Social disruption induces lung inflammation

Brain Behav Immun. 2010 Mar;24(3):394-402. doi: 10.1016/j.bbi.2009.10.019. Epub 2009 Nov 10.


Social disruption (SDR) is a well-characterized mouse stressor that causes changes in immune cell reactivity in response to inflammatory stimuli. In this study, we found that SDR in the absence of an immune challenge induced pulmonary inflammation and increased pulmonary myeloperoxidase activity. The percentage of neutrophils within the lungs increased 2-fold after social disruption. Monocyte accumulation in the lungs was also significantly increased. In addition, SDR increased the percentage of neutrophils that expressed CD11b, indicating that more neutrophils were in an activated state. In the lungs, we observed an increased level of the inflammatory cytokine, IL-1beta, as well as higher levels of KC/CXCL1, MIP-2/CXCL2, and MCP-1/CCL2, which are chemokines responsible for neutrophil and monocyte recruitment. Furthermore, social disruption led to increased lung expression of the adhesion molecules P-selectin, E-selectin, and ICAM-1, which localize and recruit immune cells. These data support previous findings of an inflammatory environment induced by SDR. We demonstrate that this effect also occurs in the pulmonary milieu and in the absence of an inflammatory stimulus.

MeSH terms

  • Animals
  • Capillary Permeability / physiology
  • Cell Adhesion Molecules / metabolism
  • Cell Count
  • Chemokines / metabolism
  • Cytokines / metabolism
  • Evans Blue
  • Flow Cytometry
  • Immunity, Cellular / physiology
  • Lung / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neutrophils / physiology
  • Peroxidase / metabolism
  • Pneumonia / metabolism
  • Pneumonia / pathology*
  • Pneumonia / psychology*
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Social Environment*
  • Stress, Psychological / pathology*
  • Stress, Psychological / psychology*


  • Cell Adhesion Molecules
  • Chemokines
  • Cytokines
  • RNA, Messenger
  • Evans Blue
  • Peroxidase