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Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System

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Published on: October 22, 2020

Social disruption induces lung inflammation.

Jennifer M Curry¹, Mark L Hanke, Melissa G Piper

¹Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Internal Medicine, The Ohio State University, Columbus, OH 43210, USA.

Brain, Behavior, and Immunity

|November 12, 2009

Summary

Social disruption (SDR) causes pulmonary inflammation in mice without an immune challenge. This stressor increases neutrophils, monocytes, and inflammatory markers in the lungs.

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Area of Science:

Immunology
Stress Physiology
Pulmonary Medicine

Background:

Social disruption (SDR) is a known stressor impacting immune cell reactivity.
Previous research indicates SDR influences immune responses to inflammatory stimuli.

Purpose of the Study:

To investigate the effects of SDR on the pulmonary immune environment in the absence of an immune challenge.
To determine if SDR induces pulmonary inflammation and alters immune cell populations and activation states.

Main Methods:

Mice were subjected to social disruption (SDR).
Pulmonary inflammation was assessed by measuring myeloperoxidase activity, immune cell counts (neutrophils, monocytes), and immune cell activation markers (CD11b expression).
Levels of inflammatory cytokines (IL-1beta) and chemokines (KC/CXCL1, MIP-2/CXCL2, MCP-1/CCL2), as well as adhesion molecules (P-selectin, E-selectin, ICAM-1) in the lungs were quantified.

Main Results:

SDR induced pulmonary inflammation and increased myeloperoxidase activity in the lungs.
A significant increase in lung neutrophils (2-fold) and monocytes was observed post-SDR.
SDR elevated neutrophil activation (CD11b expression) and increased levels of pro-inflammatory cytokines, chemokines, and adhesion molecules in the lungs.

Conclusions:

Social disruption alone is sufficient to induce a pro-inflammatory state in the pulmonary system.
SDR alters immune cell infiltration, activation, and the expression of key inflammatory mediators in the lungs, independent of an external immune challenge.