Cytokine Networks in the Regulation of Inflammation and Fibrosis in the Lung: Discussion (Part 4)

In: Pulmonary function

16 Nov 2012

They demonstrate that cytokines can stimulate fibroblast proliferation and collagen production when present individually and inhibit fibroblast proliferation and collagen production when present simultaneously. They also demonstrate that fibroblasts can produce IL-l-a, IL-6, and IL-l-p and that the highest levels of these moieties are seen in cells stimulated with rIL-1 and rTNF in combination. If one assumes that granulomas and abscesses are the result of localized insults (infectious, occupational or otherwise), one can construct a hypothesis based on these cytokine networks that explains the unique histology of these legions. It is likely that tissue damage at the site of the granuloma or abscess results in serum weepage into the lung and mononuclear cell activation with the release of large quantities of IL-1, TNF, and IFN-7. Fibroblasts located near the center of these lesions are likely to be simultaneously exposed to multiple cytokines. Thus, their proliferation and collagen production would tend to be inhibited. Simultaneously, they would be making large amounts of IL-l-a, IL-6, and pro-IL-l-p which would augment local inflammatory events. In contrast, fibroblasts at the periphery of these lesions are more likely to be exposed to individual cytokines. Their proliferation and collagen production would be stimulated by agents such as IL-1 and TNF and their production of IL-l-a, IL-l-p and IL-6 would be markedly diminished in comparison to centrally located cells. This would result in a gradient of fibrogenetic activity (fibroblast proliferation and collagen production) that is highest at the periphery and lowest in the center of granulomas and abscesses. buy prednisone

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