Chemokine response induced by Chlamydia trachomatis in prostate derived CD45+ and CD45− cells

Abstract

The role of innate cells and their receptors within the male genital tract remains poorly understood. Much less is known about the relative contribution of different genital tract cells such as epithelial/stromal cells and resident leucocytes. In this study, we examined innate immune responses to Chlamydia trachomatis by prostate epithelial/stromal cells and prostate resident leucocytes. Murine prostate primary cultures were performed and leucocyte and epithelial/stromal cells were sorted based on surface protein expression of CD45 by magnetism-activated cell sorting or fluorescence-activated cell sorting. Prostate derived CD45K and CD45C cells were infected with C. trachomatis and chemokine secretion assayed by ELISA. Similar experiments were performed using prostate CD45C and CD45K cells from myeloid differentiation factor 88 (Myd88) and Tlr4 mutant double-deficient mice. Moreover, a TLR-signalling pathway array was used to screen changes in different genes involved in TLR-signalling pathways by real-time PCR. Prostate derived CD45K and CD45C cells responded to chlamydial infection with the production of different chemokines. Both populations expressed genes involved in TLR signalling and required to respond to pathogen-associated molecular patterns and to C. trachomatis infection. Both populations required the adaptor molecule MYD88 to elicit chemokine response against C. trachomatis. TLR2-TLR4 was essential for chemokine production by CD45C prostate derived cells, but in their absence, CD45K cells still produced significant levels of chemokines. We demonstrate that C. trachomatis is differentially recognised by prostate derived CD45C and CD45K cells and suggest that diverse strategies are taking place in the local microenvironment of the host in response to the infection.

Chlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release

“…To our knowledge, all previous studies have only explored the effect of Ct on epithelial cells of the female reproductive tract 20–22 , however as we have demonstrated here, Ct can also infect and affect the function of ESC. In light of this novel finding, we propose that ascending genital Ct infection might be a more complicated process than previously thought, as Ct could breach the epithelial barrier of the endometrium and infect other cell types such as stromal cells, endothelial cells or glandular epithelial cells (endometrial structure reviewed in ref.…”

Seminal Levels of Pro-inflammatory (CXCL1, CXCL9, CXCL10) and Homeostatic (CXCL12) Chemokines in Men With Asymptomatic Chlamydia trachomatis Infection

“…Therefore, based on the current study results, it may be concluded that both CXCL1 and CXCL9 are critical chemokines involved in the innate immune responses against C. trachomatis infection. Previous studies demonstrated that CXCL1 is produced by several immune and non-immune tissue/cell systems, including macrophages, neutrophils and epithelial cells with predominant neutrophil chemoattraction activities ( 19 ). Moreover, it has also been documented that CXCL9 play important roles in infiltrating of the activated T lymphocytes towards the infected and inflamed tissues ( 20 ).…”

“…Mackern Oberti et al have examined the prostate epithelial/stromal cells dependent immune responses to C. trachomatis and observed that it could infect murine prostate cells by the development of large inclusions. Moreover, their results demonstrated that prostate cells have responded to C. trachomatis infection by production of pro-inflammatory chemokines inducing CCL2, CXCL1, and CXCL2 ( 19 ). They also observed that the chemokine productions by prostate cells were performed via activation with toll-like receptor, pathogen-associated molecular patterns interaction ( 19 ).…”

A reproducible approach to high-throughput biological data acquisition and integration

“…C . trachomatis has been implicated as a microbial driver in prostate carcinogenesis and has also been shown to elicit chemokine production from immune cells and non-immune cells isolated from the prostate ( Oberti et al, 2011 ). Our prediction suggests a more specific role for ACBD6 in prostate cancer as a potential suppressor of NF κ B activity and downstream inflammation, as it was highly co-expressed with the two NF κ B inhibitors, NF κ B IA and NF κ BIE ( Pringle et al, 2012 ; Wu et al, 2006 ) ( Fig.…”

“…Performing this task in ARepA allowed us to recover several genes already associated with NF κ B and prostate cancer ( Davis, Kucuk & Sarkar, 1999 ; Perkins, 2012 ), in addition to original findings including MEN1 as a novel putative upstream regulator ( Bouwmeester et al, 2004 ; Hacker & Karin, 2006 ; Heppner et al, 2001 ; Wen et al, 2000 ) and ACBD6 as a potential downstream suppressor of NF κ B-activation ( Oberti et al, 2011 ; Pringle et al, 2012 ; Soupene et al, 2012 ; Wu et al, 2006 ). MEN1 was linked to cancer, prostate cancer and NF κ B by two main data sources.…”