Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.27.4 (ribonuclease)
 6,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-1 (IL-1) is an important proinflammatory cytokine which may contribute to the pathogenesis of inflammatory airway disorders, such as asthma and cystic fibrosis. Interleukin-1 receptor antagonist (IL-1ra) is a naturally occurring IL-1 inhibitor which binds to IL-1 receptors without inducing agonist activity. Three IL-1ra isoforms have been identified: secreted IL-1ra (sIL-1ra), which is preferentially expressed by-inflammatory cells; intracellular IL-1ra (iIL-1ra) type I, which lacks a signal peptide and is preferentially expressed by epithelial cells; and iIL-1ra type II, which is identical to iIL-1ra type I except for the insertion of an additional 21 amino acids. The goal of this study was to assess whether airway epithelial cell iIL-1ra type I production can be regulated by corticosteroids. First, using reverse transcription-polymerase chain reaction (RT-PCR) and immunoblotting, we confirm that normal human bronchial epithelial (NHBE) cells and a human pulmonary mucoepidermoid carcinoma cell line (NCI-H292) express intracellular IL-1ra type I messenger RNA (mRNA) and protein. Second, using immunoblotting and ELISA, we report that dexamethasone induces time- and concentration-dependent increases in iIL-1ra type I protein within NCI-H292 cell lysates. Lastly, utilizing a ribonuclease protection assay, we report that dexamethasone induces concentration-dependent increases in iIL-1ra type I mRNA levels in NCI-H292 cells. These data suggest that corticosteroid-mediated induction of iIL-1ra type I mRNA and protein by human bronchial epithelial cells represents a novel mechanism by which IL-1-mediated airway inflammatory events might be regulated.
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PMID:Corticosteroids induce intracellular interleukin-1 receptor antagonist type I expression by a human airway epithelial cell line. 870 81

Mast cells produce substances with antiinflammatory properties in addition to their capacity to release proinflammatory mediators. To further probe the antiinflammatory aspect of mast-cell function we investigated the ability of human mast cells (huMCs) to produce interleukin (IL)-1 receptor antagonist (IL-1ra) in response to high-affinity Fc receptor for immunoglobulin E (Fcalpha RI) aggregation, and examined IL-1ra in bronchoalveolar lavage fluid (BALF) to determine whether it might be of mast-cell origin. Using a ribonuclease protection assay, flow cytometry, and enzyme-linked immunosorbent assay (ELISA), IL-1ra message and protein were found to be constitutively expressed in cultured huMCs. Upon stimulation through Fcalpha RI, IL-1ra message was upregulated in huMCs and IL-1ra protein secreted from cultured huMCs and isolated human lung mast cells. By immunoblot analysis, huMCs were found to produce the 17-kD form of IL-1ra and the presence of IL-1ra in human lung mast cells was confirmed by immunohistochemistry. In BALF obtained from allergic asthmatic subjects, IL-1ra production increased after specific antigen challenge, with the 17-kD isoform of IL-1ra predominating. These findings demonstrate that huMCs produce and release IL-1ra after Fcalpha RI aggregation, which may contribute to a local inhibition of IL-1-dependent effects on inflammation in the lung.
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PMID:Secretion of interleukin-1 receptor antagonist from human mast cells after immunoglobulin E-mediated activation and after segmental antigen challenge. 1172 93