immunological players from epithelial cells and antigen-presenting cells to innate lymphoid cells and regulatory T cells. We discuss recent studies that have identified diverse microbiota-derived bioactive molecules and their effects on inflammation within the intestine and distally at sites as anatomically remote as the brain. Finally, we highlight new insights into how the microbiome influences the host response to infection, vaccination and cancer, as well as susceptibility to autoimmune and neurodegenerative disorders.
The gut microbiota (GM) plays a critical role in human health and disease. Likewise, it is becoming increasingly evident that changes or disruptions to the GM can have significant effects on animal models and their expressed phenotypes, adding a complex and important variable into basic research and pre-clinical studies. In this article, we review some of the most common sources of GM variability in rodent models, and discuss measures to address this variability for improved reproducibility.
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