4.2 Article

An Artificial Silk Elastin-Like Protein Modifies the Polarization of Macrophages

Journal

ACS APPLIED BIO MATERIALS
Volume 5, Issue 12, Pages 5657-5664

Publisher

AMER CHEMICAL SOC
DOI: 10.1021/acsabm.2c00701

Keywords

Artificial silk elastin-like protein; macrophage polarization; TNF-?; IL-10; morphological changes; a pouch model

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This study demonstrates the influence of silk elastin-like protein (SELP) on the polarization of mouse bone marrow-derived macrophages. Higher concentrations of SELP solution can suppress the secretion of pro-inflammatory cytokines from inflammation-type macrophages and enhance the secretion of anti-inflammation cytokines from original-type macrophages. Additionally, SELP can induce changes in the morphology of macrophages.
A silk elastin-like protein (SELP) is an artificial compound with silk fibroin-like and elastin-like tandem repeats. The objective of this study is to evaluate the influence of SELP on the polarization of mouse bone marrow-derived macrophages. When the macrophages of inflammation-type (M1) were cultured with different concentrations of SELP solution, the secretion of a pro-inflammatory cytokine, tumor necrotizing factor (TNF)-alpha, was significantly suppressed at the higher concentrations. In addition, the secretion of an anti-inflammation cytokine, interleukin (IL)-10, was significantly enhanced from the macrophage of an original type (M0). By the incubation with soluble SELP, the morphology of M0-and M1-type macrophages changed to be of a round shape with a large size. Following incubation with the sponge of SELP, the M0-type macrophages secreted IL-10 with time. When injected into an air pouch of mice subcutis which had been prepared by the injection of air, the SELP sponge and 5 wt % of SELP solution induced IL-10 secretion to a significantly high extent compared with the saline injection. Cells isolated from the air pouch 24 h after the injection were stained by the CD206 of a M2 marker. It is concluded that the SELP itself in solution has an ability to induce the anti-inflammation M2-type macrophages.

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