Histamine inhibits chemotaxis, phagocytosis, superoxide anion production, and the production of TNF alpha and IL-12 by macrophages via H-2-receptors

Histamine is released from stimulated basophils and mast cells. and plays a n important role in the pathogenesis of allergic inflammatory processes. In vitro treatment of macrophages with histamine resulted in inhibition of ch emotaxis. Moreover, histamine at 10(-5) M markedly inhibited the production of superoxide anions by both opsonized zymosan-A and phorbol 12-myristate 13-acetate (PMA) stimulated macrophages and histamine at a concentration ra nge of 10(-7) to 10(-5) M significantly inhibited phagocytosis of Escherich ia coli by macrophages. In addition, H-2-selective receptor agonist dimapri t resulted in inhibition of macrophage chemotaxis and markedly inhibited th e production of superoxide anion by PMA-stimulated macrophages and phagocyt osis of E. coli by macrophages. On the other hand, histamine and dimaprit b oth resulted in a concentration-dependent inhibition of lipopolysaccharide- induced production of TNF alpha and IL-12 by macrophages. These results su ggest that histamine and dimaprit may inhibit chemotaxis, phagocytosis, sup eroxide anion production, and the production of TNF alpha and IL-12 by macr ophages via H-2-histamine receptors. (C) 2001 Elsevier Science BN. All righ ts reserved.