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Background: Monocyte subsets and monocyte–platelet aggregates (MPAs) play important roles in inflammation.Aim: To evaluate the association between the three human monocyte subsets and their contributions to MPAs and mortality among septic patients.Methods: Consecutive septic patients were enrolled in. Age- and gender-matched nonseptic patients were recruited as control patients. Monocyte subsets and monocyte–platelet aggregates were determined by flow cytometric analysis.Results: Elevated percentage of MPAs (MPAs%) was associated with an increased risk of mortality.Conclusions: This study demonstrated increased MPAs% enables the identification of a group of septic patients at high risk of death. [ABSTRACT FROM PUBLISHER]

Graph: Figure 4 I/R triggers gut injury and intestinal barrier disruption. Correction to: I Scientific reports i https://doi.org/10.1038/s41598-018-25387-8, published online 09 May 2018 This Article contains an error in Figure 4, where the images in panel (a) for the Sham group, Jejunuum and the I/R group, Ileum are incorrect. [Extracted from the article]

Background Inflammatory biomarkers usually start to rise earlier before the infection becomes clinically evident. This study was designed to evaluate the predictive performance of procalcitonin (PCT), C-reactive protein (CRP), and white blood cell (WBC) counts in postoperative intraabdominal infections (IAIs) after definitive operation of intestinal fistulae. Material and methods We prospectively enrolled a total of 356 consecutive patients who underwent elective digestive tract reconstruction for gastrointestinal fistulae without existing clinical infection. Plasma PCT levels, serum CRP concentration, and WBC counts were assessed preoperatively and on postoperative days (PODs) 1, 3, 5, and 7. The predictive value of each laboratory marker for IAIs was calculated. Results The occurrence rate of IAIs after elective digestive tract reconstruction for gastrointestinal fistulae in our study was 7.3%. Both PCT levels and WBC counts were significantly higher in patients with IAIs than those in patients without IAIs on POD 1, POD 3, and POD 5, whereas CRP levels differed significantly on POD 3 and POD 5. Receiver-operating characteristics demonstrated that PCT on POD 3 had the highest diagnostic accuracy for IAIs, and the area under the curve reached 0.86, with a sensitivity of 92.0% and specificity of 74.0%. Conclusions The value of PCT above 0.98 ng/L on POD 3 and 0.83 ng/L on POD 5 could predict the occurrence of IAIs after definitive operations for intestinal fistulae. [ABSTRACT FROM AUTHOR]

Abstract: Background: Acting via IL-10 and transforming growth factor-β (TGF-β), t regulatory cells (Tregs) that express the Forkhead Box P3 (Foxp3) play a vital role in maintaining intestinal immune homeostasis. Many studies have found correlation between Foxp3+ Treg cells and Crohn's disease (CD). T2, extracted from the medicinal plant Tripterygium wilfordii Hook F, has already been proved to be therapeutically effective in inducing the remission of CD. However, the mechanisms in human studies remain largely unknown. Aim: We aimed to explore the effect of T2 on the in situ levels of inflammatory cytokines and the number of Foxp3+ Tregs in inflamed mucosa of CD. Methods: Mucosal biopsies from 20 patients treated with T2 were taken by colonoscopy. The changes of Foxp3+ Tregs as well as TNF-α and IL-10 in diseased tissue were visualized by immunochemistry. Western blot and ELISA were used to quantify levels of Foxp3 protein expression and inflammatory cytokines. Results: T2 treatment ameliorated the pathological inflammation of CD. We observed that the significantly elevated Foxp3+ Tregs and IL-10 levels in the mucosa of CD patients after T2 treatment concurred with the down-regulation of proinflammatory TNF-α. Conclusion: We confirmed the efficacy of T2 treatment in CD and showed that microscopic inflammation was attenuated by the modulation of in situ levels of inflammatory cytokines. The therapeutic mechanisms might involve the up-regulation of Foxp3+ Tregs. [Copyright &y& Elsevier]