AJP - Regulatory, Integrative and Comparative Physiology, Vol 272, Issue 1 294-R301, Copyright © 1997 by American Physiological Society

ARTICLES

Interleukin-1 beta potentiates bradykinin-induced macromolecular efflux from hamster oral mucosa

X. P. Gao and I. Rubinstein
Department of Medicine, University of Illinois at Chicago, USA.

The purpose of this study was to determine whether interleukin-1 beta (IL-1 beta) elicits macromolecular efflux from the in situ oral mucosa and whether it amplifies that evoked by bradykinin. Using intravital microscopy, we found that suffusion of recombinant human IL-1 beta (50 ng/ml) had no significant effects on leaky site formation and increase in clearance of fluorescein isothiocyanate-labeled dextran (mol mass 70 kDa) from the hamster cheek pouch. However, it significantly potentiated bradykinin-induced macromolecular efflux (P < 0.05). The potentiating effects of IL-1 beta on bradykinin-induced responses were abrogated by a bradykinin B2-receptor antagonist and by a recombinant human IL-1-receptor antagonist. They were not mediated by substance P, prostaglandins, or changes in vasomotor tone. IL-1 beta had no significant effects on adenosine-induced macromolecular efflux. Collectively, these data indicate that IL-1 beta potentiates bradykinin-induced macromolecular efflux from the in situ hamster oral mucosa in a specific fashion. We suggest that this interaction could play a role in the pathogenesis of oral mucosa inflammation.

This article has been cited by other articles:

				X.-P. Gao and I. Rubinstein Methotrexate potentiates bradykinin-induced increase in macromolecular efflux from the hamster oral mucosa Am J Physiol Regulatory Integrative Comp Physiol, October 1, 1997; 273(4): R1254 - R1262. [Abstract] [Full Text] [PDF]