Asthma guidelines: a changing paradigm to improve asthma care.
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Anti-Asthmatic Agents↗
Biomedical subjects
William W Busse
Publications and source records attributed to William W Busse.
Interferon-gamma enhances rhinovirus-induced RANTES secretion by airway epithelial cells.
Respiratory viruses, including rhinoviruses, infect respiratory epithelium and induce a variety of cytokines and chemokines that can initiate an inflammatory response. Cytokines, such as interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha, could enhance epithelial cell activation by inducing virus receptors. To test this hypothesis, effects of IFN-gamma or TNF-alpha on expression of intercellular adhesion molecule (ICAM)-1, rhinovirus binding, and virus-induced chemokine secretion on A549 and human bronchial epithelial cells (HBEC) were determined. The results varied with the type of cell. IFN-gamma was a stronger inducer of ICAM-1 and viral binding on HBEC, whereas TNF-alpha had greater effects on A549 cells. In addition, IFN-gamma, but not TNF-alpha, synergistically enhanced regulated on activation, normal T cells expressed and secreted (RANTES) mRNA expression and protein secretion induced by RV16 or RV49. To determine whether IFN-gamma could enhance RANTES secretion independent of effects on ICAM-1 and RV binding, HBEC were transfected with RV16 RNA in the presence or absence of IFN-gamma. RV16 RNA alone stimulated RANTES secretion, and this effect was enhanced by IFN-gamma. These results demonstrate that IFN-gamma can enhance rhinovirus-induced RANTES secretion by increasing viral binding, and through a second receptor-independent pathway. These findings suggest that IFN-gamma, by upregulating RANTES secretion, could be an important regulator of the initial immune response to rhinovirus infections.
Antiviral Agents↗
Asthma.
Inflammation plays an integral role in the pathophysiology of asthma. With advances in molecular biological techniques and newer animal models, our insight into this process is advancing rapidly. A greater understanding of the interactions of the various elements of the inflammatory response and their interactions is thus evolving. This progress in our knowledge and understanding of the disease process appears to raise even more questions, but such is the nature of research. It is also known that no single abnormality of cells or mediators will suffice to explain the pathogenesis of asthma. Enhanced knowledge of molecular and cellular events in the inflammatory process would inevitably lead to newer, more specific, therapeutic agents, which would potentially be curative rather than palliative.
Animals↗