Neural-immune receptor cross-talk in the intestine

Bakri Assas and colleagues discuss cross-talk between neural and immune receptors in controlling immune homeostasis in the intestine. They propose a mechanism by which Gram-negative bacterial signaling via Toll-like receptor 4 can activate the sensory vanilloid receptor 1 via intracellular signaling, thereby inducing the release of anti-inflammatory calcitonin gene-related peptide to maintain mucosal homeostasis. See page 1283

Regulatory T cells promote Th17 responses to C. rodentium

Zuobai Wang et al. demonstrate that CD4+ Foxp3+ regulatory T cells promote T helper type 17 cell (Th17) responses to intestinal infection with the mouse pathogen Citrobacter rodentium. See page 1290

Malaria suppresses Salmonella-induced intestinal inflammation

Jason Mooney and colleagues found that interleukin-10 production during malaria infection suppressed inflammatory responses to intestinal infection with non-typhoidal Salmonella infection. See page 1302

NOD2 signaling inhibits NF-kB signaling

Tomohiro Watanabe and colleagues show that activation of nucleotide-binding oligomerization domain 2 (NOD2) results in increased expression of interferon regulatory factor 4 and binding to tumor necrosis factor receptor–associated factor 6 (TRAF6) and receptor interacting serine–threonine kinase (RICK), resulting in inhibition of Lys63-linked polyubiquitination of TRAF6 and RICK and thus to downregulation of nuclear factor-kB (NF-kB) activation. See page 1312

cHMOS regulates signaling in the immature intestine

Yingying He and co-workers demonstrate that human milk oligosaccharides from colostrum (cHMOS) can directly modulate the signaling pathways of the immature mucosa. See page 1326

Claudin-2 regulates intestinal homeostasis

Rizwan Ahmad and colleagues identified a critical role of claudin-2 in intestinal homeostasis: regulating epithelial permeability, inflammation, and proliferation. See page 1340

a4 Integrins in colitis

Elvira Kurmaeva et al. demonstrate a direct role for T cell–associated a4b7, but not a4b1, integrins during initiation and perpetuation of chronic colitis in mice. They found that anti-a4 (natalizumab) treatment reduced mucosal CD4 T-cell accumulation in patients with Crohn’s disease. See page 1354

IL-16 and S. aureus pneumonia

Danielle Ahn et al. provide evidence that the production of interleukin-16 (IL-16) by CD4+ T cells contributes to immune pathology and inhibits bacterial clearance in Staphylococcus aureus pneumonia. See page 1366

HIV targeting of Th17 cells in the female reproductive tract

Marta Rodriguez-Garcia and colleagues describe the phenotype of T helper type 17 (Th17) cells in the female reproductive tract and demonstrate increased susceptibility to HIV infection in vitro of cells expressing CCR5 and CD90. See page 1375

DCs and lung injury in the elderly

Sangeetha Prakash and co-workers observed that monocyte-derived dendritic cells (DCs) from elderly, but not young, subjects produced tumor necrosis factor-a that was able to induce cytokines and chemokines and alter the barrier function of primary bronchial epithelial cells. See page 1386

T-cell IL-4 drives Th2 cells in food allergy

Derek Chu et al. show that the priming of T helper type 2 (Th2) cell responses in the intestine to initiate food allergy in mice is dependent on interleukin-4 (IL-4) produced by the T cells themselves and not by other innate sources and is driven by OX40L expressed by dendritic cells. See page 1395

Vitamin D and Crohn’s disease

Serge Dionne and colleagues report a differential effect of vitamin D on Toll-like receptor– and nucleotide-binding oligomerization domain 2–induced cytokine production by mononuclear phagocytes from patients with Crohn’s disease. See page 1405

LXRb protects against colitis in mice

Tomas Jakobsson and co-workers found that the oxysterol receptor LXRb protected against dextran sodium sulfate– and 2,4,6-trinitrobenzene sulfonic acid–induced colitis in mice. See page 1416

SHIP1 promotes mucosal T-cell survival

Mi-Young Park and colleagues demonstrate that SHIP1 is important for the survival of protective T cells at mucosal surfaces, thus preventing abnormal myeloid cell activation and inflammation. See page 1429

Foxp3+ Tregs induce epithelial cell proliferation in the lung

Using an experimental model of lung injury, Jason Mock et al. obtained evidence that CD4+ Foxp3+ regulatory T cells (Tregs) contribute to epithelial cell proliferation and epithelial repair. See page 1440

CHOP regulates epithelial cell proliferation

Nadine Waldschmitt and colleagues show a role for the unfolded protein response target gene C/EBP homologous protein (CHOP) in regulating epithelial cell proliferation. They found that overexpression results in poor epithelial repair in dextran sodium sulfate–induced colitis and experimental wounding. See page 1452

SIRT1 in control of colitis

Roberta Caruso and colleagues combined analyses of human inflammatory bowel disease and mouse models to identify a role for SIRT1, an NAD-dependent deacetylase, in the control of intestinal inflammation. See page 1467

Caspase-11 protects against DSS colitis

Dieter Demon and co-workers demonstrate that caspase-11 is expressed in the colonic mucosa and protects against dextran sodium sulfate–induced (DSS) colitis, through a mechanism that is independent of inflammasome activation of interleukin-1b and -18. See page 1480

Blocking TL1A/DR3 inhibits intestinal fibrosis

David Shih et al. report evidence of a direct role for TL1A, a product of the inflammatory bowel disease–susceptibility gene TNFSF15, in mediating colitis-induced intestinal fibrosis in a mouse model. They observed that inhibition of TL1A/DR3 signaling in vivo could block the fibrotic response. See page 1492