Androgen signaling restricts glutaminolysis to drive sex-specific Th17 metabolism in allergic airway inflammation.

Female individuals have an increased prevalence of many Th17 cell-mediated diseases, including asthma. Androgen signaling decreases Th17 cell-mediated airway inflammation, and Th17 cells rely on glutaminolysis. However, it remains unclear whether androgen receptor (AR) signaling modifies glutamine metabolism to suppress Th17 cell-mediated airway inflammation.

Digital Navigation Improves No-Show Rates and Bowel Preparation Quality for Patients Undergoing Colonoscopy: A Randomized Controlled Quality Improvement Study.

Objectives: Because of high historical no-show rates and poor bowel preparation quality in our unit, we sought to evaluate whether text message navigation for patients scheduled for colonoscopy would reduce no-show rates and improve bowel preparation quality compared with usual care.

Methods: We performed a randomized controlled quality improvement study from April to August 2019 in an urban academic endoscopy unit. All patients scheduled for colonoscopy were randomly assigned to a control group that received usual care (paper instructions/nursing precalls) or to the intervention group that received usual care plus the text message program [short message service (SMS)].

Endoscopic resection is more effective than biopsy or EUS to detect residual rectal neuroendocrine tumor.

 Rectal neuroendocrine tumors (NETs) are often discovered incidentally and may be misidentified as adenomatous polyps. This can result in a partial resection at the index procedure, and lesions are often referred for staging or evaluation for residual disease at the resection site. The aim of this study was to identify the ideal method to confirm complete excision of small rectal NETs.

A Respiratory Syncytial Virus Attachment Gene Variant Associated with More Severe Disease in Infants Decreases Fusion Protein Expression, Which May Facilitate Immune Evasion.

This study identified a genotype of respiratory syncytial virus (RSV) associated with increased acute respiratory disease severity in a cohort of previously healthy term infants. The genotype (2stop+A4G) consists of two components. The A4G component is a prevalent point mutation in the 4th position of the gene end transcription termination signal of the G gene of currently circulating RSV strains.

Group 2 Innate Lymphoid Cells Coordinate Damage Response in the Stomach.

Background & Aims: Severe injury to the lining of the stomach leads to changes in the epithelium (reprogramming) that protect and promote repair of the tissue, including development of spasmolytic polypeptide-expressing metaplasia (SPEM) and tuft and foveolar cell hyperplasia. Acute gastric damage elicits a type-2 inflammatory response that includes production of type-2 cytokines and infiltration by eosinophils and alternatively activated macrophages. Stomachs of mice that lack interleukin 33 (IL33) or interleukin 13 (IL13) did not undergo epithelial reprogramming after drug-induced injury.

Dissection-enabled scaffold-assisted resection (DeSCAR): a novel technique for resection of residual or non-lifting gastrointestinal neoplasia of the colon, expanded experience and follow-up.

 Colonic lesions may not be amenable to conventional endoscopic mucosal resection (EMR) due to previous manipulation, submucosal invasion, or lesion flatness. In 2018, we described Dissection-enabled Scaffold Assisted Resection (DeSCAR) to be safe for the endoscopic resection of non-lifting or residual colonic lesions 1 In this study, we expand our original cohort to describe our expanded experience with patients undergoing DeSCAR and assess the efficacy, safety, and feasibility of DeSCAR for endoscopic resection of non-lifting or residual colonic lesions.  We retrospectively reviewed 57 patients from 2015-2019 who underwent DeSCAR for colonic lesions with incomplete lifting and/or previous manipulation.

Protocols for Studying Murine ILC Development.

Understanding the origins and developmental trajectory of innate lymphoid cell (ILC) progenitors has been of substantial interest to the fields of ILC biology and immunology. While mature ILC are rare lymphocytes, ILC progenitors represent an even smaller fraction of cells, providing additional challenges in studying them. Moreover, though the approaches to studying these cells are conceptually straightforward, the technical nuances that underlie them can substantially affect the quality of the data.

IL-33 Is a Cell-Intrinsic Regulator of Fitness during Early B Cell Development.

