Tumor necrosis factor receptor superfamily members 1a and 1b contribute to exacerbation of atherosclerosis by Chlamydia pneumoniae in mice |
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Authors: | Mark T Zafiratos Jonathan T Cottrell Srikanth Manam Kyle K Henderson Kyle H Ramsey Ashlesh K Murthy |
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Institution: | 1. College of Health Sciences, Midwestern University, Downers Grove, 60515, USA;2. Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, 60515, USA;3. College of Veterinary Medicine, Midwestern University, Glendale, 85308, USA |
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Abstract: | The host immune responses that mediate Chlamydia-induced chronic disease sequelae are incompletely understood. The role of TNF-α, TNF receptor 1 (TNFR1), and TNF receptor 2 (TNFR2), in Chlamydia pneumoniae (CPN)-induced atherosclerosis was studied using the high-fat diet-fed male C57BL/6J mouse model. Following intranasal CPN infection, TNF-α knockout (KO), TNFR1 KO, TNFR2 KO, and TNFR 1/2 double-knockout, displayed comparable serum anti-chlamydial antibody response, splenic antigen-specific cytokine response, and serum cholesterol profiles compared to wild type (WT) animals. However, atherosclerotic pathology in each CPN-infected KO mouse group was reduced significantly compared to WT mice, suggesting that both TNFR1 and TNFR2 promote CPN-induced atherosclerosis. |
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Keywords: | Atherosclerosis Pathogenesis Tumor necrosis factor Tumor necrosis factor receptor 1 Tumor necrosis factor receptor 2 |
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