| First Author | Choi YJ | Year | 2022 |
| Journal | Sci Rep | Volume | 12 |
| Issue | 1 | Pages | 1700 |
| PubMed ID | 35105928 | Mgi Jnum | J:319757 |
| Mgi Id | MGI:6865106 | Doi | 10.1038/s41598-022-05708-8 |
| Citation | Choi YJ, et al. (2022) Promotion of the inflammatory response in mid colon of complement component 3 knockout mice. Sci Rep 12(1):1700 |
| abstractText | To determine whether complement component 3 (C3) deficiency affects its receptor downstream-mediated inflammatory response, the current study was undertaken to measure alterations in the inducible nitric oxide synthase (iNOS)mediated cyclooxygenase2 (COX2) induction pathway, inflammasome pathway, nuclear factor-kappaB (NF-kappaB) activation, and inflammatory cytokine expressions in the mid colon of C3 knockout (KO) mice. Significant enhancement was observed in expressions of key components of the iNOSmediated COX2 induction pathway, and in the phosphorylation of mitogenactivated protein (MAP) kinase members. A similar pattern of increase was also observed in the expression levels of inflammasome proteins in C3 KO mice. Moreover, compared to WT mice, C3 KO mice showed remarkably enhanced phosphorylation of NF-kappaB and Inhibitor of kappaB-alpha (IkappaB-alpha), which was reflected in entirety as increased expressions of Tumor necrosis factor (TNF), IL-6 and IL-1alpha. However, the levels of E-cadherin, tight junction channels and ion channels expressions were lower in the C3 KO mice, although myeloperoxidase (MPO) activity for neutrophils was slightly increased. Taken together, results of the current study indicate that C3 deficiency promotes inflammatory responses in the mid colon of C3 KO mice through activation of the iNOSmediated COX2 induction pathway, Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC)-inflammasome pathway and NF-kappaB signaling pathway, and the enhancement of inflammatory cytokine expressions. |
