CXCL17 is a mucosal chemokine elevated in idiopathic pulmonary fibrosis that exhibits broad antimicrobial activity.
CXCL17 is a mucosal chemokine elevated in idiopathic pulmonary fibrosis that exhibits broad antimicrobial activity.
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DOI：
10.4049/jimmunol.1102903
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发表时间：
2012-06-15
期刊：
影响因子：
--
通讯作者：
Zlotnik A
中科院分区：
文献类型：
--
作者：
Burkhardt AM;Tai KP;Flores-Guiterrez JP;Vilches-Cisneros N;Kamdar K;Barbosa-Quintana O;Valle-Rios R;Hevezi PA;Zuñiga J;Selman M;Ouellette AJ;Zlotnik A
粘膜免疫网络是防止病原体进入人体的重要屏障。介导粘膜防御机制的免疫细胞网络可能是由趋化因子形成的，趋化因子吸引广泛的免疫细胞到身体的特定部位。根据趋化因子的表达模式，可分为稳态趋化因子和炎性趋化因子。此外，一些趋化因子介导入侵病原体的直接杀伤，例如CCL28，一种与粘膜相关的趋化因子，对一系列病原体具有抗菌活性。CXCL17是最后一个被描述的趋化因子配体，也是CXC趋化因子家族的第17个成员。它在105个人体组织和细胞中的表达模式表明CXCL17是一种稳态的粘膜相关趋化因子。其在粘膜组织中的战略性表达提示其参与粘膜的先天免疫和/或不育。为了验证后一种假设，我们测试了CXCL17对一组致病菌和机会性细菌的可能抗菌活性。我们的研究结果表明，CXCL17具有强大的抗菌活性，其抗菌作用机制涉及肽介导的细菌膜破坏。由于CXCL17在支气管中强烈表达，我们在支气管肺泡灌洗液中测量了它，并观察到它在特发性肺纤维化中强烈上调。我们得出结论，CXCL17是一种抗菌粘膜趋化因子，可能在间质性肺疾病的发病机制中发挥作用。
The mucosal immune network is a crucial barrier preventing pathogens from entering the body. The network of immune cells that mediates the defensive mechanisms in the mucosa is likely shaped by chemokines, which attract a wide range of immune cells to specific sites of the body. Chemokines have been divided into homeostatic or inflammatory depending upon their expression patterns. Additionally, several chemokines mediate direct killing of invading pathogens, as exemplified by CCL28, a mucosa-associated chemokine that exhibits antimicrobial activity against a range of pathogens. CXCL17 was the last chemokine ligand to be described, and the 17th member of the CXC chemokine family. Its expression pattern in 105 human tissues and cells indicates that CXCL17 is a homeostatic, mucosa-associated chemokine. Its strategic expression in mucosal tissues suggests that it is involved in innate immunity and/or sterility of the mucosa. To test the latter hypothesis, we tested CXCL17 for possible antibacterial activity against a panel of pathogenic and opportunistic bacteria. Our results indicate that CXCL17 has potent antimicrobial activities, and that its mechanism of antimicrobial action involves peptide-mediated bacterial membrane disruption. Since CXCL17 is strongly expressed in bronchi, we measured it in bronchoalveolar lavage fluids, and observed that it is strongly upregulated in idiopathic pulmonary fibrosis. We conclude that CXCL17 is an antimicrobial mucosal chemokine that may play a role in the pathogenesis of interstitial lung diseases.
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