VIP impairs acquisition of the macrophage proinflammatory polarization profile

Journal of Leukocyte Biology

Mar Carrión¹  Irene Gutiérrez-Cañas¹  Rosa P. Gomariz,, and¹  Carmen Martínez²  Yasmina Juarranz¹  Amaya Puig-Kröger³  Selene Pérez-García¹  Lizbeth Estrada-Capetillo³ 

[1]Faculty of Biology, Department of Cell Biology, Complutense University, Madrid, Spain

[2] Faculty of Medicine, Department of Cell Biology, Complutense University, Madrid, Spain

[3]Immuno-metabolism Laboratory, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, Madrid, Spain Faculty of Biology, Department of Cell Biology, Complutense University, Madrid, Spain

关键词: granulocyte;    anti-inflammatory;    rheumatoid arthritis;    human monocyte;    inflammation;   

DOI  :  10.1189/jlb.3A0116-032RR

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

This study tested the hypothesis that vasoactive intestinal peptide (VIP) is able to modify the macrophage inflammatory profile, thus supporting its therapeutic role in autoimmune diseases. Macrophages are innate immune cells that display a variety of functions and inflammatory profiles in response to the environment that critically controls their polarization. Deregulation between the pro- and anti-inflammatory phenotypes has been involved in different pathologies. Rheumatoid arthritis (RA) is an autoimmune disease, in which macrophages are considered central effectors of synovial inflammation, displaying a proinflammatory profile. VIP is a pleiotropic neuropeptide with proven anti-inflammatory actions. As modulation of the macrophage phenotype has been implicated in the resolution of inflammatory diseases, we evaluated whether VIP is able to modulate human macrophage polarization. In vitro-polarized macrophages by GM-CSF (GM-MØ), with a proinflammatory profile, expressed higher levels of VIP receptors, vasoactive intestinal polypeptide receptors 1 and 2 (VPAC1 and VPAC2, respectively), than macrophages polarized by M-CSF (M-MØ) with anti-inflammatory activities. RA synovial macrophages, according to their GM-CSF-like polarization state, expressed both VPAC1 and VPAC2. In vitro-generated GM-MØ exposed to VIP exhibited an up-regulation of M-MØ gene marker expression, whereas their proinflammatory cytokine profile was reduced in favor of an anti-inflammatory function. Likewise, in GM-MØ, generated in the presence of VIP, VIP somehow changes the macrophages physiology profile to a less-damaging phenotype. Therefore, these results add new value to VIP as an immunomodulatory agent on inflammatory diseases.

【 授权许可】

Unknown