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Editorial
. 2021 Aug 1;204(3):243-245.
doi: 10.1164/rccm.202104-0869ED.

Airway Androgen Receptor Expression: Regulator of Sex Differences in Asthma?

Ruth P Cusack  1 , Akimichi Nagashima  1 , Roma Sehmi  1
Affiliations
Editorial

Airway Androgen Receptor Expression: Regulator of Sex Differences in Asthma?

Ruth P Cusack et al. Am J Respir Crit Care Med. .
No abstract available

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Figures

Figure 1.
Figure 1.
Airway androgen and androgen receptor (AR) axis—putative modulation of asthma pathogenesis. (A) In mice, testosterone and DHEA attenuate type 2 inflammatory airway responses by inhibiting type 2 cytokine (IL-5 and IL-13) generation by ILC2 and Th2 cell populations, thereby attenuating eosinophilia (6). (B) Zein and colleagues report that AR gene and protein ligand expression levels are negatively associated with inducible nitric oxide synthase (NOS2) gene expression and fractional exhaled nitric oxide (FeNO) levels (10). The signaling from AR is postulated to cause suppression of gene expression of NOS2, an enzyme that catalyzes the production of nitric oxide from l-arginine with consequent reduction in FeNO levels. The beneficial role of androgens in the pathophysiology of asthma is partly mediated through AR modulation of the nitrosative capacity of epithelial cells. DC = dendritic cells; DHEA = dehydroepiandrosterone; DHEA-S = DHEA sulfate; DHT = 5α-dihydrotestosterone; ILC2 = group 2 innate lymphoid cell; Th2 = T-helper cell type 2; TSLP = thymic stromal lymphopoietin.
See this image and copyright information in PMC

Comment on

  • Benefits of Airway Androgen Receptor Expression in Human Asthma.
    Zein JG, McManus JM, Sharifi N, Erzurum SC, Marozkina N, Lahm T, Giddings O, Davis MD, DeBoer MD, Comhair SA, Bazeley P, Kim HJ, Busse W, Calhoun W, Castro M, Chung KF, Fahy JV, Israel E, Jarjour NN, Levy BD, Mauger DT, Moore WC, Ortega VE, Peters M, Bleecker ER, Meyers DA, Zhao Y, Wenzel SE, Gaston B. Zein JG, et al. Am J Respir Crit Care Med. 2021 Aug 1;204(3):285-293. doi: 10.1164/rccm.202009-3720OC. Am J Respir Crit Care Med. 2021. PMID: 33779531 Free PMC article.

References

    1. Zhang G-Q, Bossios A, Rådinger M, Nwaru BI. Sex steroid hormones and asthma in women: state-of-the-art and future research perspectives. Expert Rev Respir Med. 2020;14:543–545. - PubMed
    1. Yung JA, Fuseini H, Newcomb DC. Hormones, sex, and asthma. Ann Allergy Asthma Immunol. 2018;120:488–494. - PMC - PubMed
    1. Becerra-Díaz M, Strickland AB, Keselman A, Heller NM. Androgen and androgen receptor as enhancers of M2 macrophage polarization in allergic lung inflammation. J Immunol. 2018;201:2923–2933. - PMC - PubMed
    1. Dahlgren MW, Molofsky AB. All along the watchtower: group 2 innate lymphoid cells in allergic responses. Curr Opin Immunol. 2018;54:13–19. - PMC - PubMed
    1. Smith SG, Chen R, Kjarsgaard M, Huang C, Oliveria J-P, O'Byrne PM, et al. Increased numbers of activated group 2 innate lymphoid cells in the airways of patients with severe asthma and persistent airway eosinophilia. J Allergy Clin Immunol. 2016;137:75–86.e8. - PubMed