Repressed activity of peritoneal macrophages in methimazole-induced hypothyroid mice.
In this study we compared the functions of normal peritoneal macrophages with those from methimazole-induced hypothyroid C57BL/6 mice. Methimazole (MMI) suppressed the expression of the tumor necrosis factor (TNF) gene in peritoneal macrophages (MAM) at both transcriptional and translational levels. The kinetics of TNF synthesis by MAM following in vivo and in vitro lipopolysaccharide (LPS) challenge were different, but both treatments resulted in significant decreases (P < 0.05) in TNF mRNA and protein after 60 min. Similarly, the production of reactive nitrogen and oxygen intermediates by MAM were significantly (P < 0.05) lower compared with control macrophages (CAM). In addition, the serum TNF protein was significantly lower (P < 0.05) in MMI-treated mice following intravenous LPS challenge for 90 min. These data suggested that peritoneal macrophages were inactivated in MMI-induced hypothyroid mice.
Liu
W K
WK
Department of Anatomy, Faculty of Medicine, Chinese University of Hong Kong, Shatin, N.T.
Tsui
K W
KW
Wong
C C
CC
D000818:Animals; D015152:Blotting, Northern; D002478:Cells, Cultured; D015870:Gene Expression / Q000187:drug effects; D007037:Hypothyroidism / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008713:Methimazole / Q000633:toxicity*; D051379:Mice; D008807:Mice, Inbred BALB C; D009573:Nitrites / Q000378:metabolism*; D010529:Peritoneal Cavity / Q000166:cytology; D012333:RNA, Messenger / Q000737:chemistry; D013481:Superoxides / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
D008070:Lipopolysaccharides; D009573:Nitrites; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides; D008713:Methimazole