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reported that fetuin-A-deficient mice are more susceptible to lethal systemic inflammation. coli LPS-induced endotoxemia mouse model, Li et al.

However, very little is known about the role of fetuin-A in infectious diseases. Fetuin-A, which is secreted from both the liver and adipose tissue, is found in abundance in serum and has been widely recognized as a multifunctional molecule that participates in vascular calcification, bone metabolism regulation, insulin resistance, and inflammatory response. Our previous study showed that genital tract Chlamydia muridarum (Cm, adapted murine model of Chlamydia trachomatis) infection leads to an increased expression of fetuin-A (also known as alpha-2-HS-glycoprotein encoded by the AHSG gene) in C57BL/6 mice.

IntroductionĬhlamydia species are obligate intracellular bacteria and a common cause of sexually transmitted disease (STD). Although preliminary in nature, these findings are suggestive of fetuin-A involvement following Cm pulmonary infection and underscores the need to investigate further the role of fetuin-A in the immune response and the consequences of its gene deletion. Additionally, the effect of fetuin-A deficiency in mounting an adaptive immune response to Cm infection was demonstrated using a splenocyte recall assay. Assessment of expression of genes associated with inflammation revealed fetuin-A-dependent upregulation of TBX21 (a Th1 cell-specific transcription factor) in the lungs of Cm-infected WT mice that correlated with IFN- γ induction. Importantly, the observed increased IFN- γ production was abrogated in fetuin-A-deficient AHSG mice suggesting that IFN- γ induction following Cm infection is fetuin-A dependent. We report here that in wild-type mice 12 days after Chlamydia muridarum (Cm) intranasal challenge, fetuin-A content in the lungs decreased 46%, while INF- γ increased 44%, consistent with a negative regulatory role of fetuin-A in inflammation. Fetuin-A is an acute phase glycoprotein shown to counter in a regulatory manner proinflammatory cytokine production to maintain homeostasis during inflammation.