Department of Pathology and Laboratory Medicine, Medical Sciences I, University of California, Irvinegrid.266093.8, Irvine, California, USA.
Department of Biomedical Sciences, Arthur Dugoni School of Dentistry, University of the Pacific, San Francisco, California, USA.
Microbiol Spectr. 2022 Aug 31;10(4):e0161722. doi: 10.1128/spectrum.01617-22. Epub 2022 Jul 25.
The tumor necrosis factor (TNF)-related apoptosis-inducing ligand receptor (TRAIL-R) suppresses inflammation and could therefore affect the course of Chlamydia infections and their long-term sequelae. Wild-type (WT) and C57BL/6 mice were inoculated vaginally with Chlamydia muridarum; the course of the infection was followed with vaginal cultures and the presence of hydrosalpinx determined. To evaluate the role of TRAIL-R following a secondary infection, the mice were vaginally reinfected. WT and male mice were also infected and reinfected in the respiratory tract, and the course of the diseases and the infections were followed. Following the primary and secondary vaginal infection, no significant differences in vaginal shedding or hydrosalpinx formation were observed between the WT and mice. The WT and mice mounted antibody responses in serum and vaginal washes that were not significantly different. After the primary and secondary intranasal infections of the male mice, changes in body weight were determined, and no significant differences were observed between the WT and mice. Ten days after the primary and the secondary infections, the weight of the lungs and number of C. muridarum inclusion forming units (IFU) were determined. The lungs of the WT mice weighed less compared with the mice following a primary infection but not after a secondary infection. No differences in the number of C. muridarum IFU in the lungs were observed between the two groups of mice. In conclusion, despite playing a role in inflammation cell-signaling pathways , TRAIL-R does not appear to play a major role in the susceptibility, clinical outcomes, or long-term sequelae of C. muridarum infections . TNF-related apoptosis-inducing ligand receptor (TRAIL-R) is involved in suppressing inflammatory responses. Bacterial pathogens such as Chlamydia spp. elicit inflammatory responses in humans following genital, ocular, and respiratory infections. The inflammatory responses are important to control the spread of Chlamydia. However, in certain instances, these inflammatory responses can produce long-term sequelae, including fibrosis. Fibrosis, or scarring, in the genital tract, eye, and respiratory system results in functional deficiencies, including infertility, blindness, and chronic obstructive lung disease, respectively. The goal of this study was to determine if mice deficient in TRAIL-R infected in the genital and respiratory tracts with Chlamydia spp. suffer more or less severe infections, infertility, or lung diseases than wild-type mice. Our results show no differences between the immune responses, infection severity, and long-term sequelae between TRAIL-R knockout and wild-type animals following a genital or a respiratory infection with Chlamydia.
肿瘤坏死因子（TNF）相关凋亡诱导配体受体（TRAIL-R）可抑制炎症，因此可能影响沙眼衣原体感染及其长期后果。将野生型（WT）和 C57BL/6 小鼠经阴道接种沙眼衣原体鼠亚种；通过阴道培养和确定输卵管积水来跟踪感染过程。为了评估 TRAIL-R 在继发感染后的作用，对小鼠进行了阴道再感染。还对 WT 和 雄性小鼠进行了呼吸道感染和再感染，并跟踪疾病和感染的过程。在原发性和继发性阴道感染后，WT 和 小鼠在阴道脱落或输卵管积水形成方面没有明显差异。WT 和 小鼠在血清和阴道冲洗中产生的抗体反应没有明显差异。在雄性小鼠的原发性和继发性鼻内感染后，确定体重变化，WT 和 小鼠之间没有观察到明显差异。原发性和继发性感染后 10 天，测定肺重和沙眼衣原体包涵体形成单位（IFU）数量。与原发性感染后相比，WT 小鼠的肺重较轻，但继发性感染后则无差异。两组小鼠肺中的沙眼衣原体 IFU 数量无差异。总之，尽管 TRAIL-R 在炎症细胞信号通路中起作用，但它似乎在沙眼衣原体感染的易感性、临床结果或长期后果中不起主要作用。肿瘤坏死因子相关凋亡诱导配体受体（TRAIL-R）参与抑制炎症反应。细菌病原体，如沙眼衣原体，在人类生殖道、眼部和呼吸道感染后会引发炎症反应。炎症反应对于控制衣原体的传播很重要。然而，在某些情况下，这些炎症反应会产生长期后果，包括纤维化。生殖道、眼睛和呼吸系统的纤维化或瘢痕形成会导致功能缺陷，分别为不孕、失明和慢性阻塞性肺疾病。本研究的目的是确定 TRAIL-R 缺失的小鼠在生殖道和呼吸道感染沙眼衣原体后，与野生型小鼠相比，感染是否更严重、不孕或肺部疾病更严重。我们的结果表明，TRAIL-R 缺失和野生型动物在生殖道或呼吸道感染沙眼衣原体后，在免疫反应、感染严重程度和长期后果方面没有差异。
