Adipose-resident T-cells (ARTs) regulate metabolic and inflammatory responses in obesity, but ART activation signals are poorly understood. Here, we describe class II major histocompatibility complex (MHCII) as an important component of high-fat diet (HFD)-induced obesity. Microarray analysis of primary adipocytes revealed that multiple genes involved in MHCII antigen processing and presentation increased in obese women. In mice, adipocyte MHCII increased within two weeks HFD, paralleling increases in pro-inflammatory and decreases in anti-inflammatory ART markers, and preceding adipose tissue macrophage (ATM) accumulation and pro-inflammatory M1 polarization. Mouse 3T3-L1 and primary adipocytes activated T-cells in an antigen-specific, contact-dependent manner, indicating adipocyte MHCII is functional. HFD-fed MHCII−/− mice developed less adipose inflammation and insulin resistance than wild-type mice, despite developing similar adiposity. These investigations uncover a mechanism whereby a HFD-induced adipocyte/ART dialogue involving MHCII instigates adipose inflammation and, together with ATM MHCII, escalates its progression.

PreambleThe guidelines for the surgical treatment of gastroesophageal reflux disease (GERD) are a series of systematically developed statements to assist physicians and patient decisions about the appropriate use of laparoscopic surgery for GERD. The statements included in this guideline are the product of a systematic review of published literature on the topic, and the recommendations are explicitly linked to the supporting evidence. The strengths and weaknesses of the available evidence are highlighted and expert opinion sought where the evidence is lacking. This is an update of previous guidelines on this topic (last revision 06/2001) as new information has accumulated. DisclaimerGuidelines for clinical practice are intended to indicate preferable approaches to medical problems as established by experts in the field. These recommendations will be based on existing data or a consensus of expert opinion when little or no data are available. Guidelines are applicable to all physicians who address the clinical problem(s) without regard to specialty training or interests, and are intended to indicate the preferable, but not necessarily the only, acceptable approaches due to the complexity of the healthcare environment. Guidelines are intended to be flexible. Given the wide range of specifics in any health care problem, the surgeon must always choose the course best suited to the individual patient and the variables in existence at the moment of decision.Guidelines are developed under the auspices of the Society of American Gastrointestinal and Endoscopic Surgeons and its various committees, and approved by the Board of Governors. Each clinical practice guideline has been systematically researched, reviewed, and revised by the guidelines committee, and reviewed by an appropriate multidisciplinary team. The recommendations are therefore considered valid at the time of its production based on the data available. Each guideline is scheduled for periodic review to allow incorporation of pertinent new developments in medical research knowledge, and practice. Literature review methodWe identified 448 relevant articles. The abstracts were reviewed by four committee members (D.S., W.W.H., P.R.R., G.P.K.) and divided into the following categories:(a) Randomized studies, metaanalyses, and systematic reviews (b) Prospective studies (c) Retrospective studies (d) Case reports (e) Review articles Randomized controlled trials, metaanalyses, and systematic reviews were selected for further review, along with prospective and retrospective studies that included at least 50 patients. Studies with smaller samples were considered when additional evidence was lacking. The most recent reviews were also included. All case reports, older reviews, and smaller studies were excluded. According to these exclusion criteria, 227 articles were reviewed. Whenever the available evidence from level I studies was considered to be adequate, lower evidence level studies were not considered. A review of the available evidence on endoluminal treatment of...

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Adipose tissue inflammation increases with obesity, but adipocyte vs. immune cell contributions are unclear. In the present study, transcriptome analyses were performed on highly-purified subcutaneous adipocytes from lean and obese women, and differentially expressed genes/pathways were determined in both adipocyte and stromal vascular fraction (SVF) samples. Adipocyte but not SVF expression of NOD-like receptor pathway genes, including NLRP3 and PYCARD, which regulate caspase-1-mediated IL-1β secretion, correlated with adiposity phenotypes and adipocyte class II major histocompatibility complex (MHCII) gene expression, but only MHCII remained after adjusting for age and body mass index. IFNγ stimulated adipocyte MHCII, NLRP3 and caspase-1 expression, while adipocyte MHCII-mediated CD4+ T cell activation, an important factor in adipose inflammation, induced IFNγ-dependent adipocyte IL-1β secretion. These results uncover a dialogue regulated by interactions among T cell IFNγ and adipocyte MHCII and NLRP3 inflammasome activity that appears to initiate and escalate adipose tissue inflammation during obesity.

These cases illustrate the benefit of a laparoscopic approach with brief hospitalizations, early resumption of diet and regular activity, and minimal use of postoperative narcotic analgesics.