%A Gärtner,Fabian
%A Gihring,Adrian
%A Roth,Aileen
%A Bischof,Joachim
%A Xu,Pengfei
%A Elad,Leonard
%A Wabitsch,Martin
%A Burster,Timo
%A Knippschild,Uwe
%D 2021
%J Frontiers in Immunology
%C
%F
%G English
%K Obesity,immune response,Severe trauma,Inflammatory reflex,Monocyte compartment,Mass cytometry (CyTOF)
%Q
%R 10.3389/fimmu.2021.745132
%W
%L
%M
%P
%7
%8 2021-November-15
%9 Original Research
%+ Prof Uwe Knippschild,Department of General and Visceral Surgery, Surgery Center, Ulm University Medical Center,Germany,uwe.knippschild@uniklinik-ulm.de
%#
%! Obesity impacts trauma immune response
%*
%<
%T Obesity Prolongs the Inflammatory Response in Mice After Severe Trauma and Attenuates the Splenic Response to the Inflammatory Reflex
%U https://www.frontiersin.org/articles/10.3389/fimmu.2021.745132
%V 12
%0 JOURNAL ARTICLE
%@ 1664-3224
%X 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.