Requirement of tumor necrosis factor for development of silica-induced pulmonary fibrosis

Article Abstract:

Silicosis is a chronic pulmonary disease where fibrous tissue develops in the lungs due to the presence of silica particles. Macrophages, immune system cells that engulf and destroy foreign organisms, are known to engulf silica particles. The engulfment of the silica by the macrophages is thought to induce the secretion of factors which cause fibrosis (the deposition of connective tissue fibers). Several factors have been identified that are secreted by macrophages and are capable of causing fibrosis. These factors include: interleukin-1, tumor necrosis factor-alpha (TNF), platelet-derived growth factor, basic fibroblast growth factor, and transforming growth factor-beta. The results of this study indicated that TNF is important in the development of silica-induced pulmonary fibrosis in mice. The evidence for TNF's involvement includes a marked increase in the messenger ribose nucleic acid (mRNA) which is translated into the TNF protein in the lung after a single instillation of silica; mRNA levels persisted for more than 70 days. There was no increase noted in other factors such as interleukin-1 or transforming growth factor-beta. Antibodies against TNF, which would normally bind with TNF and inhibit TNF function, did not inhibit the formation of nodules which are formed containing the silica, but almost completely inhibited collagen deposition in these nodules. The deposition of collagen was increased when purified TNF was given to the mice. Corticosteroids are known to decrease TNF production and may provide a new treatment for fibrosis of the lung in patients with silicosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Macrophages, Silica, Lung diseases, Silicon dioxide, Silicosis, Fibrosis

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Tumours and Coley's toxins

Article Abstract:

Coley's toxins work as treatments for tumors in a more involved way than simply by stimulating tumor necrosis factor (TNF). Three considerations allow TNF to be discounted in the effort to account for the therapeutic value of Coley's toxins: the toxins become effective after two to three weeks rather than the 24 hours observed for TNF, the daily or every-other-day administration of the toxins by Coley when TNF cannot be triggered that frequently, and Coley's ability to produce his results using a skin infection caused by group A streptococci.

Drug therapy, Bacterial toxins, Tumors

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Phosphorylation of Raf by ceramide-activated protein kinase

Article Abstract:

The phosphorylation of Raf1 on threonine (Thr) 269 and 268 occurs due to a ceramide-activated protein (CAP) kinase. There is a preference for threonine 269 as the phosphoacceptor site. The CAP kinase indirectly activates MAP kinase, by the activation of Raf1. A complex formation occurs between CAP kinase and Raf1 in intact HL-60 cells. The tumor necrosis factor and ceramide analogues stimulate the phosphorylation and activation of Raf1.

Analysis, Protein kinases, Phosphorylation

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