The concurrent expression of Griffonia simplicifolia-IB4 binding and tumor necrosis factor-alpha differs between alveolar and peritoneal macrophages.
As a corollary to their anatomic location, alveolar macrophages (AM) have a lower threshold for generating some physiologic functions than peritoneal macrophages (PM). In this study, we examined both of these populations for their ability to bind the lectin Griffonia simplicifolia-IB4 (GSIB4) and to produce tumor necrosis factor (TNF)-alpha. The results showed that these two responses were concurrently expressed in activated macrophages, although they differed in magnitude when AM and PM were compared. Following in vitro incubation, AM from lipopolysaccharide-treated rats demonstrated a higher percentage of GSIB4 positivity and TNF production when compared with their respective PM. Since prostaglandin E2 can regulate the expression of some macrophage activities, experiments were conducted to determine whether this could also affect the ability of macrophages to bind the GSIB4 lectin. Neither the administration of indomethacin nor exogenous prostaglandin E2 altered the expression of this marker. Conversely, these treatments produced significant changes in TNF-alpha production in both alveolar and peritoneal macrophages. When the concurrent expression of GSIB4 lectin binding and TNF-alpha production was analyzed, AM from lipopolysaccharide-treated rats demonstrated both superior GSIB4 positivity and TNF-alpha production compared with all other macrophages examined. The results of this work show that AM and PM differ in their expression of GSIB4 binding and TNF-alpha production. These differential responses may be important in determining the level of activity of macrophages that are participating in an immune response.
Tabor
D R
DR
Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock 72205.
Theus
S A
SA
Barnett
J B
JB
Tryka
A F
AF
Jacobs
R F
RF
D000818:Animals; D002478:Cells, Cultured; D015232:Dinoprostone / Q000096:biosynthesis; D037102:Lectins / Q000378:metabolism*; D008070:Lipopolysaccharides; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism*; D016676:Macrophages, Alveolar / Q000378:metabolism*; D008297:Male; D010529:Peritoneal Cavity / Q000166:cytology; D051381:Rats; D011916:Rats, Inbred F344; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
D037102:Lectins; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D015232:Dinoprostone