Interleukin-10 limits local and body cavity inflammation during infection with muscle-stage Trichinella spiralis
Interleukin-10 limits local and body cavity inflammation during infection with muscle-stage Trichinella spiralis
复制标题
DOI：
10.1128/iai.72.6.3129-3137.2004
复制
发表时间：
2004-06-01
影响因子：
3.1
通讯作者：
Appleton, JA
中科院分区：
文献类型：
--
作者：
Beiting, DP;Bliss, SK;Appleton, JA
本研究的目的是表征细胞反应肌肉阶段旋毛虫。从其在肌肉中的细胞内栖息地，T。螺旋体分泌引起强烈的系统性宿主免疫应答的有效糖蛋白抗原。尽管这种反应的幅度和长期性质，护士细胞很少被浸润细胞破坏。我们检验了抗炎细胞因子白细胞介素-10（IL-10）调节细胞对肌肉期寄生虫的反应的假设。旋毛虫幼虫大量定植于横膈膜，促使我们评估除了肌肉局部反应之外的体腔局部反应。缺乏IL-10的小鼠在滋养细胞周围和胸膜腔中表现出过度的炎症反应。IL-10的作用在肌肉感染后20天最明显。IL-10缺陷小鼠的反应强度增加并不影响寄生虫的建立或存活。在感染后20至50天之间，野生型和IL-10缺陷型小鼠的炎症反应均减弱。肌肉感染也引起了抗体反应，其特征在于最初针对体细胞幼虫抗原的混合同种型，并改变为针对携带泰维糖的排泄或分泌抗原的免疫球蛋白G1主导的反应。我们的结论是，IL-10限制在肌肉感染的早期阶段的局部和区域炎症，但慢性炎症是由IL-10独立的机制，这是一致的Th 2反应。
The aim of this study was to characterize cellular responses to muscle-stage Trichinella spiralis. From its intracellular habitat in muscle, T. spiralis secretes potent glycoprotein antigens that elicit a strong systemic host immune response. Despite the magnitude and prolonged nature of this response, nurse cells are rarely destroyed by infiltrating cells. We tested the hypothesis that the anti-inflammatory cytoldne interleukin-10 (IL-10) moderates cellular responses to muscle-stage parasites. Trichinella larvae colonize the diaphragm in large numbers, prompting us to evaluate regional responses in body cavities in addition to local responses in muscle. Mice deficient in IL-10 demonstrated an exaggerated inflammatory response around nurse cells and in the pleural cavity. The effect of IL-10 was most evident 20 days following muscle infection. The increased intensity of the response in IL-10-deficient mice did not affect parasite establishment or survival. Between 20 and 50 days postinfection, the inflammatory response was diminished in both wild-type and IL-10-deficient mice. Muscle infection also elicited an antibody response, characterized initially by mixed isotypes directed at somatic larval antigens and changing to an immunoglobulin G1-dominated response directed at tyvelose-bearing excreted or secreted antigens. We conclude that IL-10 limits local and regional inflammation during the early stages of muscle infection but that chronic inflammation is controlled by an IL-10-independent mechanism that is coincident with a Th2 response.