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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, OBJECTIVE, METHODS, RESULTS. Meshes: Bronchi, Chemokine CCL11, Chemokine CCL26, Chemokines, CC, Humans, Interleukin-13, Interleukin-4, Myocytes, Smooth Muscle, Pneumonia, Th2 Cells, Transforming Growth Factor beta.
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Does tGF-beta differentially regulate TH2 cytokine-induced eotaxin and eotaxin-3 release by human airway smooth muscle cells? Context: Human airway smooth muscle cells (HASMs) are involved in the pathogenesis of asthma. By producing chemokines, HASMs play a role in the inflammatory processes observed in this disease. Eotaxin, eotaxin-2, and eotaxin-3 are important chemoattractants for eosinophils, and these chemokines are expressed during different phases of the allergic reaction. TH2 cytokines and TGF-beta can be found in increased levels in patients with asthma, and these cytokines may be involved in the regulation of chemokine expression. The aim of this study was to determine the effect of TH2 cytokines and TGF-beta on the regulation of expression of eotaxin, eotaxin-2, and eotaxin-3 by HASMs. HASMs were incubated for 24 hours with IL-4, IL-13, TGF-beta1, or combinations of these cytokines. Protein and mRNA levels of eotaxin and eotaxin-3 were evaluated by sandwich ELISA and reverse transcriptase-PCR. IL-4 and IL-13 induced mRNA and protein for both eotaxin and eotaxin-3. Eotaxin-2 mRNA and protein were not detected in HASMs. TGF-beta alone did not induce expression of the eotaxins. However, in combination with IL-4 or IL-13, TGF-beta enhanced eotaxin production and inhibited TH2 cytokine-induced eotaxin-3 production.
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TGF-beta differentially regulates TH2 cytokine-induced eotaxin and eotaxin-3 release. Final Decision: yes