Metabolic analyses reveal dysregulated NAD+ metabolism and altered mitochondrial state in ulcerative colitis.

Ulcerative colitis (UC) is a complex, multifactorial disease driven by a dysregulated immune response against host commensal microbes. Despite rapid advances in our understanding of host genomics and transcriptomics, the metabolic changes in UC remain poorly understood. We thus sought to investigate distinguishing metabolic features of the UC colon (14 controls and 19 patients).

Utilizing a reductionist model to study host-microbe interactions in intestinal inflammation.

Background: The gut microbiome is altered in patients with inflammatory bowel disease, yet how these alterations contribute to intestinal inflammation is poorly understood. Murine models have demonstrated the importance of the microbiome in colitis since colitis fails to develop in many genetically susceptible animal models when re-derived into germ-free environments. We have previously shown that Wiskott-Aldrich syndrome protein (WASP)-deficient mice (Was) develop spontaneous colitis, similar to human patients with loss-of-function mutations in WAS.

STAT1 signaling shields T cells from NK cell-mediated cytotoxicity.

The JAK-STAT pathway critically regulates T-cell differentiation, and STAT1 is postulated to regulate several immune-mediated diseases by inducing proinflammatory subsets. Here we show that STAT1 enables CD4 T-cell-mediated intestinal inflammation by protecting them from natural killer (NK) cell-mediated elimination. Stat1 T cells fail to expand and establish colitis in lymphopenic mice.

WASP-mediated regulation of anti-inflammatory macrophages is IL-10 dependent and is critical for intestinal homeostasis.

Mutations in Wiskott-Aldrich syndrome protein (WASP) cause autoimmune sequelae including colitis. Yet, how WASP mediates mucosal homeostasis is not fully understood. Here we show that WASP-mediated regulation of anti-inflammatory macrophages is critical for mucosal homeostasis and immune tolerance.

Interleukin 1β Mediates Intestinal Inflammation in Mice and Patients With Interleukin 10 Receptor Deficiency.

Interleukin 10 receptor (IL10R)-deficient mice develop spontaneous colitis and, similarly, patients with loss-of-function mutations in IL10R develop severe infant-onset inflammatory bowel disease. Loss of IL10R signaling in mouse and human macrophages is associated with increased production of interleukin 1β. We demonstrated that innate immune production of IL1β mediates colitis in IL10R-deficient mice.

[Assessment on the yield loss risk of longan caused by cold damage in South China].

Using daily climate variables gathered from 64 meteorological stations in South China from 1961 to 2012, recognized hazard indicators about disaster grades of cold damage for longan, and methods on agricultural meteorological disasters risk and simulation technology, the yield loss risks of longan caused by cold damage in South China during different developmental periods were assessed. The results showed that during the period of physiologic differentiation of flower bud, the disasters of longan affected by mild cold damage in South China were the most common, followed by severe cold damage and moderate cold damage. The hazards caused by cold damage under different grades varied.

Basophil-macrophage dialog in allergic inflammation.

Monocyte-macrophage differentiation under pathological conditions is poorly understood. In the present issue of Immunity, Egawa et al. (2013) report how basophils drive the differentiation of inflammatory monocytes into M2 macrophages, thereby regulating allergic skin inflammation.

Salmonella polarises peptide-MHC-II presentation towards an unconventional Type B CD4+ T-cell response.

Distinct peptide-MHC-II complexes, recognised by Type A and B CD4(+) T-cell subsets, are generated when antigen is loaded in different intracellular compartments. Conventional Type A T cells recognize their peptide epitope regardless of the route of processing, whereas unconventional Type B T cells only recognise exogenously supplied peptide. Type B T cells are implicated in autoimmune conditions and may break tolerance by escaping negative selection.