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Murine MicroRNA-214 regulates intracellular adhesion molecule (ICAM1) gene expression in genital Chlamydia muridarum
Tanvi Arkatkar1, Rishein Gupta1, Weidang Li2
1South Texas Center for Emerging Infectious Diseases and Center of Excellence in Infection Genomics, University of Texas at San Antonio, San Antonio, TX, USA.
Abstract:
The hallmark of chlamydial infection is the development of upper genital pathology in the form of hydrosalpinx and oviduct and/or tubal dilatation. Although molecular events leading to genital tissue presentation and cellular architectural remodelling are unclear, early-stage host immune responses are believed to contribute to these long-term sequelae. Recently, we reported the contribution of selected infection-associated microRNAs (miRs) in the generation of host immunity at early-stage infection (day 6 after intravaginal Chlamydia muridarum challenge in C57BL/6 mice). In this report, we describe the contribution of an infection-associated microRNA, i.e. miR-214, to host immunity. Chlamydia muridarum infection in the C57BL/6 mouse genital tract significantly down-regulated miR-214 while up-regulating intracellular adhesion molecule 1 (ICAM1) gene expression. These in vivo observations were confirmed by establishing direct regulation of ICAM-1 by miR-214 in ex vivo genital cell cultures in the presence of miR-214 mimic and inhibitor. Because, ICAM-1 contributes to recruitment of neutrophils following infection, we also demonstrated that alteration of ICAM1 by miR-214 in interleukin-17A-deficient (IL-17A(-/-) ) mice correlated with reduction of neutrophils infiltrating genital tissue at day 6 after challenge. Additionally, these early-stage events resulted in significantly decreased genital pathology in IL-17A(-/-) mice compared with C57BL/6 mice. This report provides evidence for early-stage regulation of ICAM1 by microRNAs, resulting in reduction of genital pathology associated with chlamydial infection.
Insights
MicroRNA-214 (miR-214) plays a key role in regulating the immune response to chlamydial infections. By down-regulating miR-214, chlamydia increases ICAM1 expression, leading to genital pathology.
Area of Science:
- Immunology
- Microbiology
- Molecular Biology
Background:
- Chlamydial infections often lead to upper genital pathology, including hydrosalpinx and tubal dilatation.
- Early host immune responses are implicated in the long-term sequelae of chlamydial infections.
- MicroRNAs (miRs) are increasingly recognized for their role in modulating host immunity during infection.
Purpose of the Study:
- To investigate the contribution of microRNA-214 (miR-214) to host immunity during early-stage Chlamydia muridarum infection.
- To elucidate the regulatory relationship between miR-214 and intracellular adhesion molecule 1 (ICAM1) in the context of chlamydial infection.
- To assess the impact of miR-214-mediated regulation of ICAM1 on genital pathology and neutrophil infiltration.
Main Methods:
- Chlamydia muridarum infection was established in C57BL/6 mice.
- miR-214 and ICAM1 expression levels were quantified in genital tissues.
- Ex vivo genital cell cultures were used to confirm direct regulation of ICAM1 by miR-214 using mimics and inhibitors.
- Neutrophil infiltration and genital pathology were assessed in wild-type and interleukin-17A-deficient (IL-17A(-/-)) mice.
Main Results:
- Chlamydia muridarum infection significantly down-regulated miR-214 expression while up-regulating ICAM1 gene expression in the mouse genital tract.
- Direct regulation of ICAM1 by miR-214 was confirmed in ex vivo cell cultures.
- In IL-17A(-/-) mice, miR-214-mediated alteration of ICAM1 correlated with reduced neutrophil infiltration and significantly decreased genital pathology compared to C57BL/6 mice.
Conclusions:
- This study provides evidence for the early-stage regulation of ICAM1 by miR-214 during chlamydial infection.
- miR-214 acts as a negative regulator of ICAM1, influencing neutrophil recruitment and subsequent genital pathology.
- Targeting miR-214 or ICAM1 may offer a therapeutic strategy to reduce the long-term sequelae of chlamydial infections.
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