Current Views on the Concept of Pelvic Inflammatory Disease

Bm, Lars Westr; Mårdh, Per‐Anders

doi:10.1111/j.1479-828x.1984.tb01467.x

Cited by 16 publications

(1 citation statement)

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“…Chlamydia trachomatis is a gram-negative, obligate intracellular bacterial pathogen causing the most common sexually transmitted infections (STI) worldwide, particularly among young women [1]. In women, chronic infection with the urogenital serovars (D-K) can cause pelvic inflammatory diseases (PID) and chronic pelvic pain, which can culminate into scarring and fibrosis of the Fallopian tubes leading to infertility or ectopic pregnancy [2][3][4]. According to the Centers for Disease Control and Prevention's (CDC's) report in 2016, a total of 1,598,354 Chlamydia infections were reported in USA alone, which was 4.7% higher than the reported number of cases in 2015 [5].…”

Section: Introductionmentioning

confidence: 99%

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2019

Int J Microbiol Curr Res

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Chlamydia trachomatis replicates primarily in the epithelial cells lining the genital tract and induces the innate immune response by triggering cellular pathogen recognition receptors (PRRs). Our previous studies showed that Toll-like receptor 3 (TLR3) is expressed in murine oviduct epithelial (OE) cells, is the primary PRR triggered by C. muridarum (Cm) early during infection to induce IFN-β synthesis, and that TLR3 signaling regulates the chlamydial induced synthesis of a plethora of other innate inflammatory modulators including IL-6, CXCL10, CXCL16 and CCL5. We also showed that the expression of these cytokines induced by Chlamydia was severely diminished during TLR3 deficiency; however, the replication of Chlamydiain TLR3 deficient OE cells was more robust than in WT cells. These data suggested that TLR3 had a biological impact on the inflammatory response to Chlamydia infection; however, the global effects of TLR3 signaling in the cellular response to Chlamydia infection in murine OE cells has not yet been investigated. To determine the impact of TLR3 signaling on Chlamydia infection in OE cell at the transcriptome level, we infected wild-type (OE-WT) and TLR3-deficient (OE-TLR3KO) cells with Cm, and performed transcriptome analyses using microarray. Genome-wide expression and ingenuity pathway analysis (IPA) identified enhanced expression of host genes encoding for components found in multiple cellular processes encompassing: (1) pro-inflammatory, (2) cell adhesion, (3) chemoattraction, (4) cellular matrix and small molecule transport, (5) apoptosis, and (6) antigen-processing and presentation. These results support a role for TLR3 in modulating the host cellular responses to Cm infection that extend beyond inflammation and fibrosis, and shows that TLR3 could serve a potential therapeutic target for drug and/or vaccine development.

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Section: Introductionmentioning

confidence: 99%