Post-infectious ARDS: mechanisms of lung injury and repair.
Lung infections are considered the most common causes of ARDS. Additionally, superimposed secondary lung infections may occur in the setting of ARDS and further aggravate lung damage. Substances released by neutrophils are the major mediators of lung injury, although other factors, such as endotoxin, exotoxins, macrophages, and immune mechanisms, are significant contributors. Neutrophil-induced lung injury results from the production of oxygen radicals, the release of products of arachidonate metabolism, and the activation of lysosomal enzymes. The development of ARDS is associated with high mortality. Although a large proportion of survivors eventually recover adequate lung function, some patients progress to severe fibrosis. Experimental evidence suggests that the development of fibrosis results from increased synthesis of ECM components by lung fibroblasts. Fibroblast synthesis of ECM components is normally influenced by alveolar cells, by circulating growth factors, by the external milieu, and by the extent of gene expression of the specific ECM components. These factors undergo significant alterations during the evolution of experimental lung fibrosis. Growth factors are more abundant, alveolar cells are activated, and gene expression is enhanced. These factors, which play a crucial role in promoting experimental lung fibrosis, are likely to be involved in the pathogenesis of fibrosis in post-infectious ARDS.
D000818:Animals; D005109:Extracellular Matrix / Q000502:physiology; D006801:Humans; D007239:Infections / Q000150:complications*; D008168:Lung / Q000503:physiopathology; D008171:Lung Diseases / Q000150:complications; D009504:Neutrophils / Q000502:physiology; D011379:Prognosis; D011658:Pulmonary Fibrosis / Q000209:etiology* / Q000503:physiopathology; D012128:Respiratory Distress Syndrome / Q000209:etiology* / Q000503:physiopathology