Susceptibility of prostate epithelial cells to Chlamydia muridarum infection and their role in innate immunity by recruitment of intracellular Toll-like receptors 4 and 2 and MyD88 to the inclusion.
Although Chlamydia infections are widespread throughout the world, data about immunopathogenesis of genitourinary tract infections in males are very limited. In the present work we present an in vitro model of male genital tract-derived epithelial cells, more precisely prostate epithelial cells (PEC), to analyze if they are susceptible and able to respond to Chlamydia muridarum infection. Our results demonstrate that rat PEC are susceptible to C. muridarum infection and respond to this pathogen by up-regulating different proinflammatory cytokine and chemokine genes that could participate in the recruitment and local activation of immune cells, therefore influencing innate and adaptive immune responses during Chlamydia infection. Moreover, we analyzed the expression of Toll-like receptor 4 (TLR4), TLR2, and related molecules on PEC and the effect of C. muridarum infection on their expression. Our results demonstrate that PEC express significant levels of TLR4, CD14, TLR2, and the adaptor molecule MyD88 and up-regulate these proteins in response to C. muridarum infection. Indeed, TLR4, CD14, TLR2, and the adaptor MyD88 are specifically recruited to the vicinity of the bacterial inclusion, suggesting that these TLRs are actively engaged in signaling from this intracellular location in these cells. This is, to our knowledge, the first time that an in vitro model of infection with Chlamydia of male tract-derived epithelial cells has been achieved, and it provides the opportunity to determine how these cells respond and participate in modulating innate and adaptive immune response during Chlamydia infections.
Mackern-Oberti
Juan Pablo
JP
CIBICI-CONICET, Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Haya de la Torre y Medina Allende, Ciudad Universitaria, Córdoba 5000, Argentina.
Maccioni
Mariana
M
Cuffini
Cecilia
C
Gatti
Gerardo
G
Rivero
Virginia E
VE
D021581:Active Transport, Cell Nucleus; D000818:Animals; D002478:Cells, Cultured; D002690:Chlamydia Infections / Q000276:immunology* / Q000378:metabolism; D023502:Chlamydia muridarum / Q000502:physiology*; D016207:Cytokines / Q000378:metabolism; D004847:Epithelial Cells / Q000737:chemistry / Q000276:immunology / Q000382:microbiology; D007113:Immunity, Innate; D008297:Male; D008954:Models, Biological; D053594:Myeloid Differentiation Factor 88 / Q000032:analysis / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism; D011467:Prostate / Q000737:chemistry / Q000276:immunology* / Q000382:microbiology; D051381:Rats; D051195:Toll-Like Receptor 2 / Q000032:analysis / Q000378:metabolism*; D051197:Toll-Like Receptor 4 / Q000032:analysis / Q000378:metabolism*
D016207:Cytokines; C507781:Myd88 protein, rat; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B; C495343:Tlr2 protein, rat; C495347:Tlr4 protein, rat; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4