Receptor for advanced glycation end products and its ligand high-mobility group box-1 mediate allergic airway sensitization and airway inflammation Md.

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Receptor for advanced glycation end products and its ligand high-mobility group box-1 mediate allergic airway sensitization and airway inflammation Md Ashik Ullah, M Pharm, Zhixuan Loh, B Biomed Sci, Wan Jun Gan, B Biomed Sci, Vivian Zhang, PhD, Huan Yang, PhD, Jian Hua Li, PhD, Yasuhiko Yamamoto, PhD, Ann Marie Schmidt, PhD, Carol L. Armour, PhD, J. Margaret Hughes, PhD, Simon Phipps, PhD, Maria B. Sukkar, PhD Journal of Allergy and Clinical Immunology Volume 134, Issue 2, Pages 440-450.e3 (August 2014) DOI: 10.1016/j.jaci.2013.12.1035 Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 HDM-induced allergic airway inflammation. A, Study design. B-K, Allergic inflammation in saline solution or HDM sensitized and challenged mice. Bars: mean (±SEM), n = 4-6 mice per group. ***P < .001, **P < .005, *P < .05 vs saline solution control. ###P < .001, ##P < .005, #P < .05 vs HDM-exposed WT controls. ˆP < .05 vs HDM-exposed TLR4−/− and RAGE−/− mice. Journal of Allergy and Clinical Immunology 2014 134, 440-450.e3DOI: (10.1016/j.jaci.2013.12.1035) Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 2 CR-induced allergic airway inflammation. A-F, Allergic inflammation in CR sensitized and challenged mice. Bars: mean (±SEM), n = 5-6 mice per group. ###P < .001, ##P < .005, #P < .05 vs CR-exposed WT controls. Journal of Allergy and Clinical Immunology 2014 134, 440-450.e3DOI: (10.1016/j.jaci.2013.12.1035) Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 3 RAGE is required for TH2-cell priming and DC migration. A, Study design. B, Lymph node cells from saline solution or HDM sensitized mice were restimulated with HDM and IL-13 release was measured. C and D, DC numbers 3 days after saline solution or HDM sensitization. Bars: mean (±SEM), n = 4 mice per group. ***P < .001, **P < .005, *P < .05 vs saline solution control. ##P < .005, #P < .05 vs HDM-exposed WT controls. Journal of Allergy and Clinical Immunology 2014 134, 440-450.e3DOI: (10.1016/j.jaci.2013.12.1035) Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 4 RAGE ligation in DCs is sufficient for the development of allergic airway inflammation. A, Study design. B-G, Allergic inflammation in mice administered media alone or HDM-pulsed WT-DC and then challenged with HDM. Bars: mean (±SEM), n = 4-6 mice per group. ***P < .001, **P < .005, *P < .05 vs saline solution control. NS, Not significant vs WT mice. Journal of Allergy and Clinical Immunology 2014 134, 440-450.e3DOI: (10.1016/j.jaci.2013.12.1035) Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 5 Expression and regulation of HMGB1 in AECs during allergen sensitization. A, Study design. HMGB1 expression during HDM sensitization (B) and day 3 after CR sensitization (C). D and E, Lung HMGB1 immunostaining (×400 magnification). F, HMGB1 cytoplasmic expression in AECs. Data: mean (±SEM), n = 3-9 mice per group. *P < .05 vs time 0. ###P < .001, ##P < .005, #P < .05 vs WT controls at respective time points. Journal of Allergy and Clinical Immunology 2014 134, 440-450.e3DOI: (10.1016/j.jaci.2013.12.1035) Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 6 Relationship among HMGB1, IL-1α and type 2 cytokine release during allergen sensitization. A, IL-1α expression during HDM sensitization and HMGB1 expression day 1 after HDM sensitization. B, Type 2 cytokine expression during HDM sensitization. C, HMGB1 and type 2 cytokine expression day 3 after sensitization with saline (Sal) solution or HDM. D, IL-1α-HMGB1 complexes in BALF during HDM sensitization. Data: mean (±SEM), n = 3-8 mice per group; ***P < .001, **P < .005, *P < .05 vs time 0 (A, B, D) or saline solution control (C). ###P < .001, ##P< .005, #P < .05 vs WT controls at respective time points. ˆP < .05 vs mice exposed to HDM. §P < .05 vs mice exposed to HDM and isotype control antibody. Journal of Allergy and Clinical Immunology 2014 134, 440-450.e3DOI: (10.1016/j.jaci.2013.12.1035) Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 7 HMGB1 is an effector molecule of allergic airway inflammation. A-I, Allergic inflammation in saline (Sal) solution or HDM sensitized and challenged mice. Bars: mean (±SEM), n = 4-6 mice per group. ***P < .001, **P < .005, *P < .05 vs saline solution control. §§P < .005, §P < .05 vs mice exposed to HDM and isotype control antibody. Journal of Allergy and Clinical Immunology 2014 134, 440-450.e3DOI: (10.1016/j.jaci.2013.12.1035) Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig E1 Schematic representation of HMGB1-RAGE signaling during allergic sensitization. HDM-induced activation of TLR4 in AECs (1) triggers IL-1α release, activation of IL-1R signaling (2), and HMGB1 release (3). HMGB1 induces the expression of the epithelial-derived TH2 instructive cytokines IL-25 and IL-33. It remains to be determined whether this occurs via activation of RAGE on AECs (4). Activation of RAGE signaling acts to sustain and/or amplify HMGB1 expression at the level of the airway epithelium (5) and also is required for DC activation and orchestration of TH2 immune responses (6). It remains to be determined whether epithelial-derived HMGB1 engages RAGE signaling in DCs (7). We speculate that bidirectional cross-talk between epithelial cells and DCs drives HMGB1-RAGE feed-forward loops that contribute to the development and propagation of the allergic inflammatory response (8). We also speculate that the formation of IL-1α-HMGB1 complexes contributes to the process of allergic sensitization. Journal of Allergy and Clinical Immunology 2014 134, 440-450.e3DOI: (10.1016/j.jaci.2013.12.1035) Copyright © 2014 American Academy of Allergy, Asthma & Immunology Terms and Conditions