Retinoid X receptor gamma dictates the activation threshold of group 2 innate lymphoid cells and limits type 2 inflammation in the small intestine.

Group 2 innate lymphoid cells (ILC2s) are crucial in promoting type 2 inflammation that contributes to both anti-parasite immunity and allergic diseases. However, the molecular checkpoints in ILC2s that determine whether to immediately launch a proinflammatory response are unknown. Here, we found that retinoid X receptor gamma (Rxrg) was highly expressed in small intestinal ILC2s and rapidly suppressed by alarmin cytokines.

Parkin increases the risk of colitis by downregulation of VDR via autophagy-lysosome degradation.

Parkin, an E3 ubiquitin ligase, plays an essential role in mitophagy. Emerging evidence indicates that mitophagy is involved in various processes closely related to immune diseases, including inflammatory bowel diseases (IBD). Here, the authors show that Parkin increases the occurrence of colitis and severe inflammation.

Vitamin D receptor enhances NLRC4 inflammasome activation by promoting NAIPs-NLRC4 association.

Inflammasomes are cytosolic multiprotein complexes that initiate host defense against bacterial pathogens. The nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family caspase-associated recruitment domain-containing protein 4 (NLRC4) inflammasomes plays a critical role in the inflammatory response against intracellular bacterial infection. The NLR family apoptosis inhibitory proteins (NAIPs) detect Flagellin or type III secretion system (T3SS) microbial components to activate NLRC4 inflammasome.

Effects of Dietary Protein Levels on Fecal Amino Acids Excretion and Apparent Digestibility, and Fecal and Ileal Microbial Amino Acids Composition in Weaned Piglets.

The purpose of this study was to determine the effects of low protein diets with the same Lys, Met + Cys, Thr, and Trp levels as in high protein diets on the fecal amino acid excretion and apparent digestibility, and ileal and fecal microbial amino acids composition in weaned piglets. Fifty-four 21-day-old Duroc × Landrace × Yorkshire weaned piglets were randomly divided into three groups and fed with corn-soybean meal basal diets, in which the crude protein (CP) content was 20% (H-CP), 17% (M-CP), and 14% (L-CP), respectively. The experiment included a 7-day adaptation period and a 45-day trial period.

Vitamin D Receptor Inhibits NLRP3 Activation by Impeding Its BRCC3-Mediated Deubiquitination.

The NLRP3 inflammasome is a multiprotein oligomer responsible for activation of the inflammatory response by promoting the maturation and secretion of the pro-inflammatory cytokines IL-1β and IL-18. Dysregulation of this inflammasome has been linked to several autoimmune diseases, indicating that NLRP3 is tightly regulated to prevent aberrant activation. The regulation of NLRP3 activation remains unclear.

Sphingosine kinase 2 cooperating with Fyn promotes kidney fibroblast activation and fibrosis via STAT3 and AKT.

Sphingosine kinases (Sphks) are the rate-limiting enzymes in the conversion of sphingosine to biologically active sphingosine-1-phosphate. The present study aimed to determine the role of Sphk2 and its downstream targets in renal fibroblast activation and interstitial fibrosis. In the kidney interstitium of patients with renal fibrosis, Sphk2-expressing cells (mainly interstitial fibroblasts) were significantly elevated and highly correlated with disease progression in patients.

Corrigendum: 1,25-Dihydroxyvitamin D Inhibits LPS-Induced High-Mobility Group Box 1 (HMGB1) Secretion Targeting the NF-E2-Related Factor 2-Hemeoxygenase-1-HMGB1 Pathway in Macrophages.

[This corrects the article on p. 1308 in vol. 8, PMID: 29085368.

1,25-Dihydroxyvitamin D Inhibits LPS-Induced High-Mobility Group Box 1 (HMGB1) Secretion Targeting the NF-E2-Related Factor 2-Hemeoxygenase-1-HMGB1 Pathway in Macrophages.

1,25-Dihydroxyvitamin D [1,25(OH)D] is recognized as a key mediator of inflammatory diseases, including sepsis. Clinical studies demonstrate that 1,25 (OH)D protects patients from sepsis, but clinical treatment with 1,25(OH)D is rare. In this study, we report that 1,25(OH)D treatment has beneficial effects and improves the survival rate in LPS-induced mouse sepsis model by blocking the secretion of high-mobility group box 1 (HMGB1), a key late regulator of sepsis.