Kurata Osamu, Nakabayashi Madoka, Hatai Kishio
Laboratory of Fish Diseases, Department of Veterinary Science, Nippon Veterinary and Life Science University, Musashino, Tokyo 180-8602, Japan.
Dev Comp Immunol. 2008;32(6):726-34. doi: 10.1016/j.dci.2007.11.003. Epub 2007 Dec 3.
We developed an in vitro model to study the cellular and molecular mechanisms of granulomatous inflammation in response to invading pathogens. Ichthyophonus hoferi was used as a target for encapsulation by cultivated leukocytes from the kidney of the rainbow trout (Oncorhynchus mykiss). The encapsulation process was observed over 1 week. The leukocytes were identified as either macrophages in the inner layer, or neutrophils and lymphocytes in the outer layer. The encapsulation response was inhibited by treatment with heat, but not formalin or methanol. The recognition of heat-unstable molecules on the pathogen surface could induce encapsulation. Increased expression of pro-inflammatory cytokines, such as interleukin (IL)-1beta, IL-8 and tumor necrosis factor-alpha2, was observed during encapsulation. These cytokines might play crucial roles in the encapsulation process. In particular, IL-8, which was expressed at a late phase, might recruit specific cell populations, such as the lymphocytes comprising the outer cellular layer around the target.
我们开发了一种体外模型，以研究针对入侵病原体的肉芽肿性炎症的细胞和分子机制。霍氏鱼醉菌被用作虹鳟（Oncorhynchus mykiss）肾脏培养白细胞进行包囊化的靶标。在1周内观察包囊化过程。白细胞在内层被鉴定为巨噬细胞，在外层被鉴定为中性粒细胞和淋巴细胞。用加热处理可抑制包囊化反应，但福尔马林或甲醇处理则无此作用。识别病原体表面热不稳定分子可诱导包囊化。在包囊化过程中观察到促炎细胞因子如白细胞介素（IL）-1β、IL-8和肿瘤坏死因子-α2的表达增加。这些细胞因子可能在包囊化过程中起关键作用。特别是在后期表达的IL-8可能募集特定的细胞群体，如构成靶标周围外层细胞层的淋巴细胞。
