2 results match your criteria: "University of California San Diego and San Diego VA Medical Center[Affiliation]"

Background & Aims: Despite the poor prognosis associated with missed or delayed spontaneous bacterial peritonitis (SBP) diagnosis, <15% get timely paracentesis, which persists despite guidelines/education in the United States. Measures to exclude SBP non-invasively where timely paracentesis cannot be performed could streamline this burden.

Methods: Using Veterans Health Administration Corporate Data Warehouse (VHA-CDW) we included patients with cirrhosis between 2009 and 2019 who underwent timely paracentesis and collected relevant clinical information (demographics, cirrhosis severity, medications, vitals, and comorbidities).

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Chemokine receptor CCR7 regulates the intestinal TH1/TH17/Treg balance during Crohn's-like murine ileitis.

J Leukoc Biol

June 2015

*Mucosal Inflammation Program, School of Medicine, Gastrointestinal Eosinophilic Disease Program, Section of Pediatric Gastroenterology, Hepatology and Nutrition, Children's Hospital Colorado, and Department of Pathology, University of Colorado Denver, Colorado, USA; Department of Inflammation Research, Amgen, Thousand Oaks, California, USA; and Inflammatory Bowel Disease Center, Division of Gastroenterology, University of California San Diego and San Diego VA Medical Center, San Diego, California, USA.

The regulation of T cell and DC retention and lymphatic egress within and from the intestine is critical for intestinal immunosurveillance; however, the cellular processes that orchestrate this balance during IBD remain poorly defined. With the use of a mouse model of TNF-driven Crohn's-like ileitis (TNF(Δ) (ARE)), we examined the role of CCR7 in the control of intestinal T cell and DC retention/egress during experimental CD. We observed that the frequency of CCR7-expressing TH1/TH17 effector lymphocytes increased during active disease in TNF(Δ) (ARE) mice and that ΔARE/CCR7(-/-) mice developed exacerbated ileitis and multiorgan inflammation, with a marked polarization and ileal retention of TH1 effector CD4(+) T cells.

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