The beta2-adrenergic agonist salbutamol is a potent suppressor of established collagen-induced arthritis: mechanisms of action.

Important note: Information in this article was accurate in 1999. The state of the art may have changed since the publication date.

The beta2-adrenergic agonist salbutamol is a potent suppressor of established collagen-induced arthritis: mechanisms of action.

J Immunol. 1999 May 15;162(10):6278-83. Unique Identifier : AIDSLINE MED/99248217
Malfait AM; Malik AS; Marinova-Mutafchieva L; Butler DM; Maini RN; Feldmann M; Kennedy Institute of Rheumatology, Hammersmith, London, United; Kingdom.

Abstract: The therapeutic potential of salbutamol, a beta2-adrenergic agonist, was explored in collagen-induced arthritis. This study was based on a report that salbutamol, by elevating intracellular cAMP, inhibits IL-12 production by macrophages and dendritic cells, thus preventing Th1 development. Ten-week-old male DBA/1 mice were immunized by intradermal injection of type II collagen in CFA. Arthritis developed 15-30 days later and the mice were treated after onset of disease with salbutamol, 200 microgram i.p. After 10 days, the mice were sacrificed, and the hind paws were evaluated histologically. Salbutamol, 200 microgram daily or every other day, had a profound therapeutic effect on the clinical progression of arthritis, as assessed by clinical score and paw thickness. The therapeutic effect was dose dependent. Daily administration of 200 microgram of salbutamol offered the best protection against joint damage, as assessed by histology. In vitro, salbutamol reduced IL-12 and TNF-alpha release by peritoneal macrophages in a dose-dependent manner, as well as TNF release by synovial cells from arthritic mice. Ex vivo, draining lymph node cells of the salbutamol-treated arthritic mice showed a diminished CII-specific IFN-gamma production and proliferation. In vivo, salbutamol specifically blocked mast cell degranulation in joint tissues. In conclusion, salbutamol has important effects on the immunoinflammatory response and a significant therapeutic action in collagen-induced arthritis.

Keywords: JOURNAL ARTICLE Adrenergic beta-Agonists/*THERAPEUTIC USE Albuterol/*THERAPEUTIC USE Animal Arthritis, Rheumatoid/CHEMICALLY INDUCED/*DRUG THERAPY/IMMUNOLOGY Cell Degranulation/DRUG EFFECTS Cells, Cultured Collagen/TOXICITY Hindlimb/PATHOLOGY Interleukin-12/BIOSYNTHESIS Joints/PATHOLOGY Macrophages/CYTOLOGY/DRUG EFFECTS Male Mast Cells/DRUG EFFECTS Mice Mice, Inbred DBA Receptors, Adrenergic, beta-2/*DRUG EFFECTS Single-Blind Method Support, Non-U.S. Gov't Synovial Membrane/CYTOLOGY/DRUG EFFECTS Th1 Cells/DRUG EFFECTS/IMMUNOLOGY Tumor Necrosis Factor/BIOSYNTHESIS
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