Title:Human Umbilical Cord Mesenchymal Stem Cells Alleviate Chronic Salpingitis by Modulating Macrophage-Associated Inflammatory Factors
Volume: 19
Issue: 11
Author(s): Wenjuan Liao, Xiaomao Li*Xinrang Tang
Affiliation:
- Department of Obstetrics and Gynecology, Third Affiliated Hospital of Sun Yat-Sen University, 600, Tianhe Road,
Tianhe District, Guangzhou, 510630, Guangdong, China
Keywords:
Mesenchymal stem cells (MSCs), human umbilical cord (Huc), chronic salpingitis (CS), macrophage (Ma), inflammatory bowel disease, tubal tissue.
Abstract:
Introduction: Mesenchymal stem cells (MSCs) have been widely studied because of
their established anti-inflammatory properties. During chronic salpingitis (CS), infiltrated
macrophages have vital roles in inflammation and tissue remodeling.
Methods: We employed the type of MSCs, human umbilical cord (huc) MSCs in an experimental
CS model and therapeutic efficacy was assessed. hucMSCs exerted this therapeutic effect by regulating
macrophage function. To verify the regulatory effects of hucMSCs on the macrophage,
macrophage line RAW264.7 markers were analyzed under LPS stimulation with or without co-culturing
with hucMSCs for 12h and 24h. In addition, flow cytometry analysis was applied to reveal
the interaction of co-culture. For animal studies, CS was induced by the MoPn strain Chlamydia
trachomatis (CT), hucMSCs were intravaginally injected in the CS, and we analyzed the infiltrated
macrophage by immunofluorescence.
Results: We found the markers IL-10 was markedly increased and IL-1β, caspase-1 was notably
downregulated after co-culturing with hucMSCs by RT-PCR. hucMSCs promote macrophage line
RAW264.7 apoptosis. We also found that hucMSCs treatment can alleviate CS by decreasing the
mRNA expression of IL-1β, caspase-1 and MCP-1 in the tubal tissue by RT-PCR and decreasing
the protein expression of IL-1β, caspase-1 and TGF-β by western blotting.
Conclusion: These results suggest that macrophage function may be related to the immune-modulating
characteristics of hucMSCs that contribute to CS.