Host Defense against Opportunist Microorganisms Following Trauma.
Abstract
Previous studies from our laboratory have demonstrated reduction in alternative complement pathway activity and serum-mediated inhibition of bacterial phagocytosis by polymorphonuclear leukocytes (PMNL) following burn injury in humans. In the present investigation, the abnormalities were documented in a guinea pig model of burn injury, and preliminary evidence was presented to suggest that burn wound injection as a primary determinant in induction of these abnormalities. Studies in burned humans failed to demonstrate a correlation between the abnormalities and nutritional status as assessed by measurement of total caloric and protein intake. Burn serum inhibitor(s) of PMNL function were shown to be heat-stable and distinct from IgG and proteases with sensitivity to inactivation by benzamidine hydrochloride. Reduction in alternative pathway activity was not found to be caused by an aberrant factor that augments the functions of the regulatory proteins, H and I, or to elevation of these proteins as compared with C3 and B. Rather, this abnormality was associated with diminution in the functional activity of D. Preliminary evidence was provided to suggest that the burn serum inhibitor(s) of alternative pathway activity and PMNL function are alpha globulin-associated and bear a relationship with burn serum inhibitor(s) of lymphocyte function.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 31, 1982
- Accession Number
- ADA144114
Entities
People
- A. B. Bjornson
- H. S. Bjornson
- J. E. Fischer
- W. A. Altemeier
Organizations
- University of Cincinnati