Tehran University of Medical Sciences

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Immunomodulation in Systemic Lupus Erythematosus: Induction of M2 Population in Monocyte-Derived Macrophages by Pioglitazone Publisher Pubmed



Mohammadi S1 ; Saghaeianjazi M2 ; Sedighi S3 ; Memarian A4
Authors
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Authors Affiliations
  1. 1. Department of Molecular Medicine, School of Advanced Technologies in Medicine, Golestan University of Medical Sciences, Gorgan, Iran
  2. 2. Biochemistry and Metabolic Disorders Research Center, Golestan University of Medical Sciences, Gorgan, Iran
  3. 3. Joint, Bone and Connective Tissue Research Center (JBCRC), Golestan University of Medical Sciences, Gorgan, Iran
  4. 4. Stem Cell Research Center, Golestan University of Medical Sciences, Gorgan, Iran

Source: Lupus Published:2017


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 I3 is proposed to function in the expansion of the M2 subpopulation. Pioglitazone is a peroxisome proliferator-activated receptor I3 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. © 2017 Author(s).