A gradient in the levels of proinflammatory mediators (IL-l-a, IL-6, pro-IL-l-p) would also result. However, the levels of these cytokines would be highest in the center and lowest in the periphery of granulomas and abscesses. The contrasting nature of these two gradients would tend to foster or maintain central inflammation and stimulate peripheral scarring as seen in these lesions. Additional investigation using both animal models and human material will be required to test this hypothesis.
Our studies focused on the regulatory effects of IL-1, TNF, IFN-7, and IL-6. These cytokines were chosen based on a large body of data demonstrating their regulatory importance. However, they are not the only regulatory cytokines in the lung. The importance of a number of other cytokines including transforming growth factor-P, epidermal growth factor, the insulin growth factors, the fibroblast growth factors, platelet derived growth factor, and the colony stimulating factors is well documented. The roles these cytokines play in the cytokine networks regulating inflammation and fibrosis in the lung will need to be clarified. asthma inhalers
The practicing pulmonary clinician is familiar with the beneficial and adverse effects of inflammation and fibrosis in the lung. Investigations such as those described in this report are beginning to unravel the complicated processes regulating inflammation and fibrosis that are responsible for the different outcomes that patients experience. A clearer understanding of the processes that maintain the integrity of the normal lung and of the abnormalities in these regulatory processes in specific disorders will allow physicians to more accurately predict the outcome of an inflammatory event in a given patient. In addition, with the advent of molecular biologic techniques, recombinant human cytokines are now readily available for investigative and therapeutic purposes. The knowledge derived from studies such as these will provide the rationale for the use of recombinant agents (systematically or via aerosolization) to influence the outcomes of inflammatory and fibrotic events in the human lung.
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