Journal of Applied Physiology, Vol 64, Issue 4 1615-1623, Copyright © 1988 by American Physiological Society
Bronchoalveolar cell activation after inhalation of a bronchoconstricting agent
J. A. Cooper Jr, W. W. Merrill, J. A. Rankin, Y. Sibille and M. G. Buck
Pulmonary Section, West Haven Veterans Administration Medical Center, Connecticut 06516.
Airway inflammation is thought to be an important determinant of
bronchoconstriction and bronchial hyperreactivity. We have recently
demonstrated that bronchoconstriction induced by an aqueous extract of
cotton bracts (CBE) is associated with bronchoalveolar complement
activation, release of polymorphonuclear neutrophil (PMN) chemoattractants
by pulmonary cells, and increased numbers of bronchoalveolar lavage PMN's.
In the present study we performed bronchoalveolar lavage (BAL) on subjects
after CBE or control (saline) challenge and examined whether BAL cells were
activated in vitro to produce other inflammatory agonists. After CBE
administration, cultured BAL cells released increased amounts of the
reactive O2 species, superoxide (O2-.), and the cyclooxygenase products
prostaglandin E2 and thromboxane B2. Although none of these in vitro
parameters of BAL cell activation appeared to correlate with the degree of
bronchoconstriction induced by CBE, BAL fluid levels of thromboxane B2 were
also increased after CBE administration and in vivo amounts of this
eicasanoid did correlate with the degree of bronchoconstriction induced by
CBE (r = 0.50, P less than 0.04). Finally, although cell culture
supernatants were highly chemotactic for PMN's, concentrations of
leukotriene B4 were not increased, suggesting other chemotaxins were
released by BAL cells in this setting. We conclude that CBE administration
activates bronchoalveolar cells to release reactive O2 species and
cyclooxygenase products that may be important in the bronchoconstricting
response to CBE.
