Obesity Prolongs the Inflammatory Response in Mice After Severe Trauma and Attenuates the Splenic Response to the Inflammatory Reflex

Thoracic traumas with extra-thoracic injuries result in an immediate, complex host response. The immune response requires tight regulation and can be influenced by additional risk factors such as obesity, which is considered a state of chronic inflammation. Utilizing high-dimensional mass and regula...

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Autores principales: Fabian Gärtner, Adrian Gihring, Aileen Roth, Joachim Bischof, Pengfei Xu, Leonard Elad, Martin Wabitsch, Timo Burster, Uwe Knippschild
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Publicado: Frontiers Media S.A. 2021
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Acceso en línea:https://doaj.org/article/ab0c9b3255ae41f583bd5de956d4e05b
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spelling oai:doaj.org-article:ab0c9b3255ae41f583bd5de956d4e05b2021-11-15T06:54:49ZObesity Prolongs the Inflammatory Response in Mice After Severe Trauma and Attenuates the Splenic Response to the Inflammatory Reflex1664-322410.3389/fimmu.2021.745132https://doaj.org/article/ab0c9b3255ae41f583bd5de956d4e05b2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.745132/fullhttps://doaj.org/toc/1664-3224Thoracic traumas with extra-thoracic injuries result in an immediate, complex host response. The immune response requires tight regulation and can be influenced by additional risk factors such as obesity, which is considered a state of chronic inflammation. Utilizing high-dimensional mass and regular flow cytometry, we define key signatures of obesity-related alterations of the immune system during the response to the trauma. In this context, we report a modification in important components of the splenic response to the inflammatory reflex in obese mice. Furthermore, during the response to trauma, obese mice exhibit a prolonged increase of neutrophils and an early accumulation of inflammation associated CCR2+CD62L+Ly6Chi monocytes in the blood, contributing to a persistent inflammatory phase. Moreover, these mice exhibit differences in migration patterns of monocytes to the traumatized lung, resulting in decreased numbers of regenerative macrophages and an impaired M1/M2 switch in traumatized lungs. The findings presented in this study reveal an attenuation of the inflammatory reflex in obese mice, as well as a disturbance of the monocytic compartment contributing to a prolonged inflammation phase resulting in fewer phenotypically regenerative macrophages in the lung of obese mice.Fabian GärtnerAdrian GihringAileen RothJoachim BischofPengfei XuLeonard EladMartin WabitschTimo BursterUwe KnippschildFrontiers Media S.A.articleobesityimmune responsesevere traumainflammatory reflexmonocyte compartmentmass cytometry (CyTOF)Immunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic obesity
immune response
severe trauma
inflammatory reflex
monocyte compartment
mass cytometry (CyTOF)
Immunologic diseases. Allergy
RC581-607
spellingShingle obesity
immune response
severe trauma
inflammatory reflex
monocyte compartment
mass cytometry (CyTOF)
Immunologic diseases. Allergy
RC581-607
Fabian Gärtner
Adrian Gihring
Aileen Roth
Joachim Bischof
Pengfei Xu
Leonard Elad
Martin Wabitsch
Timo Burster
Uwe Knippschild
Obesity Prolongs the Inflammatory Response in Mice After Severe Trauma and Attenuates the Splenic Response to the Inflammatory Reflex
description Thoracic traumas with extra-thoracic injuries result in an immediate, complex host response. The immune response requires tight regulation and can be influenced by additional risk factors such as obesity, which is considered a state of chronic inflammation. Utilizing high-dimensional mass and regular flow cytometry, we define key signatures of obesity-related alterations of the immune system during the response to the trauma. In this context, we report a modification in important components of the splenic response to the inflammatory reflex in obese mice. Furthermore, during the response to trauma, obese mice exhibit a prolonged increase of neutrophils and an early accumulation of inflammation associated CCR2+CD62L+Ly6Chi monocytes in the blood, contributing to a persistent inflammatory phase. Moreover, these mice exhibit differences in migration patterns of monocytes to the traumatized lung, resulting in decreased numbers of regenerative macrophages and an impaired M1/M2 switch in traumatized lungs. The findings presented in this study reveal an attenuation of the inflammatory reflex in obese mice, as well as a disturbance of the monocytic compartment contributing to a prolonged inflammation phase resulting in fewer phenotypically regenerative macrophages in the lung of obese mice.
format article
author Fabian Gärtner
Adrian Gihring
Aileen Roth
Joachim Bischof
Pengfei Xu
Leonard Elad
Martin Wabitsch
Timo Burster
Uwe Knippschild
author_facet Fabian Gärtner
Adrian Gihring
Aileen Roth
Joachim Bischof
Pengfei Xu
Leonard Elad
Martin Wabitsch
Timo Burster
Uwe Knippschild
author_sort Fabian Gärtner
title Obesity Prolongs the Inflammatory Response in Mice After Severe Trauma and Attenuates the Splenic Response to the Inflammatory Reflex
title_short Obesity Prolongs the Inflammatory Response in Mice After Severe Trauma and Attenuates the Splenic Response to the Inflammatory Reflex
title_full Obesity Prolongs the Inflammatory Response in Mice After Severe Trauma and Attenuates the Splenic Response to the Inflammatory Reflex
title_fullStr Obesity Prolongs the Inflammatory Response in Mice After Severe Trauma and Attenuates the Splenic Response to the Inflammatory Reflex
title_full_unstemmed Obesity Prolongs the Inflammatory Response in Mice After Severe Trauma and Attenuates the Splenic Response to the Inflammatory Reflex
title_sort obesity prolongs the inflammatory response in mice after severe trauma and attenuates the splenic response to the inflammatory reflex
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/ab0c9b3255ae41f583bd5de956d4e05b
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