IL-33 is an IL-1 family member protein that is a potent driver of inflammatory responses in both allergic and nonallergic disease. This proinflammatory effect is mediated primarily by extracellular release of IL-33 from stromal cells and binding of the C-terminal domain of IL-33 to its receptor ST2 on targets such as CD4 Th2 cells, ILC2, and mast cells. Notably, IL-33 has a distinct N-terminal domain that mediates nuclear localization and chromatin binding.

Host and Viral Determinants of Respiratory Syncytial Virus-induced Airway Mucus.

Respiratory syncytial virus (RSV) is a leading cause of hospitalization of infants worldwide each year. Both host and viral factors host factors predispose a subset of what appear to be healthy infants to severe RSV-induced disease. In this review, we outline many genetic and immunologic factors that contribute to airway obstruction that contributes to the severity of RSV infection.

Calciphylaxis in end-stage liver and renal disease patients before and after transplant.

Calciphylaxis is a rare vascular disorder characterized by calcification of arterioles which causes tissue inflammation and necrosis. It is associated with the metabolic disturbances seen in end-stage renal disease (ESRD) and has also been described in patients with cirrhosis with preserved kidney function. Characteristic calciphylaxis lesions are black eschars surrounded by retiform purpura, and the gold standard for diagnosis is skin biopsy.

Glucagon-like peptide 1 receptor signaling attenuates respiratory syncytial virus-induced type 2 responses and immunopathology.

GLP-1R signaling, an emerging anti-inflammatory therapeutic 59 target, 60 attenuated type 2-associated immunopathology in mice infected with a strain of RSV that was 61 isolated from a hospitalized infant with severe lower respiratory tract infection and bronchiolitis.

Lumen-Apposing Metal Stents: Which One and Why?

Numerous lumen-apposing metal stents (LAMS) have been designed for transluminal applications, including complex pancreatic fluid collections (PFCs) and difficult biliary access. Limited high-quality data exist directly comparing the various LAMS models, and their use remains largely dependent on availability and operator expertise. LAMS placement has been streamlined by the addition of electrocautery, allowing for single-step or modified "hot" approach, if desired.

Glucagon-like peptide 1 signaling inhibits allergen-induced lung IL-33 release and reduces group 2 innate lymphoid cell cytokine production in vivo.

Background: IL-33 is one of the most consistently associated gene candidates for asthma identified by using a genome-wide association study. Studies in mice and in human cells have confirmed the importance of IL-33 in inducing type 2 cytokine production from both group 2 innate lymphoid cells (ILC2s) and T2 cells. However, there are no pharmacologic agents known to inhibit IL-33 release from airway cells.

IL-33 promotes the egress of group 2 innate lymphoid cells from the bone marrow.

Group 2 innate lymphoid cells (ILC2s) are effector cells within the mucosa and key participants in type 2 immune responses in the context of allergic inflammation and infection. ILC2s develop in the bone marrow from common lymphoid progenitor cells, but little is known about how ILC2s egress from the bone marrow for hematogenous trafficking. In this study, we identified a critical role for IL-33, a hallmark peripheral ILC2-activating cytokine, in promoting the egress of ILC2 lineage cells from the bone marrow.

Testosterone Attenuates Group 2 Innate Lymphoid Cell-Mediated Airway Inflammation.

Sex hormones regulate many autoimmune and inflammatory diseases, including asthma. As adults, asthma prevalence is 2-fold greater in women compared to men. The number of group 2 innate lymphoid cells (ILC2) is increased in patients with asthma, and we investigate how testosterone attenuates ILC2 function.

Dietary Manganese Promotes Staphylococcal Infection of the Heart.

Diet, and specifically dietary metals, can modify the risk of infection. However, the mechanisms by which manganese (Mn), a common dietary supplement, alters infection remain unexplored. We report that dietary Mn levels dictate the outcome of systemic infections caused by Staphylococcus aureus, a leading cause of bacterial endocarditis.

STAT1 Represses Cytokine-Producing Group 2 and Group 3 Innate Lymphoid Cells during Viral Infection.

The appropriate orchestration of different arms of the immune response is critical during viral infection to promote efficient viral clearance while limiting immunopathology. However, the signals and mechanisms that guide this coordination are not fully understood. IFNs are produced at high levels during viral infection and have convergent signaling through STAT1.