Important note: Information in this article was accurate in 1994. The state of the art may have changed since the publication date.
Interleukin-6 and the lung.
Lung Biol Health Dis; 61:229-80 1993. Unique Identifier : AIDSLINE ICDB/94606665 Zitnik RJ; Elias JA; Dept. of Internal Medicine, Yale Univ. Sch. of Medicine, New; Haven, CT
Abstract:
Interleukin-6 (IL6) is a pleiotropic cytokine produced by a wide variety of cells, including many of the major cells in the lung, and in response to a broad spectrum of stimuli (eg, viral infection, bacterial endotoxin, agonists of cAMP, PKC, and calcium 2nd-messenger systems). Regulation of IL6 production is complex and can occur at the level of both gene transcription and mRNA degradation. The biological effects of IL6 are protean, and newly discovered activities continue to be described. IL6 production and activities are reviewed as follows: the IL6 protein (structure, molecular heterogeneity, and structure-function analysis), structure and regulation of the IL6 gene, the IL6 receptor, biological effects of IL6 (B-cell and T-cell effects, plasmacytoma and hybridoma growth, acute-phase response, hematopoiesis, and endocrine, neurobiologic, and cutaneous effects), IL6 in human homeostasis (acute inflammatory disorders, trauma and surgery, chronic inflammatory disorders, neoplastic disorders, transplant rejection, and HIV and Kaposi's sarcoma), and IL6 in the lung. IL6 causes disease by three major mechanisms: (1) IL6 can be overproduced, causing disease as a direct result of its systemic effects; (2) IL6 can be elevated as a protective reaction to stress, injury, or infections; and (3) IL6 may function as a part of dysregulated autocrine and paracrine feedback loops in chronic inflammatory disease and neoplastic disorders. In the pathogenesis of several neoplastic disorders, the effects of IL6 are mediated principally through two major mechanisms: some tumors constitutively produce large amounts of IL6, and the oversecreted cytokine produces the systemic manifestations of the tumor; other tumors constitutively produce and proliferate in response to IL6. The autocrine or paracrine (or both) effects of IL6 on the tumor are responsible for stimulating tumor cell proliferation and induction of the malignant phenotype. Hematological malignancies (multiple myeloma, leukemias, and lymphomas) and solid tumors are discussed. Several questions remain to be answered concerning IL6 and its role in the lung. Particular attention needs to be directed toward determining whether dysregulated autocrine or paracrine IL6 feedback loops play an important role in the pathogenesis of diseases such as sarcoidosis, asthma, hypersensitivity pneumonitis, allograft rejection, and lung cancer. (247 Refs)
Keywords: Cell Division Gene Expression Regulation Human Interleukin-6/GENETICS/*METABOLISM Lung/*METABOLISM Lung Diseases/METABOLISM Phenotype RNA, Messenger/METABOLISM Transcription, Genetic MONOGRAPH 941230
M94C4340
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Important note: Information in this article was accurate in 1994. The state of the art may have changed since the publication date.
