SM-induced increases in inflammatory proteins including soluble receptor for glycation end products, its ligand, high mobility group box-1, and matrix metalloproteinase-9 were also reduced by anti-TNFα antibody administration, along with increases in numbers of lung macrophages expressing TNFα, cyclooxygenase-2 and inducible nitric oxide synthase. Anti-TNFα antibody was found to blunt SM-induced peribronchial edema, perivascular inflammation and alveolar plasma protein and inflammatory cell accumulation in the lung this was associated with reduced expression of PCNA in histologic sections and decreases in BAL levels of fibrinogen. This was followed 15–30 min later by anti-TNFα antibody (15 mg/kg, i.v.) or PBS control. Rats were treated with SM vapor (0.4 mg/kg) or air control by intratracheal inhalation. In these studies, we analyzed the effects of blocking TNFα on lung injury, inflammation and oxidative stress induced by inhaled SM. This is accompanied by an accumulation of macrophages in the lung and the release of the proinflammatory cytokine, tumor necrosis factor (TNF)α. Sulfur mustard (SM) is a bifunctional alkylating agent that causes severe injury to the respiratory tract.
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