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IL-33/ST2 Signaling Excites Sensory Neurons and Mediates Itch

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IL-33/ST2 Signaling Excites Sensory Neurons and Mediates Itch IL-33/ST2 signaling excites sensory neurons and PNAS PLUS mediates itch response in a mouse model of poison ivy contact allergy Boyi Liua,b,1, Yan Taib, Satyanarayana Achantab, Melanie M. Kaelbererb, Ana I. Caceresb, Xiaomei Shaoa, Jianqiao Fanga, and Sven-Eric Jordtb,1 aDepartment of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310053, People’s Republic of China; and bDepartment of Anesthesiology, Duke University School of Medicine, Durham, NC 27710 Edited by Diana M. Bautista, University of California, Berkeley, CA, and accepted by Editorial Board Member David E. Clapham October 14, 2016 (received for review April 27, 2016) Poison ivy-induced allergic contact dermatitis (ACD) is the most itch usually triggers scratching that is hard to control, especially common environmental allergic condition in the United States. Case among children, and further injures the skin (10). Scratching exac- numbers of poison ivy ACD are increasing due to growing biomass erbates the inflammation and stimulates nerve fibers, leading to and geographical expansion of poison ivy and increasing content of even more itch and scratching. This itch–scratch cycle can cause skin the allergen, urushiol, likely attributable to rising atmospheric CO2. infections that require antibiotic treatment. Antihistamines are Severe and treatment-resistant itch is the major complaint of af- usually ineffective for treating pruritus associated with poison ivy fected patients. However, because of limited clinical data and poorly ACD, although they are still commonly used (2, 11). Patients with characterized models, the pruritic mechanisms in poison ivy ACD severe symptoms are treated with high-dose corticosteroid regi- remain unknown. Here, we aim to identify the mechanisms of itch mens, which frequently have side effects and are effective only if in a mouse model of poison ivy ACD by transcriptomics, neuronal administered shortly after exposure. imaging, and behavioral analysis. Using transcriptome microarray The pruritic mechanisms in poison ivy ACD remain largely un- analysis, we identified IL-33 as a key cytokine up-regulated in the known because of very limited clinical data and poorly characterized inflamed skin of urushiol-challenged mice. We further found that animal models. Itch signals are generated by a subset of primary af- NEUROSCIENCE the IL-33 receptor, ST2, is expressed in small to medium-sized dorsal ferent sensory neurons that innervate the skin (12). Recent studies root ganglion (DRG) neurons, including neurons that innervate the 2+ using rodent models of pruritic conditions identified a range of non- skin. IL-33 induces Ca influx into a subset of DRG neurons through histaminergic endogenous itch mediators acting on sensory neurons neuronal ST2. Neutralizing antibodies against IL-33 or ST2 reduced and neuronal receptor systems signaling itch. These include cytokines scratching behavior and skin inflammation in urushiol-challenged such as IL-31, CXCL-10, or TSLP (thymic stromal lymphopoietin); mice. Injection of IL-33 into urushiol-challenged skin rapidly exacer- transmitters such as serotonin; and their cognate receptors and cou- bated itch-related scratching via ST2, in a histamine-independent – manner. Targeted silencing of neuronal ST2 expression by intrathecal pled ion channels (13 15). These studies used either chemicals elic- ST2 siRNA delivery significantly attenuated pruritic responses caused iting acute itch (such as chloroquine) or ACD rodent models induced by urushiol-induced ACD. These results indicate that IL-33/ST2 signal- by synthetic allergens not present in the environment [2,4-dinitro- ing is functionally present in primary sensory neurons and contrib- fluorobenzene (DNFB) oxazolone, and others] (14, 16–18). utes to pruritus in poison ivy ACD. Blocking IL-33/ST2 signaling may We contributed to these efforts, identifying the ion channel represent a therapeutic approach to ameliorate itch and skin inflam- TRPA1 (transient receptor potential ankyrin 1) as a key target to mation related to poison ivy ACD. Significance itch | pain | cytokine | IL-33 | allergic contact dermatitis In the United States, the most common cause of allergic con- llergic contact dermatitis (ACD) is a common allergic skin tact dermatitis (ACD) is contact with poison ivy. Severe itch and Acondition caused by environmental or occupational aller- skin inflammation are the major manifestations of poison ivy- gens (1). In the United States, the most common cause of ACD induced ACD. In this study, we have established a critical role is contact with poison ivy, which affects >10 million Americans of IL-33/ST2 (interleukin 33/growth stimulation expressed gene per year (2, 3). Poison ivy ACD is also a serious occupational 2) signaling in both itch and skin inflammation of poison