Luminal mapping reveals mesenteric predominance of colonic adenomas and adenocarcinomas.

Background: Previous studies have examined the relationship between colorectal tumor distribution and metastasis, but the tumor luminal location and associative risk factors promoting tumor growth remain unknown.

Methods: In this study, we mapped the luminal distribution of human colonic adenomas/adenocarcinomas and their association with various physiologic parameters.

Results: We identified a mesenteric predominance for colonic adenomas and adenocarcinomas.

Agr2-associated ER stress promotes adherent-invasive E. coli dysbiosis and triggers CD103 dendritic cell IL-23-dependent ileocolitis.

Endoplasmic reticulum (ER) stress is associated with Crohn's disease (CD), but its impact on host-microbe interaction in disease pathogenesis is not well defined. Functional deficiency in the protein disulfide isomerase anterior gradient 2 (AGR2) has been linked with CD and leads to epithelial cell ER stress and ileocolitis in mice and humans. Here, we show that ileal expression of AGR2 correlates with mucosal Enterobactericeae abundance in human inflammatory bowel disease (IBD) and that Agr2 deletion leads to ER-stress-dependent expansion of mucosal-associated adherent-invasive Escherichia coli (AIEC), which drives Th17 cell ileocolitis in mice.

Using checklists to improve care in the nonoperating room environment.

Purpose Of Review: As the number and complexity of cases performed in the nonoperating room environment continue to increase to a higher share of all anesthetic procedures, checklists are needed to ensure staff and patient safety.

Recent Findings: Providing anesthesia care in the nonoperating room environment poses specific challenges. Closed claims data base analysis shows a higher morbidity and mortality in this setting.

Innate lymphoid cells link gut microbes with mucosal T cell immunity.

Despite continuous exposure to trillions of microbes, the intestinal immune system protects the mucosa by balancing barrier protection, tolerance, and immunity. As both sentinel and effector, the mucosal innate immune system plays a central role in coordinating these responses. By integrating signals from the intestinal microbiota, mononuclear phagocytes (MNPs) serve as a critical link in regulating effector functions of group 3 innate lymphoid cells (ILC3s).

The balance of power: innate lymphoid cells in tissue inflammation and repair.

Over the last ten years, immunologists have recognized the central importance of an emerging group of innate lymphoid cells (ILCs) in health and disease. Characterization of these cells has provided a molecular definition of ILCs and their tissue-specific functions. Although the lineage-defining transcription factors, cytokine production, and nomenclature parallel those of T helper cells, ILCs do not require adaptive immune programming.

Microbiota-Induced TNF-like Ligand 1A Drives Group 3 Innate Lymphoid Cell-Mediated Barrier Protection and Intestinal T Cell Activation during Colitis.

Inflammatory bowel disease (IBD) results from a dysregulated interaction between the microbiota and a genetically susceptible host. Genetic studies have linked TNFSF15 polymorphisms and its protein TNF-like ligand 1A (TL1A) with IBD, but the functional role of TL1A is not known. Here, we found that adherent IBD-associated microbiota induced TL1A release from CX3CR1 mononuclear phagocytes (MNPs).

IgA-coated enriched in Crohn's disease spondyloarthritis promote T17-dependent inflammation.

Peripheral spondyloarthritis (SpA) is a common extraintestinal manifestation in patients with active inflammatory bowel disease (IBD) characterized by inflammatory enthesitis, dactylitis, or synovitis of nonaxial joints. However, a mechanistic understanding of the link between intestinal inflammation and SpA has yet to emerge. We evaluated and functionally characterized the fecal microbiome of IBD patients with or without peripheral SpA.

T helper type 1 and 17 cells determine efficacy of interferon-beta in multiple sclerosis and experimental encephalomyelitis.

Interferon-beta (IFN-beta) is the major treatment for multiple sclerosis. However, this treatment is not always effective. Here we have found congruence in outcome between responses to IFN-beta in experimental autoimmune encephalomyelitis (EAE) and relapsing-remitting multiple sclerosis (RRMS).