College of Health Sciences, Midwestern University, Downers Grove, 60515, USA.
Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, 60515, USA.
Microbes Infect. 2019 Mar;21(2):104-108. doi: 10.1016/j.micinf.2018.09.003. Epub 2018 Oct 4.
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.
介导衣原体引起的慢性疾病后遗症的宿主免疫反应尚不完全清楚。本研究使用高脂肪饮食喂养的雄性 C57BL/6J 小鼠模型，研究了肿瘤坏死因子-α（TNF-α）、肿瘤坏死因子受体 1（TNFR1）和肿瘤坏死因子受体 2（TNFR2）在肺炎衣原体（CPN）诱导的动脉粥样硬化中的作用。经鼻腔 CPN 感染后，TNF-α 敲除（KO）、TNFR1 KO、TNFR2 KO 和 TNFR1/2 双重敲除小鼠与野生型（WT）动物相比，血清抗衣原体抗体反应、脾抗原特异性细胞因子反应和血清胆固醇谱相当。然而，与 WT 小鼠相比，每种 CPN 感染的 KO 小鼠组的动脉粥样硬化病理明显减少，表明 TNFR1 和 TNFR2 均促进 CPN 诱导的动脉粥样硬化。
