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Role of Arginase 1 from Myeloid Cells in Th2-Dominated Lung Inflammation

Lookup NU author(s): Dr Lee Borthwick

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Abstract

Th2-driven lung inflammation increases Arginase 1 (Arg1) expression in alternatively-activated macrophages (AAMs). AAMs modulate T cell and wound healing responses and Arg1 might contribute to asthma pathogenesis by inhibiting nitric oxide production, regulating fibrosis, modulating arginine metabolism and restricting T cell proliferation. We used mice lacking Arg1 in myeloid cells to investigate the contribution of Arg1 to lung inflammation and pathophysiology. In six model systems encompassing acute and chronic Th2-mediated lung inflammation we observed neither a pathogenic nor protective role for myeloid-expressed Arg1. The number and composition of inflammatory cells in the airways and lungs, mucus secretion, collagen deposition, airway hyper-responsiveness, and T cell cytokine production were not altered if AAMs were deficient in Arg1 or simultaneously in both Arg1 and NOS2. Our results argue that Arg1 is a general feature of alternative activation but only selectively regulates Th2 responses. Therefore, attempts to experimentally or therapeutically inhibit arginase activity in the lung should be examined with caution.

Publication metadata

Author(s): Barron L, Smith AM, El Kasmi KC, Qualls JE, Huang XZ, Cheever A, Borthwick LA, Wilson MS, Murray PJ, Wynn TA

Publication type: Article

Publication status: Published

Journal: PLoS ONE

Year: 2013

Volume: 8

Issue: 4

Online publication date: 24/04/2013

Date deposited: 04/11/2014

ISSN (electronic): 1932-6203

Publisher: Public Library of Science

URL: http://dx.doi.org/10.1371/journal.pone.0061961

DOI: 10.1371/journal.pone.0061961

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