Abstract
Endometriosis is defined as the growth of endometrial tissue in ectopic locations, and is associated with altered immune and microbial phenotypes. It is unclear if these changes are the result of the disease or may be causative. We induced endometriosis in non-human primates (Papio Anubis) to test our hypothesis that the growth of endometriotic lesions results in alterations in immune and microbial dynamics that may advance disease progression. Baboon samples were collected pre-inoculation (prior to disease induction), at 3, 6, 9, and 15 months after disease induction. Tolerant regulatory T-cells (Tregs) and inflammatory T-helper 17 (Th17) cells were identified in peripheral blood and within the eutopic/ectopic endometrial tissues. Microbiome communities were identified in fecal/urine samples. The induction of endometriosis decreased peripheral Tregs cells while Th17 cells increased at all post-induction collections, thus reducing the Tregs:Th17 cells ratio, indicating systemic inflammation. Microbiome diversity and abundance were altered at each sample site after disease induction. Thus, induction of endometriosis in baboons caused an immune shift toward an inflammatory profile and altered mucosal microbial profiles, which may drive inflammation through production of inflammatory mediators. Immune and microbial profiling may lead to innovative diagnostic tools and novel therapies for endometriosis treatment.
Highlights
Endometriosis is defined as the growth of endometrial tissue in ectopic locations, and is associated with altered immune and microbial phenotypes
To determine if induction of endometriosis altered peripheral immune cell populations, we identified natural Tregs (nTregs) (CD4+CD25+Foxp3+), inducible Tregs (iTregs) (CD4+CD25−Foxp3+) and T-helper 17 (Th17) cell populations in blood samples collected over time (Fig. 1)
Utilizing a non-human primate animal model of induced endometriosis in olive baboons, this study investigated the alteration of immune populations and microbial dynamics in response to establishment of disease
Summary
Endometriosis is defined as the growth of endometrial tissue in ectopic locations, and is associated with altered immune and microbial phenotypes It is unclear if these changes are the result of the disease or may be causative. We induced endometriosis in non-human primates (Papio Anubis) to test our hypothesis that the growth of endometriotic lesions results in alterations in immune and microbial dynamics that may advance disease progression. Earlier studies using the baboon model demonstrated that the induction of endometriosis resulted in reduction of Tregs in the peripheral circulation and e ndometrium[12] Together, these findings prompted us to characterize both Tregs and Th17 cell populations during the pathogenesis of endometriosis in the induced non-human primate model of disease. It is reasonable to hypothesize that inflammation associated with endometriosis can shift the microbial dynamics of the GI/ UG tracts and that these shifts may correlate with presence of the disease and the disease severity
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