Incisional hernia, a serious complication after laparotomy is associated with high morbidity and costs. This trial examines the value of prophylactic intraperitoneal onlay mesh (IPOM) to reduce the risk of incisional hernia after a median follow-up time of 5.3 years. Methods:We conducted a parallel group, open-label, single centre, randomised controlled trial (NCT01003067). After midline incision the participants were either allocated to abdominal wall closure according to Everett with a PDS-loop running suture reinforced by an intraperitoneal composite mesh strip (Group A) or the same procedure without the additional mesh strip (Group B). Results:A total of 276 patients were randomized (Group A=131; Group B=136). Follow-up data after a median of 5.3 years after surgery was available from 183 patients (Group A=95; Group B=88). Incisional hernia was diagnosed in 25/95 (26%) patients in Group A and in 46/88 (52%) patients in Group B (risk ratio 0.52; 95% CI 0.36-0.77; p<0.001).Eighteen patients with asymptomatic incisional hernia went for watchfull waiting instead of hernia repair and remained free of symptoms after of a median follow up of 5.1 years.Between the 2nd and 5th year follow-up period no complication associated with the mesh could be detected. Conclusion:

ObjectiveMucosal-associated invariant T (MAIT) cells are the most abundant T cells in human liver. They respond to bacterial metabolites presented by major histocompatibility complex-like molecule MR1. MAIT cells exert regulatory and antimicrobial functions and are implicated in liver fibrogenesis. It is not well understood which liver cells function as antigen (Ag)-presenting cells for MAIT cells, and under which conditions stimulatory Ags reach the circulation.DesignWe used different types of primary human liver cells in Ag-presentation assays to blood-derived and liver-derived MAIT cells. We assessed MAIT cell stimulatory potential of serum from healthy subjects and patients with portal hypertension undergoing transjugular intrahepatic portosystemic shunt stent, and patients with inflammatory bowel disease (IBD).ResultsMAIT cells were dispersed throughout healthy human liver and all tested liver cell types stimulated MAIT cells, hepatocytes being most efficient. MAIT cell activation by liver cells occurred in response to bacterial lysate and pure Ag, and was prevented by non-activating MR1 ligands. Serum derived from peripheral and portal blood, and from patients with IBD stimulated MAIT cells in MR1-dependent manner.ConclusionOur findings reveal previously unrecognised roles of liver cells in Ag metabolism and activation of MAIT cells, repression of which creates an opportunity to design antifibrotic therapies. The presence of MAIT cell stimulatory Ags in serum rationalises the observed activated MAIT cell phenotype in liver. Increased serum levels of gut-derived MAIT cell stimulatory ligands in patients with impaired intestinal barrier function indicate that intrahepatic Ag-presentation may represent an important step in the development of liver disease.

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In the original version of the article, Philippe M. Glauser’s, Philippe Brosi’s, Benjamin Speich’s, Samuel A. Käser’s, Andres Heigl’s, and Christoph A. Maurer’s first and last names were interchanged. The names are correct as reflected here. The original article has been corrected.