Hemorrhage decreases macrophage inflammatory protein 2 and interleukin-6 release - A possible mechanism for increased wound infection

Citation
Mk. Angele et al., Hemorrhage decreases macrophage inflammatory protein 2 and interleukin-6 release - A possible mechanism for increased wound infection, ANN SURG, 229(5), 1999, pp. 651-661
Citations number
45
Categorie Soggetti
Surgery,"Medical Research Diagnosis & Treatment
Journal title
ANNALS OF SURGERY
ISSN journal
00034932 → ACNP
Volume
229
Issue
5
Year of publication
1999
Pages
651 - 661
Database
ISI
SICI code
0003-4932(199905)229:5<651:HDMIP2>2.0.ZU;2-N
Abstract
Objective To determine whether alteration in wound exudate cell immune func tion occurs after trauma-hemorrhage. Background Although clinical and experimental studies indicate that the rat e of wound infection is increased after trauma and hemorrhagic shock, the u nderlying mechanism for this increased susceptibility remains unknown. Methods Male C3H/HeN mice were subjected to a midline laparotomy and polyvi nyl alcohol sponges were implanted subcutaneously in the abdominal wound be fore hemorrhage (35 +/- 5 mm Hg for 90 minutes and resuscitation) or sham o peration. The wound exudate cells from the sponges were harvested on the fi rst, third, and fifth postoperative day and cultured for 24 hours in the pr esence of lipopolysaccharide (10 mu g/ml) or heat-killed Staphylococcus aur eus. Interleukin (IL)-1 beta, IL-6, monocyte chemotactic protein i, macroph age inflammatory protein 2, and nitrite levels were determined in the super natants. The distribution of macrophages and polymorphonuclear leukocytes w as assessed in the sponge with and without in vivo injection of S. aureus. The phagocytic activity of isolated wound exudate cells was determined usin g fluorescent S. aureus. Results The composition of exudate cells was unaltered by hemorrhagic shock ; however, in vivo injection of S. aureus significantly decreased the perce ntage of macrophages under such conditions. Wound exudate cell phagocytic a ctivity and the release of IL-1 beta, IL-6, monocyte chemotactic protein i, and macrophage inflammatory protein 2 was decreased on the first postopera tive day. The release of IL-1 beta and IL-6 was also decreased on the third postoperative day in hemorrhaged mice. On the fifth postoperative day, wou nd 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 hem orrhage might contribute to the increased incidence of wound infections. Th erefore, attempts to enhance or restore wound cell immune function might be helpful for decreasing the incidence of wound infections in trauma victims .