Lechner F, Vogt H R, Seow H F, von Bodungen U, Bertoni G, Zurbriggen A, Peterhans E
Institute of Veterinary Virology, University of Berne, Switzerland.
Vet Immunol Immunopathol. 1996 Nov;54(1-4):281-9. doi: 10.1016/s0165-2427(96)05701-7.
Goats infected with caprine arthritis encephalitis virus (CAEV) develop chronic arthritis sharing many features with human rheumatoid arthritis (RA). TNF is thought to be a key mediator contributing to the formation of the arthritic lesion in RA. We studied this cytokine in goats suffering from chronic arthritis. TNF alpha expressing cells were detected by in situ hybridization in synovial membranes of arthritic carpal joints. Expression of TNF alpha did not correlate with the degree of viral replication as assessed by in situ hybridization for viral RNA. In line with the lack of correlation between the degree of viral replication and TNF expression in vivo, we failed to detect increased cytokine RNA in goat macrophages infected with CAE virus in vitro and no TNF protein was found in culture supernatants. In addition, virus infection failed to prime goat macrophages for enhanced TNF expression in response to lipopolysaccharide. Taken together, these findings argue against a direct role of CAE virus in increasing the expression of TNF alpha in caprine arthritis.
感染山羊关节炎脑炎病毒(CAEV)的山羊会患上慢性关节炎,其具有许多与人类类风湿性关节炎(RA)相同的特征。肿瘤坏死因子(TNF)被认为是导致RA中关节炎病变形成的关键介质。我们对患有慢性关节炎的山羊体内的这种细胞因子进行了研究。通过原位杂交在关节炎腕关节的滑膜中检测到表达TNFα的细胞。通过对病毒RNA进行原位杂交评估,TNFα的表达与病毒复制程度无关。鉴于体内病毒复制程度与TNF表达之间缺乏相关性,我们在体外感染CAE病毒的山羊巨噬细胞中未检测到细胞因子RNA增加,并且在培养上清液中未发现TNF蛋白。此外,病毒感染未能使山羊巨噬细胞对脂多糖刺激产生增强的TNF表达。综上所述,这些发现表明CAE病毒在山羊关节炎中增加TNFα表达方面没有直接作用。