Johansson Sofi, Andersson Kerstin, Wennergren Göran, Wennerås Christine, Rudin Anna
Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, University of Gothenburg, Guldhedsgatan 10A, 413 46, Göteborg, Sweden.
Inflammation. 2009 Apr;32(2):65-9. doi: 10.1007/s10753-008-9103-1.
Clara cell 16-kDa (CC16) is an anti-inflammatory protein chiefly produced in the lung epithelium. CC16 has been shown to inhibit the migration of rabbit neutrophils and human monocytes toward the formyl peptide N-formyl-methionine-leucin-phenylalanin (fMLF). Eosinophils migrate towards prostaglandin D2 (PGD(2)) and CC16 has been shown to bind to PGD(2). Therefore we investigated if CC16 could inhibit the migration of human eosinophils and neutrophils towards fMLF and/or PGD(2). Migration of eosinophils and neutrophils was assessed in a microplate migration system using specific ligands and receptor antagonists. CC16 inhibited the migration of eosinophils and neutrophils toward fMLF, which is likely to result from the interaction of CC16 with members of the formyl-peptide receptor family. However, CC16 did not inhibit eosinophil migration towards PGD(2). We therefore propose that CC16 may down-modulate the entry of human eosinophils and neutrophils into the airways during inflammation in the lung.
克拉拉细胞16千道尔顿蛋白（CC16）是一种主要在肺上皮细胞中产生的抗炎蛋白。研究表明，CC16可抑制兔中性粒细胞和人单核细胞向甲酰肽N-甲酰甲硫氨酸-亮氨酸-苯丙氨酸（fMLF）的迁移。嗜酸性粒细胞会向前列腺素D2（PGD2）迁移，且已证实CC16可与PGD2结合。因此，我们研究了CC16是否能抑制人嗜酸性粒细胞和中性粒细胞向fMLF和/或PGD2的迁移。使用特异性配体和受体拮抗剂，在微孔板迁移系统中评估嗜酸性粒细胞和中性粒细胞的迁移情况。CC16抑制了嗜酸性粒细胞和中性粒细胞向fMLF的迁移，这可能是CC16与甲酰肽受体家族成员相互作用的结果。然而，CC16并未抑制嗜酸性粒细胞向PGD2的迁移。因此，我们认为CC16可能在肺部炎症期间下调人嗜酸性粒细胞和中性粒细胞进入气道的过程。
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