Hemorrhage decreases macrophage inflammatory protein 2 and interleukin-6 release: a possible mechanism for increased wound infection.
OBJECTIVE
To determine whether alteration in wound exudate cell immune function occurs after trauma-hemorrhage.


BACKGROUND
Although clinical and experimental studies indicate that the rate of wound infection is increased after trauma and hemorrhagic shock, the underlying mechanism for this increased susceptibility remains unknown.


METHODS
Male C3H/HeN mice were subjected to a midline laparotomy and polyvinyl alcohol sponges were implanted subcutaneously in the abdominal wound before hemorrhage (35+/-5 mm Hg for 90 minutes and resuscitation) or sham operation. The wound exudate cells from the sponges were harvested on the first, third, and fifth postoperative day and cultured for 24 hours in the presence of lipopolysaccharide (10 microg/ml) or heat-killed Staphylococcus aureus. Interleukin (IL)-1beta, IL-6, monocyte chemotactic protein 1, macrophage inflammatory protein 2, and nitrite levels were determined in the supernatants. The distribution of macrophages and polymorphonuclear leukocytes was assessed in the sponge with and without in vivo injection of S. aureus. The phagocytic activity of isolated wound exudate cells was determined using fluorescent S. aureus.


RESULTS
The composition of exudate cells was unaltered by hemorrhagic shock; however, in vivo injection of S. aureus significantly decreased the percentage of macrophages under such conditions. Wound exudate cell phagocytic activity and the release of IL-1beta, IL-6, monocyte chemotactic protein 1, and macrophage inflammatory protein 2 was decreased on the first postoperative day. The release of IL-1beta and IL-6 was also decreased on the third postoperative day in hemorrhaged mice. On the fifth postoperative day, wound exudate cell cytokine production was comparable to that in shams.


CONCLUSIONS
Because most wound infections occur early after severe trauma, these results suggest that the dysfunction of wound exudate cells after hemorrhage might contribute to the increased incidence of wound infections. Therefore, attempts to enhance or restore wound cell immune function might be helpful for decreasing the incidence of wound infections in trauma victims.
Angele
M K
MK
Center for Surgical Research and Department of Surgery, Brown University School of Medicine and Rhode Island Hospital, Providence 02903, USA.
Knöferl
M W
MW
Schwacha
M G
MG
Ayala
A
A
Bland
K I
KI
Cioffi
W G
WG
Josephson
S L
SL
Chaudry
I H
IH
D000818:Animals; D054426:Chemokine CXCL2; D002630:Chemotactic Factors / Q000378:metabolism*; D005122:Exudates and Transudates / Q000166:cytology / Q000276:immunology; D015850:Interleukin-6 / Q000378:metabolism*; D008264:Macrophages; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D015846:Monokines / Q000378:metabolism*; D009504:Neutrophils; D012771:Shock, Hemorrhagic / Q000150:complications*; D014946:Wound Infection / Q000209:etiology / Q000276:immunology*
D054426:Chemokine CXCL2; D002630:Chemotactic Factors; D015850:Interleukin-6; D015846:Monokines