Distribution Of M1 Macrophages Research Articles

NLRP3 inflammasome mediates M1 macrophage polarization and IL-1β production in inflammatory root resorption.

To explore the involvement of NOD-like receptor protein 3 (NLRP3) inflammasome and M1 macrophage in root resorption (RR). A rat RR model was established by excessive orthodontic force. After different force-loading time, the expression levels of NLRP3, caspase-1, and interleukin-1β (IL-1β) and distribution of M1 macrophages were analysed by immunohistochemistry and immunofluorescence staining in vivo. Then, the mechanism of NLRP3 activation was further verified by macrophage and human periodontal ligament cell (hPDLC) co-culture system in vitro. The production levels of NLRP3, caspase-1, pro-caspase-1, and IL-1β in M1 macrophages in the co-culture system were detected by Western blot, and the polarization of CD68+IL-1β+ M1 macrophages was detected by immunofluorescence staining. In the rat RR model, NLRP3, caspase-1, IL-1β, and M1 macrophages were expressed in periodontal ligament, mainly concentrated around RR areas. Force-pre-treated hPDLCs promoted M1 macrophage polarization and the production of NLRP3, caspase-1, and IL-1β in M1 macrophages in co-culture system. When MCC950, an inhibitor of NLRP3 inflammasome, was added, NLRP3 activation and M1 macrophage polarization were inhibited. In periodontal tissues, hPDLCs stimulated by force promoted M1 macrophage polarization and increased IL-1β production by activating NLRP3 inflammasome in M1 macrophages, thus initiating the occurrence of RR.

ECM hydrogel coating mitigates the chronic inflammatory response to polypropylene mesh

Polypropylene has been used as a surgical mesh material for several decades. This non-degradable synthetic polymer provides mechanical strength, a predictable host response, and its use has resulted in reduced recurrence rates for ventral hernia and pelvic organ prolapse. However, polypropylene and similar synthetic materials are associated with a chronic local tissue inflammatory response and dense fibrous tissue deposition. These outcomes have prompted variations in mesh design to minimize the surface area interface and increase integration with host tissue. In contrast, biologic scaffold materials composed of extracellular matrix (ECM) are rapidly degraded in-vivo and are associated with constructive tissue remodeling and minimal fibrosis. The objective of the present study was to assess the effects of an ECM hydrogel coating on the long-term host tissue response to polypropylene mesh in a rodent model of abdominal muscle injury. At 14 days post implantation, the ECM coated polypropylene mesh devices showed a decreased inflammatory response as characterized by the number and distribution of M1 macrophages (CD86+/CD68+) around mesh fibers when compared to the uncoated mesh devices. At 180 days the ECM coated polypropylene showed decreased density of collagen and amount of mature type I collagen deposited between mesh fibers when compared to the uncoated mesh devices. This study confirms and extends previous findings that an ECM coating mitigates the chronic inflammatory response and associated scar tissue deposition characteristic of polypropylene.