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Effect of Both Ultraviolet B Irradiation and Histamine Receptor Function on Allergic Responses to an Inhaled Antigen¹

Jacqueline P. McGlade^*, Shelley Gorman^*, Jason C. Lenzo^*, Jamie W. Tan^*, Takeshi Watanabe, John J. Finlay-Jones^*, Wayne R. Thomas^* and Prue H. Hart^2,*

^* Telethon Institute for Child Health Research and Centre for Child Health Research, University of Western Australia, Perth, Australia and Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan

Exposure of skin to UVB radiation (290–320 nm) modulates the immune system, with most studies showing a suppression of Th1-driven immune responses. This study investigated the effects of UVB on Th2-associated immune responses using a murine model of allergic respiratory inflammation. C57BL/6, histamine receptor-1 knockout (H1RKO), and histamine receptor-2 knockout (H2RKO) mice were exposed to a single 4 kJ/m² dose of UVB (twice a minimal edemal dose) on shaved dorsal skin 3 days before intranasal sensitization with papain, a cysteine protease homologue of the dust mite allergen Der p 1. H1RKO mice demonstrated enhanced papain-specific inflammatory responses in the lung-draining lymph nodes (LDLNs), whereas the responses of H2RKO mice closely mimicked those of C57BL/6 mice. UVB irradiation 3 days before sensitization reduced in vitro papain-specific proliferation of LDLN cells of C57BL/6 and H1RKO mice but not H2RKO mice 24 h after challenge. The regulatory effect of UVB was transferred by adoptive transfer of unfractionated LDLN cells from UVB-irradiated, papain-sensitized C57BL/6 and H1RKO donor mice in naive recipients of the corresponding strain that were subsequently sensitized and challenged with papain. Additionally, UVB exposure suppressed papain-induced IL-5 and IL-10 production in vitro by LDLN cells from H1RKO mice but not from C57BL/6 mice or H2RKO mice. The results of this study demonstrate systemic immunomodulation of responses to intranasally delivered Ag by UVB irradiation and implicate a role for the H2 receptor in UVB-induced suppression of Ag-specific responses in the draining lymph nodes.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grant 229920 from the National Health and Medical Research Council of Australia (to P.H.H. and J.J.F.-J.). J.P.M. is supported by an Australian Postgraduate Award from University of Western Australia and a Stan and Jean Perron Award.

² Address correspondence and reprint requests to Dr. Prue H. Hart, Telethon Institute for Child Health Research, P.O. Box 855, West Perth, Western Australia, Australia. E-mail address: prueh{at}ichr.uwa.edu.au

³ Abbreviations used in this paper: BALF, bronchoalveolar lavage fluid; H1R, histamine receptor-1; H1RKO, H1R knockout; H2R, histamine receptor-2; H2RKO, H2R knockout; LDLN, lung-draining lymph node; RT, room temperature; rm, recombinant murine; H4R, histamine receptor-4.

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