Immunomodulation in systemic lupus erythematosus: induction of M2 population in monocyte-derived macrophages by pioglitazone. (October 2017)

• Record Type: Journal Article
• Authors: Mohammadi, S; Saghaeian-Jazi, M; Sedighi, S; Memarian, A
• Is Part Of: Lupus. Volume 26:Number 12(2017)
• Page Start: 1318
• Page End: 1327
• Publication Date: 2017-10
• Subjects: Efferocytosis -- immunomodulation -- macrophage polarization -- peroxisome proliferator-activated receptor γ -- pioglitazone -- systemic lupus erythematosus; Systemic lupus erythematosus -- Periodicals; 616.772005
• DOI: 10.1177/0961203317701842
• Languages: English
• ISSNs: 0961-2033

Abstract

Macrophages have recently gained attention in systemic lupus erythematosus (SLE) pathogenesis for their role in the anti-inflammatory clearance of apoptotic cells. The M1/M2 polarization of macrophages improves efferocytic capability. Peroxisome proliferator-activated receptor γ is proposed to function in the expansion of the M2 subpopulation. Pioglitazone is a peroxisome proliferator-activated receptor γ agonist with a variety of anti-inflammatory effects. In this paper, we investigated the ex vivo alterations of monocyte-derived macrophages of 15 newly diagnosed SLE patients and 10 normal subjects triggered by apoptotic cells among SLE patients following pioglitazone treatment. The phagocytosis capacity of macrophages and M1/M2 polarization (CD86/CD163) was evaluated. The supernatants were also analyzed for the expression of interleukin (IL)-10, IL-12, transforming growth factor β1 and TNF-α. The mRNA expression of IL-1β and mannose receptor C-type 1 were also quantified among treated and non-treated monocyte-derived macrophages. We found that efferocytosis is defective among monocyte-derived macrophages of SLE patients and might be a major underlying mechanism involved in the sustained inflammation. Pioglitazone could enhance alternative activation of monocyte-derived macrophages and consequently immunomodulation in these patients.