Macrophages-Neutrophil-Platelet Interaction as a Mechanism for Byssinosis?

Ragnar Rylander and Patrick G. Holt


Data from animal experiments as well as observations on humans exposed in cotton cardrooms demonstrate that an invasion of neutrophils into the airways or the respiratory epithelium, is a primary response after exposure to cotton dust. Previous researchers have demonstrated that the mechanism for the neutrophil invasion is a secretion of leucotactic substances from alveolar macrophages. In vitro experiments with a Boyden chamber technique indicated that macrophages exposed to endotoxin increase the chemotaxis of blood neutrophils. After phagocytosis, neutrophils are known to secrete substances which activate platelets. The accumulation of neutrophils and activation of platelets at the site of cotton dust deposition will lead to the liberation of vasoactive and bronchoconstricting agents. These reactions are discussed as a possible mechanism behind the airway constriction and a feeling of chest tightness reported among persons exposed to cotton dusts. In the cardroom environment, these reactions are probably mediated by endotoxin, although other, as yet unidentified chemical compounds, may be present in amounts large enough to contribute to the reaction.

Reprinted from Proceedings of the 1983 Beltwide Cotton Dust Conference pp. 32 - 33
©National Cotton Council, Memphis TN

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Document last modified Sunday, Dec 6 1998