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The Tick Salivary Protein, Salp15, Inhibits the Development of Experimental Asthma¹

Sara A. Paveglio^*, Jenna Allard^*, Jana Mayette^*, Laurie A. Whittaker^*, Ignacio Juncadella, Juan Anguita and Matthew E. Poynter^2,*

^* Department of Medicine, Vermont Lung Center and University of Vermont, Burlington, VT 05405; and Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA 01003

Activation of Th2 CD4⁺ T cells is necessary and sufficient to elicit allergic airway disease, a mouse model with many features of human allergic asthma. Effectively controlling the activities of these cells could be a panacea for asthma therapy. Blood-feeding parasites have devised remarkable strategies to effectively evade the immune response. For example, ticks such as Ixodes scapularis, which must remain on the host for up to 7 days to feed to repletion, secrete immunosuppressive proteins. Included among these proteins is the 15-kDa salivary protein Salp15, which inhibits T cell activation and IL-2 production. Our objective for these studies was to evaluate the T cell inhibitory properties of Salp15 in a mouse model of allergic asthma. BALB/cJ mice were Ag sensitized by i.p. injection of OVA in aluminum hydroxide, with or without 50 µg of Salp15, on days 0 and 7. All mice were challenged with aerosolized OVA on days 14–16 and were studied on day 18. Compared with control mice sensitized with Ag, mice sensitized with Ag and Salp15 displayed significantly reduced airway hyperresponsiveness, eosinophilia, Ag-specific IgG1 and IgE, mucus cell metaplasia, and Th2 cytokine secretion in vivo and by CD4⁺ T cells restimulated with Ag in vitro. Our results demonstrate that Salp15 can effectively prevent the generation of a Th2 immune response and the development of experimental asthma. These studies, and those of others, support the notion that a lack of ectoparasitism may contribute to the increasing prevalence of allergic asthma.

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 National Institutes of Health/National Heart, Lung, and Blood Institute Predoctoral Pulmonary Training Grant T32 HL076122 (to S.A.P.), by Institutional Research Support from the University of Vermont, College of Medicine (to M.E.P.), by National Institutes of Health National Center for Research Resources Center of Biomedical Research Excellence Grant RR15557 (to M.E.P. and L.A.W.), and by National Institutes of Health Grant AI053064 (to J.A.).

² Address correspondence and reprint requests to Dr. Matthew E. Poynter, Department of Medicine, Division of Pulmonary Disease and Critical Care, University of Vermont, 149 Beaumont Avenue, HSRF 220, Burlington, VT 05405. E-mail address: matthew.poynter{at}uvm.edu

³ Abbreviations used in this paper: BAL, bronchoalveolar lavage; alum, aluminum hydroxide; BALF, BAL fluid; PAS, periodic acid-Schiff; C_T, threshold cycle.