Phenotypic and functional modulations of porcine macrophages by interferons and interleukin-4. (July 2018)

• Record Type: Journal Article
• Authors: Sautter, Carmen A.; Auray, Gaël; Python, Sylvie; Liniger, Matthias; Summerfield, Artur
• Is Part Of: Developmental and comparative immunology. Volume 84(2018)
• Page Start: 181
• Page End: 192
• Publication Date: 2018-07
• Subjects: Pig -- Macrophages -- Polarization -- IL-4 -- IFNγ -- IFNβ; CSF-1 colony-stimulating factor-1 (also known as M-CSF) -- CSF-2 colony-stimulating factor-2 (also known as GM-CSF) -- ENPP1 ectonucleotide pyrophosphatase/phosphodiesterase 1 -- FBS fetal bovine serum -- iNOS inducible nitric oxide synthase -- MDM monocyte-derived macrophage -- PS porcine serum; Immunology -- Periodicals; Developmental immunology -- Periodicals; 616.079
• DOI: 10.1016/j.dci.2018.01.018
• Languages: English
• ISSNs: 0145-305X

Abstract

Abstract: Considering that macrophage functions are strongly impacted by the local tissue environment and the type of immune response, the aim of this study was to carefully set the methodological baseline for phenotype and functions of polarized porcine monocyte-derived macrophages. To this end, macrophages were generated in autologous serum alone or with colony-stimulating factor (CSF)-1 or CSF-2, and subsequently polarized with interferon (IFN)γ, interleukin-4 or IFNβ. IFNγ promoted expression of MHC class I, MHC class II, CD11a, and CD40 as well as LPS-induced IL-6 and IL-12. A hallmark of interleukin-4 was Arginase 1 and CD203a upregulation, without abrogating pro-inflammatory cytokine production. IFNβ induced CD169, MHC class I, CD40, CD80/86, but suppressed IL-6, IL-12 and tumor-necrosis-factor secretion. CSF-2 alone altered macrophage differentiation and promoted an IFNγ-like polarization. Altogether, the results provide a comprehensive overview of porcine macrophage polarization, and demonstrate commonalities with other species as well as peculiarities of the pig. Highlights: Antigen presentation molecule induction is a hallmark of IFNγ and IFNβ polarization. IFNγ-priming strongly promotes LPS-induced IL-6 and IL-12 secretion. IFNβ treatment suppresses LPS-induced TNF responses. High CD203a expression and IL-12 prevention are hallmarks of IL-4 polarization. LPS-induced IL-1β, IL-8 and IL-10 are not impacted by polarizing cytokine treatments.