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Mannan-induced Nos2 in macrophages enhances IL-17-driven psoriatic arthritis by innate lymphocytes

Jianghong Zhong1, Tatjana Scholz2, Anthony C Y Yau1

  • 1Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm 171 77, Sweden.

Science Advances
|May 19, 2018
PubMed

Insights

Inducible nitric oxide synthase (NOS2) produces nitric oxide (NO), a key factor in developing psoriasis and psoriatic arthritis. Targeting NOS2 may offer new therapeutic strategies for these inflammatory skin and joint conditions.

Area of Science:

  • Immunology
  • Dermatology
  • Rheumatology

Background:

  • The inducible nitric oxide synthase (NOS2) gene is a risk factor for psoriasis (Ps) and psoriatic arthritis (PsA).
  • Nitric oxide (NO) may play a pathogenic role in PsA, contrasting with the regulatory role of reactive oxygen species (ROS) from macrophages.

Purpose of the Study:

  • To investigate the role of NOS2-derived NO in a mouse model of mannan-induced Ps and PsA (MIP).
  • To examine NOS2 expression in patients with PsA and its contribution to disease pathogenesis.

Main Methods:

  • Utilized a mouse model of mannan-induced Ps and PsA (MIP).
  • Assessed NO levels and NOS2 expression in mice and PsA patient monocytes.
  • Investigated the effects of Nos2 deletion and NOS inhibition on MIP development.

Main Results:

  • NO was detected before disease onset in the MIP model, independent of NADPH oxidase 2.
  • Nos2 deletion or NOS inhibition suppressed MIP, confirming Nos2-derived NO is pathogenic.
  • NOS2 was upregulated in PsA monocytes; Nos2-dependent IL-1α release from macrophages was crucial for IL-17 production and arthritis.

Conclusions:

  • Nos2-derived NO from tissue macrophages promotes PsA development in the MIP model.
  • This contrasts with the protective role of ROS in this model.
  • Findings highlight NOS2 as a potential therapeutic target for PsA.

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