ivy- hazard, particularly among firefighters, forestry workers, and induced ACD and revealed a previously unidentified interaction farmers, accounting for 10% of total U.S. Forest Services lost- of IL-33/ST2 signaling with primary sensory neurons that may time injuries, and it often torments outdoor enthusiasts as well underlie the pruritic mechanisms of poison ivy-induced ACD. (3, 4). The major allergen in poison ivy is urushiol, contained in Blocking IL-33/ST2 signaling may represent a therapeutic ap- the oleoresinous sap of the plant and of related plants (e.g., proach to ameliorate itch and skin inflammation related to poi- poison oak and poison sumac) (5). An estimated 50–75% son ivy dermatitis and, possibly, other chronic itch conditions in of Americans are sensitized to urushiol (6). Elevated atmo- which IL-33/ST2 signaling may participate. spheric carbon dioxide and warming temperatures have in- creased the biomass of poison ivy and related plants, widened Author contributions: B.L. and S.-E.J. designed research; B.L., Y.T., and A.I.C. performed research; M.M.K., X.S., and J.F. contributed new reagents/analytical tools; B.L., Y.T., S.A., their geographic distribution, and increased plant urushiol and A.I.C. analyzed data; and B.L. and S.-E.J. wrote the paper. content (7). These factors will likely increase allergenicity and The authors declare no conflict of interest. result in even larger case numbers of poison ivy ACD in the This article is a PNAS Direct Submission. D.M.B. is a Guest Editor invited by the Editorial future (8). Board. The clinical manifestations of poison ivy-induced ACD are in- 1To whom correspondence may be addressed. Email: [email protected] or boyi.liu@ tense and persistent itch (pruritus), burning sensation, skin rashes, foxmail.com. and swelling, followed by the appearance of vesicles in severe cases This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10. (2, 3, 9). Skin inflammation and pruritus last for weeks. The severe 1073/pnas.1606608113/-/DCSupplemental. www.pnas.org/cgi/doi/10.1073/pnas.1606608113 PNAS Early Edition | 1of8 Downloaded by guest on October 2, 2021 suppress itch in a mouse ACD model induced by the synthetic A Uru or Oxa 2% Uru or Oxa 0.5% allergen oxazolone (16). To examine whether these pathways Sensitization Challenge Uru/Oxa also contribute to itch in poison ivy ACD, we established a Tissue collection mouse model induced by cutaneous sensitization and challenge -5 0 246 8 with urushiol. This model mimics many key clinical features of Time, day poison ivy-induced ACD, including skin inflammation and severe B Veh1 Veh3Veh2 Oxa1Oxa2 Oxa3 Uru1 Uru2 Uru3 itch (16). TRPA1 inhibition was less efficacious in this model, Oxa Uru suggesting that poison ivy ACD engages as-yet-unknown in- Il1f6 86.44** 294.47*** flammatory and pruritic pathways (16). Il1b 288.11*** 215.75*** The aim of the present study is to reveal these pathways through Il24 183.14*** 121.9*** an unbiased approach by using transcriptome microarray analysis Cxcl2 97.87*** 103.97*** of urushiol-induced genes in the mouse skin, validation by quan- Il1f8 46.65** 66.61** Ccl3 52.31*** 59.89*** titative PCR (qPCR) and biochemistry, neuronal functional im- Il19 13.33** 59.81** aging, and pharmacological and behavioral testing. Il1f9 23.28** 29.47** Il33 15.26*** 19.35*** Results Il1a 21.06** 16.35** Urushiol-Induced ACD Triggers the Release of IL-33 from the Inflamed Il6 24.1** 7.68** Skin. To search for potential endogenous pruritogens involved in Ccl8 8.1** 7.49** the pruritus caused by urushiol-induced ACD, we carried out a Il1f5 4.26* 5.87** Cxcl3 6.36** 5.72*** mouse transcriptome microarray analysis to study gene expression Ccl4 5.9** 4.86*** profiles of the skin isolated from urushiol-challenged and un- -4.0 0.0 4.0 challenged (acetone-treated) mice. For comparison, we included the well-established oxazolone-induced ACD mouse model. Mice C D E were sensitized with 2.0% (wt/vol) oxazolone or urushiol on the Skin/qPCR Skin/ELISA Plasma/ELISA 6 ** 2.0 30 abdominal skin, followed by challenges on the nape of neck 5 d ** later with 0.5% oxazolone or urushiol, a concentration known to ** 1.6 ** +Veh 4 20 +Oxa elicit ACD in sensitized humans (Fig. 1A) (19). We found that, 1.2 during the third and fifth urushiol challenge, mice usually de- +Uru 0.8 pg/ml 2 10 veloped a stable dermatitis condition and long-lasting scratching Fold change toward the neck. Therefore, mouse neck skin samples were col- ng/mg protein 0.4 ND ND ND lected after the fifth challenge. Total RNA from neck skins of 0 0.0 0 unchallenged mice and from the mice that had received urushiol or F G 50 oxazolone treatment were analyzed by using hybridization with a Control +Oxazolone +Urushiol ** mouse transcriptome microarray. A total of 3,612 genes, which 40 ** represents 5.5% of total genes (65,956), was identified to be sig- 30 nificantly up- or down-regulated (greater than twofold; P < 0.05) in 20 mouse skin upon urushiol treatment (Tables S1 and S2).
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