![cm 01 02 real time editor cm 01 02 real time editor](https://fmshots.com/images/2020/04/07/cm0102-screenshot-440c3497af320d828.jpg)
Fetuin-A knock out mice backcrossed onto C57BL/6 mice (referred to as AHSG mice) were used in this study.
![cm 01 02 real time editor cm 01 02 real time editor](https://usermanual.wiki/Document/SQLWorkbenchManual.24942592-User-Guide-Page-1.png)
MiceĬ57BL/6 (WT) were purchased from Jackson Laboratory (Bar Harbor, ME). To date, the influence of fetuin-A following chlamydial pulmonary infection has not been reported prompting our examining albeit in a preliminary fashion, the focus of this report. While CD8+ T cells contribute to control of bacterial growth via IFN- γ and TNF- α early in the infection, CD4+ T cells have been shown to be more important in the later stages of infection, especially in cases of reinfection. Upregulation of proinflammatory cytokines and chemokines followed by CD4 + T cell-mediated type 1 immune response has been shown to confer protective immunity against chlamydial lung infection through NO production by iNOS pathway activation. Initially, Chlamydia encounters and infects lung epithelial cells and alveolar macrophages leading to infiltration of macrophages, dendritic cells, and neutrophils. However, Chlamydia also causes lung infections ranging from community-acquired pneumonia, bronchitis, pharyngitis, sinusitis, chronic asthma, and obstructive pulmonary disease. Ĭhlamydia is best known as an infectious agent for STD, and recurrent infection can lead to chronic inflammatory complications, including pelvic inflammatory disease and infertility. Additionally, fetuin-A was found to suppress LPS-induced production of interleukin 1 β (IL-1 β), nitric oxide (NO), and tumor necrosis factor-alpha (TNF- α) in cultured macrophages, suggesting that fetuin-A is a potent anti-inflammatory acute phase protein. 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.
![cm 01 02 real time editor cm 01 02 real time editor](https://www.mdpi.com/remotesensing/remotesensing-13-02694/article_deploy/html/images/remotesensing-13-02694-g006-550.jpg)
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.