Macrophage function during the development of adjuvant disease.
Using rat peritoneal macrophages and blood monocytes we examined the relationship of developing adjuvant disease (AD) with the expression of class I and II antigens, release of interleukin-1 (IL-1) and production of prostaglandin E2 (PGE2). We observed that class I and II antigens initially decreased; class II remained low throughout, whereas class I returned to normal. PGE2 and IL-1 gradually increased. Treatment in vivo with the NSAID Na-diclofenac lowered PGE2 and IL-1 release and partly reversed the observed reduction of class I and II antigens. Also, exposure of the cells in vitro to lipopolysaccharide increased class I antigen expression.
Schenkelaars
E J
EJ
Erasmus University, Rotterdam, The Netherlands.
Bonta
I L
IL
Ferrone
S
S
Quagliata
F
F
D000818:Animals; D001168:Arthritis / Q000503:physiopathology*; D001169:Arthritis, Experimental / Q000378:metabolism / Q000503:physiopathology*; D001835:Body Weight / Q000187:drug effects; D015232:Dinoprostone / Q000096:biosynthesis; D007375:Interleukin-1 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000378:metabolism / Q000502:physiology*; D008285:Major Histocompatibility Complex / Q000187:drug effects; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D007375:Interleukin-1; D008070:Lipopolysaccharides; D015232:Dinoprostone