EurekaMag.com logo
+ Site Statistics
References:
53,869,633
Abstracts:
29,686,251
+ Search Articles
+ Subscribe to Site Feeds
EurekaMag Most Shared ContentMost Shared
EurekaMag PDF Full Text ContentPDF Full Text
+ PDF Full Text
Request PDF Full TextRequest PDF Full Text
+ Follow Us
Follow on FacebookFollow on Facebook
Follow on TwitterFollow on Twitter
Follow on LinkedInFollow on LinkedIn

+ Translate

Inhalant corticosteroids inhibit mechanical strain-induced RANTES and eotaxin production by human airway smooth muscle cells



Inhalant corticosteroids inhibit mechanical strain-induced RANTES and eotaxin production by human airway smooth muscle cells



Allergology International 51(1): 13-20, March



Background: RANTES and eotaxin play an important role in the production of allergic inflammation of the airway through a chemotactic activity for eosinophils. Airway smooth muscle (ASM) cells are known to produce these cytokines in response to pro-inflammatory stimuli, such as tumor necrosis factor (TNF)-alpha; however, it has not been determined whether mechanical strain could induce cytokine production by ASM cells. In addition, in the present study we also examined the effect of inhalant corticosteroids, namely fluticasone propionate (FP) and budesonide (BUD), on RANTES and eotaxin production. Methods: To clarify these issues, human ASM cells cultured on silicone culture rubber dishes that had been incubated with or without inhalant corticosteroids were stretched or compressed. The ASM cells were simultaneously stimulated with TNF-alpha. The concentration of RANTES and eotaxin in the culture supernatants was determined. Results: The results showed that: (i) mechanical strain, including stretch and compression, stimulated ASM cells to produce RANTES and eotaxin; and (ii) FP and BUD inhibited mechanical strain-induced and TNF-alpha-stimulated RANTES and eotaxin production by ASM cells. These results indicate that mechanical strain is capable of inducing RANTES and eotaxin production by ASM cells and that inhalant corticosteroids effectively inhibit RANTES and eotaxin production by mechanical strain-loaded ASM cells, as well as by TNF-alpha-stimulated cells. Conclusions: Mechanical strain and inflammatory stimuli are capable of inducing chemokine production; therefore, suppressing the contraction of, as well as chemokine production by, ASM cells is important for controlling the production and the progression of allergic inflammation.

(PDF emailed within 0-6 h: $19.90)

Accession: 010845983

Download citation: RISBibTeXText

DOI: 10.1046/j.1440-1592.2002.00242.x



Related references

Inhalant corticosteroids inhibit hyperosmolarity-induced, and cooling and rewarming-induced interleukin-8 and RANTES production by human bronchial epithelial cells. American Journal of Respiratory and Critical Care Medicine 162(3 Pt 1): 1075-1080, 2000

Regulation of TNF-a-induced eotaxin release from cultured human airway smooth muscle cells by b2-agonists and corticosteroids. The FASEB Journal 15(1): 1-9, 2001

Regulation of TNF-alpha-induced eotaxin release from cultured human airway smooth muscle cells by beta2-agonists and corticosteroids. Faseb Journal 15(1): 261-269, 2001

TGF-beta differentially regulates TH2 cytokine-induced eotaxin and eotaxin-3 release by human airway smooth muscle cells. Journal of Allergy and Clinical Immunology 114(4): 791-798, 2004

PAF-induced RANTES production by human airway smooth muscle cells requires both p38 MAP kinase and Erk. American Journal of Respiratory and Critical Care Medicine 161(3 Pt 1): 922-929, 2000

Induction of eotaxin expression and release from human airway smooth muscle cells by IL-1beta and TNFalpha: effects of IL-10 and corticosteroids. British Journal of Pharmacology 127(5): 1145-1150, 1999

Th2- and to a lesser extent Th1-type cytokines upregulate the production of both CXC (IL-8 and gro-alpha) and CC (RANTES, eotaxin, eotaxin-2, MCP-3 and MCP-4) chemokines in human airway epithelial cells. International Archives of Allergy and Immunology 131(4): 264-271, 2003

Zinc chelators inhibit eotaxin, RANTES, and MCP-1 production in stimulated human airway epithelium and fibroblasts. American Journal of Physiology. Lung Cellular and Molecular Physiology 285(3): L719-L729, 2003

Cyclic mechanical strain-induced proliferation and migration of human airway smooth muscle cells: role of EMMPRIN and MMPs. Faseb Journal 19(11): 1507-1509, 2005

Modulation by cAMP of IL-1 -induced eotaxin and MCP-1 expression and release in human airway smooth muscle cells. European Respiratory Journal 22(2): 220-226, 2003

Mechanical strain-induced DNA synthesis and cell proliferation in human airway smooth muscle cells through extracellular signal-regulated kinase. Allergology International 50(1): 63-72, 2001

Modulation by cAMP of IL-1beta-induced eotaxin and MCP-1 expression and release in human airway smooth muscle cells. European Respiratory Journal 22(2): 220-226, 2003

Role of c-jun N-terminal kinase in the induced release of GM-CSF, RANTES and IL-8 from human airway smooth muscle cells. British Journal of Pharmacology 139(6): 1228-1234, July, 2003

Cigarette smoke induces IL-8, but inhibits eotaxin and RANTES release from airway smooth muscle. Respiratory Research 6(): 74-74, 2005

Mechanical Strain-Induced Extracellular Matrix Production by Human Vascular Smooth Muscle Cells : Role of TGF- 1. Hypertension 36(3): 319-324, 2000