Faculty Research Labs

Derbigny Lab

Research in the lab of Wilbert A. Derbigny, PhD is focused on characterizing the cellular immune responses of epithelial cells lining the lumen of the oviduct. This team of investigators is describing their contributions to the overall immune response to Chlamydia infections.

The central focus of the laboratory addresses the hypothesis that the IFN-β produced within the oviduct during genital tract Chlamydia infection is Toll-like receptor-3 (TLR3) dependent, and that the synthesis of this important regulatory cytokine has significant impact on the synthesis of a multitude of other inflammatory mediators that are required to clear Chlamydia infections.  This hypothesis was proven correct in vitro by disrupting TLR3 expression in wild-type murine oviduct epithelial (OE) cells via si-RNA, and in experiments using OE cells derived from TLR3-deficient mice. The Derbigny Lab’s most recent in vivo findings show that TLR3-deficient mice exhibit higher bacterial loads, altered CD4+ T-cell recruitment, and more severe genital tract damage during intravaginal Chlamydia muridarum infection when compared to wild type mice.  Collectively, our data implicate TLR3 as an important modulator of the immune response during genital tract Chlamydia infections in mice.

Active Research

The Derbigny Lab was the first to demonstrate a protective role for TLR3 during genital tract chlamydial infections. The laboratory’s findings represent a novel look into the impact of TLR3 on outcomes of bacterial infection. Future research includes looking into the impact of TLR3-dependent pathways that are NOT related to IFN-β expression, and to ascertain whether TLR3 has a similar impact on human genital tract infections in vitro.

Research Funding

The role of TLR3 signaling in Chlamydia caused urogenital pathology

Role: PI

Training Grant in Immunology and Infectious Diseases

Role: Investigator/mentor

Recent Publications

Hu S, Hosey KL, Derbigny WA. Analyses of the pathways involved in early- and late-phase induction of IFN-beta during C. muridarum infection of oviduct epithelial cells. PloS one. 2015; 10(3):e0119235. PubMed [journal] PMID: 25798928, PMCID: PMC4370658

Hosey KL, Hu S, Derbigny WA. Role of STAT1 in Chlamydia-Induced Type-1 Interferon Production in Oviduct Epithelial Cells. J Interferon Cytokine Res.2015 Aug 11. [Epub ahead of print] PubMed PMID: 26262558.

Derbigny WA, Shobe LR, Kamran JC, Toomey KS, Ofner S. Identifying a role for Toll-like receptor 3 in the innate immune response to Chlamydia muridarum infection in murine oviduct epithelial cells. Infection and immunity. 2012; 80(1):254-65. PubMed [journal] PMID: 22006569, PMCID: PMC3255657

Seye CI, Agca Y, Agca C, Derbigny W. P2Y2 receptor-mediated lymphotoxin-α secretion regulates intercellular cell adhesion molecule-1 expression in vascular smooth muscle cells. The Journal of biological chemistry. 2012; 287(13):10535-43. PubMed [journal] PMID: 22298782, PMCID: PMC3323005

Research Team

Ramesh Kumar, PhD

Ramesh Kumar, PhD

Postdoctoral Fellow in Pediatrics