Porcine IL12A and IL12B gene mapping, variation and evidence of association with lytic complement and blood leucocyte proliferation traits
INTERNATIONAL JOURNAL OF IMMUNOGENETICS
Authors: Wimmers, K.; Kumar, K. G.; Schellander, K.; Ponsuksili, S.
Abstract
Interleukin-12, a heterodimeric cytokine consisting of glycosylated subunits of 35 and 40 kDa, is a central molecule in controlling innate as well as adaptive immunity. This study was aimed to investigate the role of IL12A and IL12B as candidate genes for immune competence in pigs. The porcine genes were screened for polymorphism and association analysis was carried out by mixed model analysis with parameters of innate immunity, in vitro haemolytic complement activity in the classical and alternative pathways, in vivo complement activation expressed as C3c serum concentration, and blood leucocyte proliferation measured in F2 animals of a pig resource population based on cross of Duroc and Berlin miniature pig (DUMI resource population). A single nucleotide polymorphism (SNP) in the promoter region (C > A) of IL12A was identified. Two SNPs were detected in intron 4 of IL12B at positions 192 (A > G) and 437 (C > T). Significant effects of IL12 genotypes on complement activity traits and mitogen-induced leucocyte proliferation were found. The IL12A and IL12B genes were assigned to chromosome13 and 16, respectively, by using radiation hybrid analysis and genetic mapping in the DUMI resource population. Mapping and association analyses promote the IL12 genes as functional and positional candidate gene for disease resistance in pigs.
Administration of Akkermansia muciniphila Ameliorates Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice
FRONTIERS IN MICROBIOLOGY
Authors: Bian, Xiaoyuan; Wu, Wenrui; Yang, Liya; Lv, Longxian; Wang, Qing; Li, Yating; Ye, Jianzhong; Fang, Daiqiong; Wu, Jingjing; Jiang, Xianwan; Shi, Ding; Li, Lanjuan
Abstract
Inflammatory bowel diseases (IBDs) develop as a result of complex interactions among genes, innate immunity and environmental factors, which are related to the gut microbiota. Multiple clinical and animal data have shown that Akkermansia muciniphila is associated with a healthy mucosa. However, its precise role in colitis is currently unknown. Our study aimed to determine its protective effects and underlying mechanisms in a dextran sulfate sodium (DSS)-induced colitis mouse model. Twenty-four C57BL/6 male mice were administered A. muciniphila Muc(T) or phosphate-buffered saline (PBS) once daily by oral gavage for 14 days. Colitis was induced by drinking 2% DSS from days 0 to 6, followed by 2 days of drinking normal water. Mice were weighed daily and then sacrificed on day 8. We found that A. muciniphila improved DSS-induced colitis, which was evidenced by reduced weight loss, colon length shortening and histopathology scores and enhanced barrier function. Serum and tissue levels of inflammatory cytokines and chemokines (TNF-alpha, IL1 alpha, IL6, IL12A, MIP-1A, G-CSF, and KC) decreased as a result of A. muciniphila administration. Analysis of 16S rDNA sequences showed that A. muciniphila induced significant gut microbiota alterations. Furthermore, correlation analysis indicated that pro-inflammatory cytokines and other injury factors were negatively associated with Verrucomicrobia, Akkermansia, Ruminococcaceae, and Rikenellaceae, which were prominently abundant in A. muciniphila-treated mice. We confirmed that A. muciniphila treatment could ameliorate mucosal inflammation either via microbe-host interactions, which protect the gut barrier function and reduce the levels of inflammatory cytokines, or by improving the microbial community. Our findings suggest that A. muciniphila may be a potential probiotic agent for ameliorating colitis.
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