Scholars@Duke publication: Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity.

Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity.

Publication , Journal Article

Suwanpradid, J; Shih, M; Pontius, L; Yang, B; Birukova, A; Guttman-Yassky, E; Corcoran, DL; Que, LG; Tighe, RM; MacLeod, AS

Published in: J Immunol

September 1, 2017

Published version (DOI) Link to item

The innate immune components that modulate allergic contact hypersensitivity (CHS) responses are poorly defined. Using human skin from contact dermatitis patients and a mouse model of CHS, we find that hapten allergens disrupt the Arginase1 (Arg1) and inducible NO synthase (iNOS) dynamic in monocytes/macrophages (mono/MΦ), which renders those cells ineffectual in suppressing skin inflammation. Mice lacking Arg1 in MΦ develop increased CHS characterized by elevated ear thickening, mono/MΦ-dominated dermal inflammation, and increased iNOS and IL-6 expression compared with control mice. Treatment of Arg1flox/flox; LysMCre+/- mice with a selective NOS inhibitor or knockout of Nos2, encoding iNOS, significantly ameliorates CHS. Our findings suggest a critical role for Arg1 in mono/MΦ in suppressing CHS through dampening Nos2 expression. These results support that increasing Arg1 may be a potential therapeutic avenue in treating allergic contact dermatitis.

Duke Scholars

Author Loretta Georgina Que Medicine, Pulmonary, Allergy, and Critical Care Medicine

Author Robert Matthew Tighe Medicine, Pulmonary, Allergy, and Critical Care Medicine

Author Amanda S MacLeod Dermatology

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Published In

J Immunol

DOI

10.4049/jimmunol.1700739

EISSN

1550-6606

Publication Date

September 1, 2017

Volume

199

Issue

Start / End Page

1827 / 1834

Location

United States

Related Subject Headings

Skin
Nitric Oxide Synthase Type II
Mice, Knockout
Mice, Inbred C57BL
Mice
Macrophages
Interleukin-6
Immunology
Immunity, Innate
Humans

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Chicago

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Suwanpradid, J., Shih, M., Pontius, L., Yang, B., Birukova, A., Guttman-Yassky, E., … MacLeod, A. S. (2017). Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity. J Immunol. United States. https://doi.org/10.4049/jimmunol.1700739

Suwanpradid, Jutamas, Michael Shih, Lauren Pontius, Bin Yang, Anastasiya Birukova, Emma Guttman-Yassky, David L. Corcoran, Loretta G. Que, Robert M. Tighe, and Amanda S. MacLeod. “Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity.” J Immunol, September 1, 2017. https://doi.org/10.4049/jimmunol.1700739.

Suwanpradid J, Shih M, Pontius L, Yang B, Birukova A, Guttman-Yassky E, et al. Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity. Vol. 199, J Immunol. 2017. p. 1827–34.

Suwanpradid, Jutamas, et al. “Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity.” J Immunol, vol. 199, no. 5, 1 Sept. 2017, pp. 1827–34. Pubmed, doi:10.4049/jimmunol.1700739.

Suwanpradid J, Shih M, Pontius L, Yang B, Birukova A, Guttman-Yassky E, Corcoran DL, Que LG, Tighe RM, MacLeod AS. Arginase1 Deficiency in Monocytes/Macrophages Upregulates Inducible Nitric Oxide Synthase To Promote Cutaneous Contact Hypersensitivity. J Immunol. 2017. p. 1827–1834.