Trauma serum suppresses superoxide production by normal neutrophils.
The effect of trauma serum on superoxide production by normal neutrophils was studied in 47 serum samples from 18 patients with multiple trauma. Ten patients became septic and eight patients remained nonseptic. Incubation in trauma serum significantly suppressed superoxide production by normal neutrophils compared with incubation in normal serum: 3.6 +/- 1.44 vs 4.04 +/- 1.64 nmole of superoxide produced by 10(6) neutrophils (mean +/- SD). There was no difference in the suppressive effect between septic and nonseptic trauma serum samples. The chemiluminescence response of normal neutrophils was likewise suppressed following incubation in trauma serum compared with incubation in normal serum. The chemiluminescence response correlated with superoxide reduction of cytochrome C. In addition, the chemiluminescence response was significantly less in septic-trauma serum than in nonseptic-trauma serum. Suppressive serum was found to inhibit the neutrophil-membrane depolarization response to latex particles, as measured by flow cytometry. We conclude that trauma serum suppresses superoxide production by normal neutrophils, and that such suppression can be detected reliably using the clinically applicable technique of chemiluminescence. A normal chemiluminescence response excludes serum-mediated suppression of neutrophil superoxide production. In addition, chemiluminescence may be of value in detecting altered resistance to sepsis following injury, while superoxide determinations do not seem to be helpful in this regard. The mechanism of action of the suppressor may involve reversible inhibition of membrane depolarization necessary for the production of bactericidal oxygen species.
D000293:Adolescent; D000328:Adult; D003182:Complement C5 / Q000502:physiology; D015936:Complement C5a; D005260:Female; D006801:Humans; D008163:Luminescent Measurements; D008297:Male; D008564:Membrane Potentials; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism* / Q000502:physiology; D009895:Opsonin Proteins; D018805:Sepsis / Q000097:blood / Q000209:etiology; D013481:Superoxides / Q000096:biosynthesis*; D014946:Wound Infection / Q000097:blood; D014947:Wounds and Injuries / Q000097:blood*; D015054:Zymosan / Q000494:pharmacology
D003182:Complement C5; D009895:Opsonin Proteins; D013481:Superoxides; D015936:Complement C5a; D015054:Zymosan