Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsiveness.

Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsiveness. Research Abstract Details 

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Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsiveness. Abstract Text:

Ming Yang,Danny Rangasamy,Klaus I Matthaei,Ailsa J Frew,Nives Zimmmermann,Suresh Mahalingam,Dianne C Webb,David J Tremethick,Philip J Thompson,Simon P Hogan,Marc E Rothenberg,William B Cowden,Paul S Foster,

Increased arginase I activity is associated with allergic disorders such as asthma. How arginase I contributes to and is regulated by allergic inflammatory processes remains unknown. CD4+ Th2 lymphocytes (Th2 cells) and IL-13 are two crucial immune regulators that use STAT6-dependent pathways to induce allergic airways inflammation and enhanced airways responsiveness to spasmogens (airways hyperresponsiveness (AHR)). This pathway is also used to activate arginase I in isolated cells and in hepatic infection with helminths. In the present study, we show that arginase I expression is also regulated in the lung in a STAT6-dependent manner by Th2-induced allergic inflammation or by IL-13 alone. IL-13-induced expression of arginase I correlated directly with increased synthesis of urea and with reduced synthesis of NO. Expression of arginase I, but not eosinophilia or mucus hypersecretion, temporally correlated with the development, persistence, and resolution of IL-13-induced AHR. Pharmacological supplementation with l-arginine or with NO donors amplified or attenuated IL-13-induced AHR, respectively. Moreover, inducing loss of function of arginase I specifically in the lung by using RNA interference abrogated the development of IL-13-induced AHR. These data suggest an important role for metabolism of l-arginine by arginase I in the modulation of IL-13-induced AHR and identify a potential pathway distal to cytokine receptor interactions for the control of IL-13-mediated bronchoconstriction in asthma.

Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsiveness. Publishing Authors By Initials

M Yang,D Rangasamy,KI Matthaei,AJ Frew,N Zimmmermann,S Mahalingam,DC Webb,DJ Tremethick,PJ Thompson,SP Hogan,ME Rothenberg,WB Cowden,PS Foster,

For similar cells: blood cells: leukocytes: leukocytes, mononuclear: lymphocytes: t-lymphocytes: cd4-positive t-lymphocytes: t-lymphocytes, helper-inducer: th2 cells research abstracts see: cells: blood cells: leukocytes: leukocytes, mononuclear: lymphocytes: t-lymphocytes: cd4-positive t-lymphocytes: t-lymphocytes, helper-inducer: th2 cells research

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Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsiveness. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 177

Page Numbers: 5595-603

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 15

MONTH: Oct

YEAR: 2006

Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsiveness. Information

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LANGUAGE: eng

NlmUniqueID: 2985117

Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsiveness. Keywords Mesh Terms:

KEYWORDS: Th2 Cells

MESH TERMS: metabolism

Chemical & Substance for Abstract: Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsiveness. Information

Substance Name: Arginase

Registry Number: EC 3.5.3.1

Grant and Affiliation Information for Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsiveness.

AFFILIATION: Division of Molecular Biosciences, The John Curtin School of Medical Research, Australian National University, Canberra, Australia.

Country: United States

AGENCY: United States NIAID

GRANT: R01 AI1053479

ACRONYM: AI

MEDLINETA: J Immunol

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