Demographic data of all patients of the control and study group.

<p>Demographic data of all patients of the control and study group.</p

Chromium and nickel concentrations in blood preoperatively and at the time of bar removal.

<p>Bars show mean concentrations of chromium and nickel in blood and error bars show standard error of the mean. The difference between nickel concentrations preoperatively and at the time of bar removal was statistically significant (**p<0.001).</p

Chromium and nickel contamination in tissue preoperatively and at the time of bar removal.

<p>Chromium and nickel contamination in tissue preoperatively and at the time of bar removal.</p

Chromium and nickel concentration in blood and urine preoperatively and at the time of bar removal.

<p>Chromium and nickel concentration in blood and urine preoperatively and at the time of bar removal.</p

Chromium and nickel concentrations in urine preoperatively and at the time of bar removal.

<p>Bars show mean concentrations of chromium and nickel in urine and error bars show standard error of the mean. The difference between chromium concentrations preoperatively and at the time of bar removal was statistically significant (**p<0.001).</p

Conventional alpha beta (αβ) T cells do not contribute to acute intestinal ischemia-reperfusion injury in mice

<div><p>Purpose</p><p>Ischemia-reperfusion injury (IRI) is associated with significant patient mortality and morbidity. The complex cascade of IRI is incompletely understood, but inflammation is known to be a key mediator. In addition to the predominant innate immune responses, previous research has also indicated that αβ T cells contribute to IRI in various organ models. The aim of this study was to clarify the role αβ T cells play in IRI to the gut.</p><p>Methods</p><p>Adult <i>wild-type</i> (WT) and <i>αβ T cell-deficient</i> mice were subjected to acute intestinal IRI with 30min ischemia followed by 4h reperfusion. The gene expression of pro-inflammatory cytokines was measured by qPCR, and the influx of leukocyte subpopulations in the gut was assessed via flow cytometry and histology. Pro-inflammatory cytokines in the serum were measured, and transaminases were assessed as an indicator of distant organ IRI.</p><p>Results</p><p>Intestinal IRI led to an increased expression of pro-inflammatory cytokines in the gut tissue and an influx of leukocytes that predominantly consisted of neutrophils and macrophages. Furthermore, intestinal IRI increased serum IL-6, TNF-α, and ALT/AST levels. The αβ T cell-deficient mice did not exhibit a more significant increase in pro-inflammatory cytokines in the gut or serum following IR than the WT mice. There was also no difference between WT- and αβ T cell-deficient mice in terms of neutrophil infiltration or macrophage activation. Furthermore, the increase in transaminases was equal in both groups indicating that the level of distant organ injury was comparable.</p><p>Conclusion</p><p>An increasing body of evidence demonstrates that αβ T cells play a key role in IRI. In the gut, however, αβ T cells are not pivotal in the first hours following acute IRI as deficiency does not impact cytokine production, neutrophil recruitment, macrophage activation, or distant organ injury. Thus, αβ T cells may be considered innocent bystanders during the acute phase of intestinal IRI.</p></div

Neutrophils and inflammatory macrophages infiltration of the gut after IR was equally strong in WT and αβ T cell deficient mice.

<p>Intraepithelial leukocytes (IEL) and lamina propria leukocytes were isolated from small intestines and at least 1×10⁵ leukocytes per sample were analyzed using flow cytometry in wild-type (WT) mice and mice deficient of αβ T cells (Tcra^tm1Mom) after intestinal ischemia reperfusion (IR) or sham operation (ctrl). Representative density plots of live CD45⁺CD11b⁺ leukocytes in IEL are displayed in (A), and LPL in (B) showing an increase of Ly6G⁺ neutrophils and a reciprocal relative decrease of F4/80⁺ macrophages. C) Percentage of CD11b⁺ myeloid cells in WT and Tcra^tm1/mom following IR or ctrl treatment. Data for IEL are displayed in the upper row, LPL in the lower row. D) Fraction of cells from (C) expressing the neutrophil specific marker Ly6G. E) Subgroup of cells from (C) expressing the macrophage marker F4/80. F) Percentages of macrophages expressing Ly6C indicating an inflammatory phenotype. Each data point represents the result of the analysis of an individual mouse. Bars represent group mean and error bar depicts ± SD. N = 6/group. ns = not significant. *** = p<0.001. Data are representative of two independent experiments.</p

Neutrophils and inflammatory macrophages infiltrate gut after IR equally strong in WT and αβ T cell deficient mice.

<p>The relative expression of mRNA of CXCL1/KC, CXCL2/MIP-2, IL-6, and TNF-α in lysed tissue of small intestine of wild-type (WT) mice and mice deficient in αβ T cells after intestinal ischemia reperfusion (IR) or sham operation (ctrl) were assessed using quantitative reverse transcription PCR (RT-qPCR). The results are presented as the mean normalized expression value with GAPDH as the housekeeping gene. Data are represented as mean ± SD (n≥4). ns = not significant. *** = p<0.001. Data are representative of two independent experiments.</p

Increase of transaminases following intestinal IRI, with no effect of αβ T cell deficiency.

<p>Levels of serum transaminases AST and ALT (A) and IL-6 and TNF-α (B) of wild-type (WT) mice and mice deficient in αβ T cells (Tcra^tm1Mom) after intestinal ischemia reperfusion (IR) or sham operation (ctrl). Each data point represents the results of the serum analysis of an individual mouse. The bars represent group mean and the error bar depicts SD. N = 5-6/group. ns = not significant. * = p<0.05, *** = p<0.001. Data are representative of two independent experiments.</p

Pulmonary PMN infiltration after AFS cell application.

<p>Pulmonary infiltration with PMNs was significantly increased in positive-controls (+) compared to negative-controls (−) 24 h after LPS injection. Mice treated with hom AFS cells showed significantly decreased pulmonary neutrophil influx compared to positive-controls (+).</p