Lack of gamma delta T cells ameliorates inflammatory response after acute intestinal ischemia reperfusion in mice

Abstract T-cells have been demonstrated to modulate ischemia–reperfusion injury (IRI) in the kidney, lung, liver, and intestine. Whereas most T-cell subpopulations contribute primarily to the antigen-specific effector and memory phases of immunity, γδ-T-cells combine adaptive features with rapid, in...

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Autores principales: Dominik Funken, Yi Yu, Xiaoyan Feng, Tawan Imvised, Faikah Gueler, Immo Prinz, Omid Madadi-Sanjani, Benno M. Ure, Jochen F. Kuebler, Christian Klemann
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Publicado: Nature Portfolio 2021
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spelling oai:doaj.org-article:52b8cb0e1cb9406eaf61fb5dfebc15132021-12-02T17:27:03ZLack of gamma delta T cells ameliorates inflammatory response after acute intestinal ischemia reperfusion in mice10.1038/s41598-021-96525-y2045-2322https://doaj.org/article/52b8cb0e1cb9406eaf61fb5dfebc15132021-09-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-96525-yhttps://doaj.org/toc/2045-2322Abstract T-cells have been demonstrated to modulate ischemia–reperfusion injury (IRI) in the kidney, lung, liver, and intestine. Whereas most T-cell subpopulations contribute primarily to the antigen-specific effector and memory phases of immunity, γδ-T-cells combine adaptive features with rapid, innate-like responses that can place them in the initiation phase of immune reactions. Therefore, we aimed to clarify the role of γδ-T-cells in intestinal IRI. Adult wild-type (WT) and γδ-T-cell-deficient mice were subjected to acute intestinal IRI. Gene expression of pro-inflammatory cytokines and influx of leukocyte subpopulations in the gut were assessed by qPCR and flow cytometry. Serum transaminases were measured as an indicator of distant organ IRI. Intestinal IRI led to increased influx of neutrophils, pro-inflammatory cytokine expression and LDH/ALT/AST elevation. Selective deficiency of γδ-T-cells significantly decreased pro-inflammatory cytokine levels and neutrophil infiltration in the gut following IRI compared to controls. Furthermore, γδ-T-cell deficiency resulted in decreased LDH and transaminases levels in sera, indicating amelioration of distant organ injury. Increasing evidence demonstrates a key role of T-cell subpopulations in IRI. We demonstrate that γδ-T-cell deficiency ameliorated pro-inflammatory cytokine production, neutrophil recruitment and distant organ injury. Thus, γδ-T-cells may be considered as mediators contributing to the inflammatory response in the acute phase of intestinal IRI.Dominik FunkenYi YuXiaoyan FengTawan ImvisedFaikah GuelerImmo PrinzOmid Madadi-SanjaniBenno M. UreJochen F. KueblerChristian KlemannNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-9 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Dominik Funken
Yi Yu
Xiaoyan Feng
Tawan Imvised
Faikah Gueler
Immo Prinz
Omid Madadi-Sanjani
Benno M. Ure
Jochen F. Kuebler
Christian Klemann
Lack of gamma delta T cells ameliorates inflammatory response after acute intestinal ischemia reperfusion in mice
description Abstract T-cells have been demonstrated to modulate ischemia–reperfusion injury (IRI) in the kidney, lung, liver, and intestine. Whereas most T-cell subpopulations contribute primarily to the antigen-specific effector and memory phases of immunity, γδ-T-cells combine adaptive features with rapid, innate-like responses that can place them in the initiation phase of immune reactions. Therefore, we aimed to clarify the role of γδ-T-cells in intestinal IRI. Adult wild-type (WT) and γδ-T-cell-deficient mice were subjected to acute intestinal IRI. Gene expression of pro-inflammatory cytokines and influx of leukocyte subpopulations in the gut were assessed by qPCR and flow cytometry. Serum transaminases were measured as an indicator of distant organ IRI. Intestinal IRI led to increased influx of neutrophils, pro-inflammatory cytokine expression and LDH/ALT/AST elevation. Selective deficiency of γδ-T-cells significantly decreased pro-inflammatory cytokine levels and neutrophil infiltration in the gut following IRI compared to controls. Furthermore, γδ-T-cell deficiency resulted in decreased LDH and transaminases levels in sera, indicating amelioration of distant organ injury. Increasing evidence demonstrates a key role of T-cell subpopulations in IRI. We demonstrate that γδ-T-cell deficiency ameliorated pro-inflammatory cytokine production, neutrophil recruitment and distant organ injury. Thus, γδ-T-cells may be considered as mediators contributing to the inflammatory response in the acute phase of intestinal IRI.
format article
author Dominik Funken
Yi Yu
Xiaoyan Feng
Tawan Imvised
Faikah Gueler
Immo Prinz
Omid Madadi-Sanjani
Benno M. Ure
Jochen F. Kuebler
Christian Klemann
author_facet Dominik Funken
Yi Yu
Xiaoyan Feng
Tawan Imvised
Faikah Gueler
Immo Prinz
Omid Madadi-Sanjani
Benno M. Ure
Jochen F. Kuebler
Christian Klemann
author_sort Dominik Funken
title Lack of gamma delta T cells ameliorates inflammatory response after acute intestinal ischemia reperfusion in mice
title_short Lack of gamma delta T cells ameliorates inflammatory response after acute intestinal ischemia reperfusion in mice
title_full Lack of gamma delta T cells ameliorates inflammatory response after acute intestinal ischemia reperfusion in mice
title_fullStr Lack of gamma delta T cells ameliorates inflammatory response after acute intestinal ischemia reperfusion in mice
title_full_unstemmed Lack of gamma delta T cells ameliorates inflammatory response after acute intestinal ischemia reperfusion in mice
title_sort lack of gamma delta t cells ameliorates inflammatory response after acute intestinal ischemia reperfusion in mice
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/52b8cb0e1cb9406eaf61fb5dfebc1513
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