Influx of podoplanin‐expressing inflammatory macrophages into the genital tract following Chlamydia infection

Author:

Chan Yee Teng1,Cheok Yi Ying1,Cheong Heng Choon1,Tan Grace Min Yi1,Seow Shi Rui1,Tang Ting Fang1,Sulaiman Sofiah2,Looi Chung Yeng3,Gupta Rishein4,Arulanandam Bernard45,Wong Won Fen1ORCID

Affiliation:

1. Department of Medical Microbiology, Faculty of Medicine University of Malaya Kuala Lumpur Malaysia

2. Department of Obstetrics and Gynecology, Faculty of Medicine University of Malaya Kuala Lumpur Malaysia

3. School of Bioscience, Faculty of Health & Medical Sciences Taylor's University Subang Jaya Malaysia

4. Center of Excellence in Infection Genomics, South Texas Center for Emerging Infectious Diseases University of Texas at San Antonio San Antonio TX USA

5. Department of Immunology Tufts University School of Medicine Boston MA USA

Abstract

AbstractGenital Chlamydia trachomatis infection remains a major health issue as it causes severe complications including pelvic inflammatory disease, ectopic pregnancy and infertility in females as a result of infection‐associated chronic inflammation. Podoplanin, a transmembrane receptor, has been previously reported on inflammatory macrophages. Thus, strategies that specifically target podoplanin might be able to reduce local inflammation. This study investigated the expression level and function of podoplanin in a C. trachomatis infection model. C57BL/6 mice infected with the mouse pathogen Chlamydia muridarum were examined intermittently from days 1 to 60 using flow cytometry analysis. Percentages of conventional macrophages (CD11b+CD11cF4/80+) versus inflammatory macrophages (CD11b+CD11c+F4/80+), and the expression of podoplanin in these cells were investigated. Subsequently, a podoplanin‐knockout RAW264.7 cell was used to evaluate the function of podoplanin in C. trachomatis infection. Our findings demonstrated an increased CD11b+ cell volume in the spleen at day 9 after the infection, with augmented podoplanin expression, especially among the inflammatory macrophages. A large number of podoplanin‐expressing macrophages were detected in the genital tract of C. muridarum–infected mice. Furthermore, analysis of the C. trachomatis–infected patients demonstrated a higher percentage of podoplanin‐expressing monocytes than that in the noninfected controls. Using an in vitro infection in a transwell migration assay, we identified that macrophages deficient in podoplanin displayed defective migratory function toward C. trachomatis–infected HeLa 229 cells. Lastly, using immunoprecipitation–mass spectrometry method, we identified two potential podoplanin interacting proteins, namely, Cofilin 1 and Talin 1 actin‐binding proteins. The present study reports a role of podoplanin in directing macrophage migration to the chlamydial infection site. Our results suggest a potential for reducing inflammation in individuals with chronic chlamydial infections by targeting podoplanin.

Publisher

Wiley

Subject

Cell Biology,Immunology,Immunology and Allergy

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