Anti-ITGAX monoclonal antibody, clone CV26

Neonatal sepsis is one of the most prevalent causes of death of the neonates. However, the mechanisms underlying neonatal sepsis remained unclear. The present study identified a total of 1128 upregulated mRNAs and 1008 downregulated mRNAs, 28 upregulated lncRNAs, and 61 downregulated lncRNAs in neonatal sepsis. Then, we constructed PPI networks to identify key regulators in neonatal sepsis, including ITGAM, ITGAX, TLR4, ITGB2, SRC, ELANE, RPLP0, RPS28, RPL26, and RPL27. lncRNA coexpression analysis showed HS.294603, LOC391811, C12ORF47, LOC729021, HS.546375, HNRPA1L-2, LOC158345, and HS.495041 played important roles in the progression of neonatal sepsis. Bioinformatics analysis showed DEGs were involved in the regulation cellular extravasation, acute inflammatory response, macrophage activation of NF-kappa B signaling pathway, TNF signaling pathway, HIF-1 signaling pathway, Toll-like receptor signaling pathway, and ribosome, RNA transport, and spliceosome. lncRNAs were involved in regulating ribosome, T cell receptor signaling pathway, RNA degradation, insulin resistance, ribosome biogenesis in eukaryotes, and hematopoietic cell lineage. We thought this study provided useful information for identifying novel therapeutic markers for neonatal sepsis.

Obesity is associated with increased macrophage and extracellular matrix accumulation in adipose tissue, which can be partially reversed following weight loss by daily caloric restriction. This study examined the effects of 8 weeks of intermittent fasting (IF; 24-hour fast on 3 nonconsecutive days per week) in mice fed a chow or high-fat diet (HFD; 43% fat) on markers of adipose tissue inflammation and fibrosis. We found that IF decreased energy intake, body weight, and fat cell size in HFD-fed mice and decreased fat mass and improved glucose tolerance in chow- and HFD-fed mice. IF decreased mRNA levels of macrophage markers (Lgals3, Itgax, Ccl2, and Ccl3) in inguinal and gonadal fat, as well as adipose tissue macrophage numbers in HFD-fed mice only, and altered genes involved in NLRP3 inflammasome pathway in both diet groups. IF increased mRNA levels of matrix metallopeptidase 9, which is involved in extracellular matrix degradation, and reduced mRNA levels of collagen 6 alpha-1 and tissue inhibitor of matrix metallopeptidase 1, as well as fibrosis in gonadal fat in HFD-fed mice. In summary, our results show that intermittent fasting improved glucose tolerance in chow- and HFD-fed mice and ameliorated adipose tissue inflammation and fibrosis in HFD-fed mice.