DNaseI protects lipopolysaccharide-induced endometritis in mice by inhibiting neutrophil extracellular traps formation. (January 2021)

• Record Type: Journal Article
• Authors: Hao, Haoyang; Yu, Huiyuan; Sun, Haowen; Zhao, Caijun; Zhang, Naisheng; Hu, Xiaoyu; Fu, Yunhe
• Is Part Of: Microbial pathogenesis. Volume 150(2021)
• Publication Date: 2021-01
• Subjects: DNaseI -- Endometritis -- NETs -- LPS; Pathogenic microorganisms -- Periodicals; Pathology, Molecular -- Periodicals; Communicable Diseases -- microbiology -- Periodicals; Communicable Diseases -- parasitology -- Periodicals; Micro-organismes pathogènes -- Périodiques; Pathologie moléculaire -- Périodiques; Electronic journals; 616.9041
• DOI: 10.1016/j.micpath.2020.104686
• Languages: English
• ISSNs: 0882-4010

Abstract

Abstract: Endometritis is an inflammatory of the inner lining of the uterus caused by bacterial infections that affect female reproductive health in humans and animals. Neutrophil extracellular traps (NETs) have the ability to resist infections that caused by pathogenic invasions. It has been proved that the formation of NETs is related to certain inflammatory diseases, such as mastitis and chronic obstructive pulmonary disease (COPD). However, there are sparse studies related to NETs and endometritis. In this study, we investigated the role of NETs in lipopolysaccharide (LPS)-induced acute endometritis in mice and evaluated the therapeutic efficiency of DNaseI. We established LPS-induced endometritis model in mice and found that the formation of NETs can be detected in the mice uterine tissues in vivo. In addition, DNaseI treatment can inhibit NETs construction in LPS-induced endometritis in mice. Moreover, myeloperoxidase (MPO) activity assay indicated that DNaseI treatment remarkably alleviated the inflammatory cell infiltrations. ELISA test indicated that the treatment of DNaseI significantly inhibited the expression of the proinflammatory cytokines TNF-α, and IL-1β. Also, DNaseI was found to increase proteins expression of the uterine tissue tight junctions and suppress LPS-induced NF-κB activation. All the results indicated that DNaseI effectively inhibits the formation of NETs by blocking the NF-κB signaling pathway and enhances the expression of tight junction proteins, consequently, alleviates inflammatory reactions in LPS-induced endometritis in mice. Highlights: DNaseI inhibited the formation of NETs in the uterine tissues. DNaseI inhibited the inflammatory response in uterus induced by LPS. DNaseI inhibited the permeability of uterus barrier induced by LPS. DNaseI inhibited the production of pro-inflammatory cytokines via inhibiting the activation of NF-κB signal pathway.