Aberrant T cell immune responses appear central to the development of systemic lupus erythematosus (SLE). We previously reported that Gαq, the alpha subunit of Gq, regulates T and B cell immune responses, promoting autoimmunity. To address whether Gαq contributes to the pathogenesis of SLE, Gαq mRNA expression was studied using real time-PCR in PBMCs and T cells from SLE patients as well as age- and sex-matched healthy controls. Our results showed that Gαq mRNA expression was decreased in PBMCs and T cells from SLE patients compared to healthy individuals. Correlation analyses showed that Gαq expression in T cells from SLE patients was associated with disease severity (as per SLE Disease Activity Index), the presence of lupus nephritis, and expression of Th1, Th2 and Th17 cytokines. In keeping with clinical results, T-helper cell subsets (Th1, Th2 and Th17) were over-represented in Gαq knockout mice. In addition, Gαq expression in SLE T cells was negatively correlated with the expression of Bcl-2, an anti-apoptotic gene, and positively correlated with the expression of Bax, a pro-apoptotic gene. These data suggest that reduced Gαq levels in T cells may promote enhanced and prolonged T cell activation, contributing to the clinical manifestations of SLE.

Accumulated data have shown that alternatively activated macrophage exerts a modulatory role in many diseases, including colitis. Interleukin-33 (IL-33), a critical modulator in adaptive and innate immune, has been implicated in autoimmunity and inflammation. Previously, we have reported that IL-33 functions as a protective modulator in TNBS-induced colitis, which is closely related to a Th1-to-Th2/Treg switch. Here, we present novel evidence suggesting that IL-33 primes macrophage into alternatively activated macrophages (AAM) in TNBS-induced colitis. The strong polarized effect of IL-33 was tightly associated with the markedly increased induction of Th2-type cytokines. To confirm the beneficial effects of AAM induced by IL-33, peritoneal AAMs isolated from IL-33-treated mice were transferred to recipient mice with TNBS colitis. The adoptive transfer resulted in prominent inhibition of disease activity and inflammatory cytokines in the TNBS-treated mice. In conclusion, our data provide clear evidence that IL-33 plays a protective role in TNBS-induced colitis, which is closely related to AAM polarization.

Salivary duct carcinomas (SDCa) are rare highly aggressive malignancies. Most patients die from distant metastatic disease within three years of diagnosis. There are limited therapeutic options for disseminated disease.

Rotavirus can lead to decreasing gut barrier function and diarrhea of children and young animals. Apple pectic oligosaccharide treatment reduced diarrhea in rotavirus-infected piglets. This study was conducted to explore whether apple pectic oligosaccharide administration could protect gut barrier function of piglets against rotavirus infection. A total of 28 crossbred weaned barrows were allotted into 2 treatments fed the diets supplementing 0 and 200 mg/kg apple pectic oligosaccharide. Half of pigs in each diet treatment were challenged by rotavirus on d 15. The whole duration of this experiment is 18 days. Rotavirus challenge increased average diarrhea index, and impaired microbiota in cecal digesta, and histology, expressions of tight-junction proteins, mucins and glucagon like peptide-2 concentrations, antioxidant capacity, endoplasmic reticulum stress, autophagy and apoptosis in jejunal mucosa of piglets. However, dietary apple pectic oligosaccharide supplementation relieved effects of rotavirus challenge on diarrhea, gut health, and antioxidant capacity, endoplasmic reticulum stress, autophagy and apoptosis of jejunal mucosa in piglets. These results suggest that apple pectic oligosaccharide administration can prevent diarrhea and damage of gut barrier function via improving antioxidant capacity that might reduce endoplasmic reticulum stress, autophagy and apoptosis of intestinal epithelial cells in rotavirus-infected piglets.