Interleukin-33 contributes to both M1 and M2 chemokine marker expression in human macrophages

BMC Immunology

Research Article

Karen E Duffy¹  Anuk Das¹  William G Finn²  Amrita D Joshi²  Cory M Hogaboam²  Sameer R Oak²  Steven L Kunkel²  Adam J Hartigan² 

[1] Centocor Inc, Radnor, PA, USA;Department of Pathology, University of Michigan Medical School, Ann Arbor, MI, USA;

关键词: Human Macrophage;    iNKT Cell;    Mouse Macrophage;    Mannose Receptor;    CCL18 Expression;   

DOI  :  10.1186/1471-2172-11-52

 received in 2010-08-19, accepted in 2010-10-19,  发布年份 2010

来源: Springer

【 摘 要 】

BackgroundInterleukin-33 is a member of the IL-1 cytokine family whose functions are mediated and modulated by the ST2 receptor. IL-33-ST2 expression and interactions have been explored in mouse macrophages but little is known about the effect of IL-33 on human macrophages. The expression of ST2 transcript and protein levels, and IL-33-mediated effects on M1 (i.e. classical activation) and M2 (i.e. alternative activation) chemokine marker expression in human bone marrow-derived macrophages were examined.ResultsHuman macrophages constitutively expressed the membrane-associated (i.e. ST2L) and the soluble (i.e. sST2) ST2 receptors. M2 (IL-4 + IL-13) skewing stimuli markedly increased the expression of ST2L, but neither polarizing cytokine treatment promoted the release of sST2 from these cells. When added to naïve macrophages alone, IL-33 directly enhanced the expression of CCL3. In combination with LPS, IL-33 blocked the expression of the M2 chemokine marker CCL18, but did not alter CCL3 expression in these naive cells. The addition of IL-33 to M1 macrophages markedly increased the expression of CCL18 above that detected in untreated M1 macrophages. Similarly, alternatively activated human macrophages treated with IL-33 exhibited enhanced expression of CCL18 and the M2 marker mannose receptor above that detected in M2 macrophages alone.ConclusionsTogether, these data suggest that primary responses to IL-33 in bone marrow derived human macrophages favors M1 chemokine generation while its addition to polarized human macrophages promotes or amplifies M2 chemokine expression.

【 授权许可】

Unknown   
© Joshi et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.