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

Frontiers in Immunology

Timo Burster¹  Adrian Gihring²  Pengfei Xu²  Leonard Elad²  Joachim Bischof²  Fabian Gärtner²  Uwe Knippschild²  Aileen Roth²  Martin Wabitsch³ 

[1] Department of Biology, School of Sciences and Humanities, Nazarbayev University, Nur-Sultan, Kazakhstan;Department of General and Visceral Surgery, Surgery Center, Ulm University Medical Center, Ulm, Germany;Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, Ulm University Medical Center, Ulm, Germany;

关键词: obesity;    immune response;    severe trauma;    inflammatory reflex;    monocyte compartment;    mass cytometry (CyTOF);   

DOI  :  10.3389/fimmu.2021.745132

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown