Pulmonary contusion causes impairment of macrophage and lymphocyte immune functions and increases mortality associated with a subsequent septic challenge.
OBJECTIVE
Pulmonary contusion is frequently followed by acute respiratory distress syndrome, pneumonia, and sepsis. However, immunologic alterations of circulating and resident immune cell populations contributing to the posttraumatic immunosuppression are poorly understood. We therefore characterized the influence of pulmonary contusion on peripheral blood mononuclear cells, peritoneal macrophages, splenocytes, and splenic macrophages. To address the significance of the immunosuppression associated with lung contusion, we investigated how the consecutive addition of moderate or severe sepsis affected survival after blunt chest trauma.


METHODS
Male C3H/HeN mice (n = 10 per group) were anesthetized and subjected to chest trauma or sham procedure.


METHODS
The cytokine release of cultured peripheral blood mononuclear cells, peritoneal macrophages, splenocytes, and splenic macrophages and plasma levels of tumor necrosis factor-alpha and interleukin-6 from those animals were quantified. Sepsis was induced via cecal ligation and puncture 24 hrs after lung contusion.


RESULTS
Two hours after blunt chest trauma, plasma tumor necrosis factor-alpha and interleukin-6 were markedly increased, as was peripheral blood mononuclear cell cytokine production, lung myeloperoxidase activity, and lung chemokine concentrations. At 24 hrs and, in part, already at 2 hrs, cytokine release from peritoneal macrophages, splenic macrophages, and splenocytes was significantly suppressed. Furthermore, pulmonary contusion when followed by moderate sepsis significantly diminished survival rate when compared with chest trauma or moderate sepsis alone.


CONCLUSIONS
These results indicate that pulmonary contusion causes severe immunodysfunction of splenocytes, macrophages, and monocytes in different local compartments and systemically. Moreover, this immunosuppression is associated with an increased susceptibility to infectious complications, which results in a decreased survival rate if blunt chest trauma is followed by a septic insult.
Perl
Mario
M
Department of Trauma, Hand, and Reconstructive Surgery, University of Ulm, Germany.
Gebhard
Florian
F
Brückner
Uwe B
UB
Ayala
Alfred
A
Braumüller
Sonja
S
Büttner
Christian
C
Kinzl
Lothar
L
Knöferl
Markus W
MW
D000704:Analysis of Variance; D000818:Animals; D002478:Cells, Cultured; D003288:Contusions / Q000276:immunology* / Q000401:mortality / Q000503:physiopathology; D016207:Cytokines / Q000378:metabolism; D007108:Immune Tolerance; D015850:Interleukin-6 / Q000097:blood; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D055370:Lung Injury; D008264:Macrophages / Q000276:immunology*; D017737:Macrophages, Peritoneal / Q000276:immunology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D011897:Random Allocation; D018805:Sepsis / Q000276:immunology* / Q000401:mortality; D013154:Spleen / Q000166:cytology / Q000276:immunology; D016019:Survival Analysis; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016207:Cytokines; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha