Calcium influx is required for tannin-mediated arachidonic acid release from alveolar macrophages
Bates, P.J.; Ralston, N.V.; Vuk-Pavlović, Z.; Rohrbach, M.S.
American Journal of Physiology 268(1 Pt 1): L33-L40
1995
ISSN/ISBN: 0002-9513 PMID: 7840226 Document Number: 448967
The role of Ca-2+ was investigated in the response of alveolar macrophages to cotton tannin, an agent implicated in the lung disease byssinosis in textile mill workers. A physiological concentration of extracellular Ca-2+ was found to be required for tannin-mediated release of radiolabeled arachidonic acid (AA). Flow cytometry using indo 1 indicated that tannin caused a rapid and dose-dependent Ca-2+ increase in macrophages that also required extracellular Ca-2+. Ethylene glycol-bis(beta-aminoethyl ether)N,N,N',N'-tetraacetic acid virtually abolished the Ca-2+ influx mediated by tannin but had little effect on intracellular Ca-2+ release induced by thapsigargin, N-formylmethionyl-leucyl-phenylalanine, or thimerosal. A mechanism for extracellular Ca-2+ influx was demonstrated by rapid Mn-2+ quenching of indo 1 by tannin. Verapamil inhibited tannin-mediated Ca-2+ influx and AA release, but the effective concentration was 100 mu-M. 1,2-Bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid chelated all Ca-2+ in the cells and effectively abolished the tannin response. Exposure to tannin was not associated with cytotoxicity, as judged by 51Cr release. The data suggest that tannin induces Ca-2+ influx in alveolar macrophages, which represents an important prerequisite for a cell-signaling pathway resulting in the accumulation of free AA.