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

Fabian Gärtner, Adrian Gihring, Aileen Roth, Joachim Bischof, Pengfei Xu, Leonard Elad, Martin Wabitsch, Timo Burster, Uwe Knippschild

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)745132
JournalFrontiers in Immunology
Volume12
DOIs
Publication statusPublished - 2021

Keywords

  • Animals
  • Cell Movement/immunology
  • Female
  • Inflammation/immunology
  • Macrophages/immunology
  • Mice
  • Mice, Inbred C57BL
  • Monocytes/immunology
  • Obesity/complications
  • Spleen/immunology
  • Thoracic Injuries/complications

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