A genetic role for macrophage migration inhibitory factor (MIF) in Epinephelus awoara infected with Vibrio parahaemolyticus. (December 2016)

• Record Type: Journal Article
• Authors: Xu, Xiaojin; Sang, Benhong; Luo, Gang
• Is Part Of: European journal of inflammation. Volume 14:Number 3(2016)
• Page Start: 184
• Page End: 189
• Publication Date: 2016-12
• Subjects: Epinephelus awoara -- interleukin-1 -- macrophage migration inhibitory factor -- tumor necrosis factor alpha -- Vibrio parahaemolyticus; Inflammation -- Periodicals; Anti-Inflammatory Agents -- therapeutic use -- Periodicals; Immunotherapy -- Periodicals; Inflammation -- Periodicals; Anti-inflammatory agents -- Periodicals; Immunotherapy -- Periodicals; Anti-inflammatory agents; Immunotherapy; Inflammation; Periodicals; 616.0473
• DOI: 10.1177/1721727X16674017
• Languages: English
• ISSNs: 1721-727X

Abstract

Macrophage migration inhibitory factor (MIF) is a key pro-inflammatory cytokine in immuno-inflammatory diseases. For the first time, we examined the expression of MIF in Epinephelus awoara ( E. awoara ). MIF expressions have been detected in the head kidney, spleen, liver, brain, intestine, gill, heart, stomach, and muscle of E. awoara infected with Vibrio parahaemolyticus . The mRNA levels observed in infected groupers were higher than those in healthy groupers. MIF, tumor necrosis factor-α (TNF-α), and interleukin-1 (IL-1) tissue levels have been measured by ELISA. A significant increase in MIF, TNF-α, and IL-1 tissue levels have been found in the treatment groups compared with those in controls. MIF, TNF-α and IL-1 tissue levels in the spleen, head kidney, intestine, and liver of E. awoara during the challenge trial with V. parahaemolyticus were significantly higher than those in controls. There was evidence of functions of MIF in a positive feedback loop with TNF-α and IL-1 that could perpetuate the inflammatory process in grouper infected with V. parahaemolyticus . In conclusion, these results indicated that MIF was related to pathogen-induced immune response.