Pattern recognition molecules activated by Chlamydia muridarum infection of cloned murine oviduct epithelial cell lines.
نویسندگان
چکیده
Chlamydia trachomatis is the most common bacterial sexually transmitted disease in the United States and a major cause of female infertility due to infection-induced Fallopian tube scarring. Epithelial cells are likely central to host defense and pathophysiology as they are the principal cell type productively infected by C. trachomatis. We generated cloned murine oviduct epithelial cell lines without viral or chemical transformation to investigate the role of the TLRs and cytosolic nucleotide binding site/leucine-rich repeat proteins Nod1 and Nod2 in epithelial responses to Chlamydia muridarum infection. RT-PCR assays detected mRNA for TLR2 (TLRs 1 and 6), TLR3, and TLR5. No mRNA was detected for TLRs 4, 7, 8, and 9. Messenger RNAs for Nod1 and Nod2 were present in the epithelial cell lines. Oviduct epithelial cell lines infected with C. muridarum or exposed to the TLR2 agonist peptidoglycan secreted representative acute phase cytokines IL-6 and GM-CSF in a MyD88-dependent fashion. Infected epithelial cell lines secreted the immunomodulatory cytokine IFN-beta, even though C. muridarum does not have a clear pathogen-associated molecular pattern (PAMP) for triggering IFN-beta transcription. The oviduct epithelial lines did not secrete IFN-beta in response to the TLR2 agonist peptidoglycan or to the TLR3 agonist poly(I:C). Our data identify TLR2 as the principal TLR responsible for secretion of acute phase cytokines by C. muridarum-infected oviduct epithelial cell lines. The pattern recognition molecule responsible for infection-induced IFN-beta secretion by oviduct epithelial cells remains to be determined.
منابع مشابه
The Chlamydia muridarum-induced IFN-β response is TLR3-dependent in murine oviduct epithelial cells.
Epithelial cells lining the murine genital tract act as sentinels for microbial infection, play a major role in the initiation of the early inflammatory response, and can secrete factors that modulate the adaptive immune response when infected with Chlamydia. C. muridarum-infected murine oviduct epithelial cells secrete the inflammatory cytokines IL-6 and GM-CSF in a TLR2-dependent manner. Furt...
متن کاملMurine oviduct epithelial cell cytokine responses to Chlamydia muridarum infection include interleukin-12-p70 secretion.
Epithelial cells play an important role in host defense as sentinels for invading microbial pathogens. Chlamydia trachomatis is an intracellular bacterial pathogen that replicates in reproductive tract epithelium. Epithelial cells lining the reproductive tract likely play a key role in triggering inflammation and adaptive immunity during Chlamydia infections. For this report a murine oviduct ep...
متن کاملIdentifying a role for Toll-like receptor 3 in the innate immune response to Chlamydia muridarum infection in murine oviduct epithelial cells.
Because epithelial cells are the major cell type productively infected with Chlamydia during genital tract infections, the overall goal of our research was to understand the contribution of infected epithelial cells to the host defense. We previously showed that Toll-like receptor 3 (TLR3) is the critical pattern recognition receptor in oviduct epithelial (OE) cells that is stimulated during Ch...
متن کاملOviduct Infection and Hydrosalpinx in DBA1/j Mice Is Induced by Intracervical but Not Intravaginal Inoculation with Chlamydia muridarum
Intravaginal infection with C. muridarum in mice often results in hydrosalpinx similar to that found in women urogenitally infected with C. trachomatis, making the C. muridarum lower genital tract infection murine model suitable for studying C. trachomatis pathogenesis. To our surprise, DBA1/j mice were highly resistant to hydrosalpinx following an intravaginal infection with C. muridarum altho...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Journal of immunology
دوره 175 9 شماره
صفحات -
تاریخ انتشار 2005