Abstract
Chlamydia trachomatis is a common sexually transmitted pathogen and is associated with infant pneumonia. Data from the female mouse model of genital tract chlamydia infection suggests a requirement for TLR2-dependent signaling in the induction of inflammation and oviduct pathology. We hypothesized that the role of TLR2 in moderating mucosal inflammation is site specific. In order to investigate this, we infected mice via the intranasal route with C. muridarum and observed that in the absence of TLR2 activation, mice had more severe disease, higher lung cytokine levels, and an exaggerated influx of neutrophils and T-cells into the lungs. This could not be explained by impaired bacterial clearance as TLR2-deficient mice cleared the infection similar to controls. These data suggest that TLR2 has an anti-inflammatory function in the lung during Chlamydia infection, and that the role of TLR2 in mucosal inflammation varies at different mucosal surfaces.
Highlights
Chlamydia trachomatis is the most common bacterial sexually transmitted pathogen worldwide [1], and the etiologic agent of blinding trachoma [2]
We compared alveolar macrophages (AM) prepared from the lungs of control and TLR2deficient mice with Bone marrow derived macrophages (BMDM) derived from the same mice to determine if alveolar macrophages differed in their response to chlamydia infection
We found TLR2 expression was required for the induction of TNF-a by Alveolar macrophages (AM), (Fig. 1C) when compared with BMDM, the absolute concentration is lower and the peak is markedly delayed
Summary
Chlamydia trachomatis is the most common bacterial sexually transmitted pathogen worldwide [1], and the etiologic agent of blinding trachoma [2]. Complications of infections in women include the development of pelvic inflammatory disease, which can lead to tubal infertility and chronic pelvic pain. Infants born to women with active cervical chlamydia infection are at risk of developing conjunctivitis and pneumonia [3,4]. While the induction of an inflammatory immune response is clearly essential for the survival of a host following an infectious challenge, it is true that an exaggerated inflammatory response can be detrimental, as in the case of severe sepsis and some autoimmune chronic inflammatory states. The pathology associated with genital chlamydia infection and ocular trachoma is thought to result from bystander injury during an aggressive inflammatory response.
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