ORIGINAL RESEARCH article
Front. Microbiol.
Sec. Infectious Agents and Disease
Volume 16 - 2025 | doi: 10.3389/fmicb.2025.1647731
This article is part of the Research TopicMechanisms and Innovations in Combating Intracellular InfectionsView all 5 articles
Intestinal IL-22RA1 signaling regulates Chlamydia Deficient in Plasmid-Encoded pGP3 spreading to Large Intestine
Provisionally accepted
- 1Hunan Provincial Maternal and Child Health Care Hospital, Changsha, China
- 2Tianjin Agricultural University, Tianjin, China
- 3Tianjin Medical University General Hospital, Tianjin, China
- 4Third Xiangya Hospital of Central South University, Changsha, China
- 5Shanghai Institute of Virology, Shanghai Jiao Tong University School of Medicine, Shanghai, China
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Chlamydia trachomatis is the most important infectious cause of tubal infertility and is frequently detected in the human gastrointestinal tract. Chlamydia muridarum, a murine pathogen, closely resembles the human pathogen C. trachomatis. Our previous studies showed that the pGP3-deficient C. muridarum mutant was restricted to the large intestine following intracolonic inoculation, suggesting that the pGP3-deficient mutant was killed by the tissue beyond the large intestine. Here, we report that the intra-ilenum, but not the intra-jejunum, to bypass the gastric barrier rescued the colonization of pGP3-deficient C. muridarum, suggesting that pGP3 is required to overcome host factors of the jejunum to help C. muridarum reach the colon. Moreover, mice genetically deficient in IL-22 not only rescued the colonization of pGP3-deficient C. muridarum following intra-jejunum inoculation but also rescued the colonization of pGP3-deficient C. muridarum in the whole gastrointestinal tract tissues following intracolonic inoculation on day 14, suggesting a critical role of IL-22 in regulating chlamydial spread. Importantly, IL-22RA1 flox/flox and Villin-cre mice rescued the colonization of pGP3-deficient C. muridarum following intra-jejunum inoculation, suggesting that intestinal epithelial-specific IL-22RA1 signaling is important for the spread of pGP3-deficient C. muridarum from the small intestine to the large intestine. These observations provide a platform for further research on intestinal IL-22RA1 signaling in regulating bacterial spread in the intestine. Therefore, host factors identified in the gastrointestinal tract may also contribute to the female lower genital tract barrier during sexually transmitted diseases.
Keywords: Chlamydia muridarum (C. muridarum), PGP3, IL-22, Gastrointestinal Tract, colonization
Received: 16 Jun 2025; Accepted: 19 Aug 2025.
Copyright: © 2025 Tian, Fang, Ma, Wang, Zuo and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Zonghui Zuo, Tianjin Agricultural University, Tianjin, China
Tianyuan Zhang, Shanghai Institute of Virology, Shanghai Jiao Tong University School of Medicine, Shanghai, China
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