Pro-inflammatory response of alveolar macrophages induced by sulphite: studies with lucigenin-dependent chemiluminescence

Abstract

Alveolar macrophages (AM) were studied for their capability to release mediators involved in modulation of neutrophil (PMN) functions. Initial responses were induced by sulphite. Supernatants obtained from canine, human and rat AM pre-treated with sulphite in concentrations of 0.1-2 mmol/L enhanced the respiratory burst of canine, human and rat PMN, measured by lucigenin-dependent chemiluminescence (CL). This PMN-stimulating activity exhibited platelet-activating factor (PAF)-like properties, as indicated by desensitization of the PAF receptor, inhibition with PAF antagonists WEB 2086 and CV 3988, and the kinetic CL response like PAF after chloroform extraction of supernatants inhibitable by PAF antagonist CV 3988. These results indicate that AM are triggered by sulphite to release mediators that activate the respiratory burst of PMN, primarily via the PAF receptor.

HEALTH EFFECTS OF SULFUR-RELATED ENVIRONMENTAL AIR POLLUTION. II. Cellular and Molecular Parameters of Injury

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Ceruloplasmin, Copper, Selenium, Iron, Zinc, and Manganese Levels in Normal and Sulfite Oxidase Deficient Rat Plasma: Effects of Sulfite Exposure

“…It is known that Cp activity can also be impacted by inflammation, as Cp is an acute phase protein and responds transcriptionally to several cytokines [39]. It has been also demonstrated that sodium sulfite increased in production of proinflammatory cytokines by macrophages [40,41]. Interestingly, we did not find a significant rise of Cp activity in SOX-deficient rats, and sulfite treatment did not affect its activity in this group.…”

Endogenous sulfur dioxide protects against isoproterenol-induced myocardial injury and increases myocardial antioxidant capacity in rats

“…Recent studies revealed that exogenous SO 2 has a role in the inflammatory response. [12][13][14] Endogenous SO 2 may be a biologically active molecule involved in the regulation of cardiovascular function, demonstrated by the regulatory role in the myocardial ischemia-reperfusion. 11 The above findings suggested that endogenous SO 2 might be an important mediator in the cardiovascular system, but it remains unclear whether and how endogenous SO 2 contributes to the pathophysiological process of myocardial injury.…”