Wuchereria bancrofti macrophage migration inhibitory factor-2 (rWbaMIF-2) ameliorates experimental colitis.
Shriram RamaniNikhil ChauhanVishal KhatriConnie VitaliRamaswamy KalyanasundaramPublished in: Parasite immunology (2020)
Immunomodulatory molecules produced by helminth parasites are receiving much attention recently as novel therapeutic agents for inflammation and autoimmune diseases. In this study, we show that macrophage migration inhibitory factor (MIF) homologue from the filarial parasite, Wuchereria bancrofti (rWbaMIF-2), can suppress inflammation in a dextran sulphate sodium salt (DSS)-induced colitis model. The disease activity index (DAI) in DSS given mice showed loss of body weight and bloody diarrhoea. At autopsy, colon of these mice showed severe inflammation and reduced length. Administration of rWbaMIF-2 significantly reduced the DAI in DSS-induced colitis mice. rWbaMIF-2-treated mice had no blood in the stools, and their colon length was similar to the normal colon with minimal inflammation and histological changes. Pro-inflammatory cytokine genes (TNF-α, IL-6, IFN-γ, IL-1β, IL-17A and NOS2) were downregulated in the colon tissue and peritoneal macrophages of rWbaMIF-2-treated mice. However, there were significant increases in IL-10-producing Treg and B1 cells in the colon and peritoneal cavity of rWbaMIF-2-treated mice. These findings suggested that rWbaMIF-2 treatment significantly ameliorated the clinical symptoms, inflammation and colon pathology in DSS given mice. This immunomodulatory effect of rWbaMIF-2 appeared to be by promoting the infiltration of Treg cells into the colon.
Keyphrases
- high fat diet induced
- oxidative stress
- rheumatoid arthritis
- disease activity
- body weight
- systemic lupus erythematosus
- gene expression
- dendritic cells
- immune response
- genome wide
- induced apoptosis
- early onset
- dna methylation
- working memory
- insulin resistance
- signaling pathway
- depressive symptoms
- cell death
- newly diagnosed
- ulcerative colitis