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首页> 外文期刊>Infection and immunity >Cryptosporidium parvum infection of human intestinal epithelial cells induces the polarized secretion of C-X-C chemokines.
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Cryptosporidium parvum infection of human intestinal epithelial cells induces the polarized secretion of C-X-C chemokines.

机译：人肠上皮细胞的小隐孢子虫感染可诱导C-X-C趋化因子的极化分泌。

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Cryptosporidium parvum infects intestinal epithelial cells and does not invade deeper layers of the intestinal mucosa. Nonetheless, an inflammatory cell infiltrate that consists of neutrophils and mononuclear cells is often present in the lamina propria, which underlies the epithelium. This study investigated the host epithelial cell response to C. parvum by assessing in vitro and in vivo the expression and production of proinflammatory cytokines by intestinal epithelial cells after infection. The human colon epithelial cell lines HCT-8 and Caco-2 and human intestinal xenografts in SCID mice were infected with C. parvum. The expression and secretion of the C-X-C chemokines interleukin-8 (IL-8) and GROalpha were determined by reverse transcription-PCR analysis and enzyme-linked immunosorbent assay. Our results demonstrate that upregulated expression and secretion of IL-8 and GROalpha after C. parvum infection of intestinal epithelial cells first occurred 16 to 24 h after infection and increased over the ensuing 1 to 2 days. The kinetics of C-X-C chemokine production by C. parvum-infected epithelial cells contrast markedly with the rapid but transient expression of C-X-C chemokines by epithelial cells infected with invasive enteric bacteria. C-X-C chemokine secretion in C. parvum-infected epithelial cells occurred predominantly from the basolateral surface in polarized monolayers of Caco-2 cells grown in Transwell cultures, whereas cell lysis occurred at the apical surface. The basolateral secretion of IL-8 and GROalpha from C. parvum-infected epithelial cells suggests that C-X-C chemokines produced by those cells contribute to the mucosal inflammatory cell infiltrate in the underlying intestinal mucosa.
机译：细小隐孢子虫感染肠上皮细胞，并且不侵入肠粘膜的更深层。然而，由嗜中性粒细胞和单核细胞组成的炎性细胞浸润通常存在于上皮层下面的固有层中。这项研究通过评估感染后肠道上皮细胞的体外和体内促炎细胞因子的表达和产生，研究了宿主对上皮衣原体的反应。 SCID小鼠中的人结肠上皮细胞系HCT-8和Caco-2和人肠异种移植物感染了小球藻。 C-X-C趋化因子白细胞介素8（IL-8）和GROalpha的表达和分泌通过逆转录PCR分析和酶联免疫吸附测定来确定。我们的结果表明，肠道小肠念珠菌感染小肠念珠菌感染后，IL-8和GROalpha的表达和分泌上调首先在感染后16至24 h发生，并在随后的1至2天内增加。细小衣原体感染的上皮细胞产生C-X-C趋化因子的动力学与侵袭性肠细菌感染的上皮细胞快速但瞬时表达C-X-C趋化因子形成鲜明对比。 C.小病毒感染的上皮细胞中C-X-C趋化因子的分泌主要发生在Transwell培养的Caco-2细胞极化单层膜的基底外侧表面，而细胞溶解发生在顶端表面。细小衣原体感染的上皮细胞的IL-8和GROalpha的基底外侧分泌表明，这些细胞产生的C-X-C趋化因子有助于粘膜炎性细胞浸润在下面的肠粘膜中。

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