Biomedical subjects
Publications and source records attributed to M T Krishna.
With advances in molecular biology, the complex inflammatory events that underlie asthma are being unraveled. The players are diverse, involving two populations each of mast cells and helper T cells, eosinophils, bronchial endothelial and epithelial cells, and an array of vasoactive and bronchoactive mediators. The clinical message is already clear: Treat the inflammation early.
Asthma is recognized as the most common treatable chronic disease of the lung, afflicting over 100 million people of all age groups yet, despite therapeutic advances, there has been little impact on the rising morbidity and mortality from the disease. This article discusses ways in which molecular medicine can inform public health policy and clinical practice in the management of asthma. It focuses on the recognition that asthma is an inflammatory disorder, and that the public health burden of the disease can be reduced by identifying environmental factors that may trigger asthma in genetically susceptible individuals.
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The health effect of atmospheric pollution is causing increasing public concern. Several controlled human-exposure studies have clearly. shown that oxidant pollutants, including ozone, nitrogen dioxide, and diesel exhaust, induce an acute inflammatory response in human airways. The main component of this response involves the influx of polymorphonuclear leukocytes (PMN) and is mediated via the upregulation of transcription factors NF-kappa B, AP-1, and NF-IL6; leukocyte-endothelial adhesion molecules, and chemokine secretion, including IL-8 and Gro-alpha. The results of recent studies also suggest that short-term exposure to ozone leads to neurogenic inflammation by causing damage to the bronchial epithelium and stimulating subepithelial sensory nerves to release substance P. In addition, such exposures lead to the consumption of endogenous antioxidants that are present in the airway lining fluid. Studies in asthmatics have shown that oxidant pollutants, including ozone and nitrogen dioxide, induce PMN influx in the airways and potentiate responses to inhaled aero-allergens. This article will review various studies addressing the toxicological mechanisms underlying oxidant pollutant-induced airways injury.
Epidemiological evidence suggests that exposure to nitrogen dioxide (NO2) through the use of unvented gas cookers in homes is associated with respiratory symptoms. Toxicological evidence, mainly in animal models, suggests that NO2 may increase the susceptibility to infection by viruses and bacteria. This review examines the evidence and proposes mechanisms whereby such exposure may occur, in particular how NO2 may aggravate respiratory symptoms in the presence of coexistent infection.