Conventional alpha beta (αβ) T cells do not contribute to acute intestinal ischemia-reperfusion injury in mice
| Autor: | Xiaoyan Feng, Gertrud Vieten, Stephanie Dippel, Yi Yu, J. F. Kuebler, Faikah Gueler, Tawan Imvised, Christian Klemann, Benno M. Ure |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male Neutrophils Physiology medicine.medical_treatment Receptors Antigen T-Cell alpha-beta T-Lymphocytes lcsh:Medicine Pathology and Laboratory Medicine urologic and male genital diseases White Blood Cells Mice Spectrum Analysis Techniques Animal Cells Immune Physiology Medicine and Health Sciences Receptor lcsh:Science Immune Response Cells Cultured Innate Immune System Multidisciplinary T Cells Flow Cytometry Acute Intestinal Ischemia Intestines Cytokine medicine.anatomical_structure Neutrophil Infiltration Spectrophotometry Reperfusion Injury Acute Disease Cytokines Cytophotometry medicine.symptom Cellular Types Anatomy Research Article T cell Immune Cells Immunology Inflammation Mice Transgenic Biology Research and Analysis Methods 03 medical and health sciences Signs and Symptoms Antigen Diagnostic Medicine medicine Animals cardiovascular diseases Innate immune system Blood Cells urogenital system Macrophages lcsh:R Biology and Life Sciences Cell Biology Molecular Development medicine.disease Gastrointestinal Tract Mice Inbred C57BL 030104 developmental biology Immune System Mesenteric Ischemia lcsh:Q Reperfusion injury Digestive System Developmental Biology |
| Zdroj: | PLoS ONE, Vol 12, Iss 7, p e0181326 (2017) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | Purpose 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. Methods Adult wild-type (WT) and αβ T cell-deficient 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. Results 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. Conclusion 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. |
| Databáze: | OpenAIRE |
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