| Literature DB >> 34462359 |
Iti Saraav1, Luisa Cervantes-Barragan2, Philipp Olias1, Yong Fu1, Qiuling Wang1, Leran Wang3, Yi Wang2, Matthias Mack4, Megan T Baldridge3, Thaddeus Stappenbeck2, Marco Colonna2, L David Sibley5.
Abstract
Oral infection with Toxoplasma gondii results in dysbiosis and enteritis, both of which revert to normal during chronic infection. However, whether infection leaves a lasting impact on mucosal responses remains uncertain. Here we examined the effect of the chemical irritant dextran sodium sulfate (DSS) on intestinal damage and wound healing in chronically infected mice. Our findings indicate that prior infection with T. gondii exacerbates damage to the colon caused by DSS and impairs wound healing by suppressing stem cell regeneration of the epithelium. Enhanced tissue damage was attributable to inflammatory monocytes that emerge preactivated from bone marrow, migrate to the intestine, and release inflammatory mediators, including nitric oxide. Tissue damage was reversed by neutralization of inflammatory monocytes or nitric oxide, revealing a causal mechanism for tissue damage. Our findings suggest that chronic infection with T. gondii enhances monocyte activation to increase inflammation associated with a secondary environmental insult.Entities:
Keywords: disbiosis; inflammation; monocytes; nitric oxide; toxoplasmosis
Mesh:
Year: 2021 PMID: 34462359 PMCID: PMC8433586 DOI: 10.1073/pnas.2106730118
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN: 0027-8424 Impact factor: 11.205