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Human airway smooth muscle cells express and release RANTES in response to T helper 1 cytokines: regulation by T helper 2 cytokines and corticosteroids.
TLDR
Airway smooth muscle cells have synthetic and secretory potential with the release of RANTES, and may participate in chronic airway inflammation by interacting with both Th1- and Th2-derived cytokines to modulate chemoattractant activity for eosinophils, activated T lymphocytes, and monocytes/macrophages.
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Anemia and inflammation in COPD.
TLDR
Anemic COPD patients show high erythropoietin levels, which may indicate presence of eryporine resistance, and the latter may be mediated through inflammatory mechanisms, which is typical for anemia of chronic illness.
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Inhaled corticosteroids increase interleukin-10 but reduce macrophage inflammatory protein-1alpha, granulocyte-macrophage colony-stimulating factor, and interferon-gamma release from alveolar…
  • M. JohnS. Lim K. Chung
  • Medicine, Biology
    American journal of respiratory and critical care…
  • 1998
TLDR
In comparison to alveolar macrophages from normal nonasthmatic volunteers, those from asthmatic patients released more MIP-1alpha, IFN-gamma, and GM-CSF but lower amounts of IL-10 particularly at baseline and after IL-1beta stimulation.
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Prevalence of anemia in chronic obstructive pulmonary disease: comparison to other chronic diseases.
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Expression and release of interleukin-8 by human airway smooth muscle cells: inhibition by Th-2 cytokines and corticosteroids.
TLDR
IL-8 release induced by TNF-alpha and IFN-gamma was partly inhibited by the Th-2-derived cytokines IL-4, IL-10, and IL-13, as well as by dexamethasone.
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Role of c‐jun N‐terminal kinase in the induced release of GM‐CSF, RANTES and IL‐8 from human airway smooth muscle cells
TLDR
Human airway smooth muscle cells (HASMC) contribute to airway inflammation in asthma by virtue of their capacity to produce several inflammatory mediators including IL‐8, GM‐CSF and RANTES, and JNK activation is involved in TNFα‐ and IL‐1β‐induced GM‐ CSF, RantES and IL-8 production from HASMC.
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Effect of inhaled budesonide on lung function and airway inflammation. Assessment by various inflammatory markers in mild asthma.
TLDR
The effect of inhaled budesonide on lung function and various markers of airway inflammation including airway responsiveness to methacholine, exhaled nitric oxide, eosinophils in induced sputum, bronchoalveolar lavage, and airway biopsies from patients with mild asthma needing beta2- agonist therapy only is examined.
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Cytokines derived from alveolar macrophages induce fever after bronchoscopy and bronchoalveolar lavage.
TLDR
Fifty consecutive patients with various pulmonary diseases who underwent FOB without further interventions or combined with BAL were enrolled and results indicate that fever after FOB and BAL is induced by proinflammatory cytokines derived from alveolar macrophages activated by instillation of fluid into the airways.
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Inhibition of macrophage inflammatory protein-1 alpha expression by IL-10. Differential sensitivities in human blood monocytes and alveolar macrophages.
TLDR
IL-10 is an inhibitor of the induced transcription of MIP-1alpha alpha mRNA and of the release of Mip-1 alpha protein, with a greater effect on monocytes as compared with alveolar macrophages.
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Cigarette smoke induces IL-8, but inhibits eotaxin and RANTES release from airway smooth muscle
TLDR
Inhibition of eotaxin and RANTES by cigarette smoke is consistent with the predominant neutrophilic but not eosinophilic inflammation found in COPD.
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