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Presentation transcript:

A new mechanism regulating the initiation of allergic airway inflammation Attila Kiss, MD, Martin Montes, MD, Sarat Susarla, MD, Elin A. Jaensson, BA, Scott M. Drouin, PhD, Rick A. Wetsel, PhD, Zhengbin Yao, PhD, Rachel Martin, PhD, Nabeel Hamzeh, MD, Rebecca Adelagun, BS, Sheila Amar, MD, Farrah Kheradmand, MD, David B. Corry, MD Journal of Allergy and Clinical Immunology Volume 120, Issue 2, Pages 334-342 (August 2007) DOI: 10.1016/j.jaci.2007.04.025 Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 Innate recruitment of allergic inflammatory cells by FAP. RAG-1−/− and wild-type mice were challenged once intranasally with either vehicle, OVA, or FAP. Eighteen hours later, the total numbers of bronchoalveolar lavage fluid (BALF) cells, including eosinophils, macrophages, neutrophils, and lymphocytes (A); BALF eosinophils (B); and whole lung homogenate IL-4–secreting cells (C), were assessed. ∗P < .05 compared with OVA-challenged mice. Representative of 4 independent experiments (n = 4 mice per group). Journal of Allergy and Clinical Immunology 2007 120, 334-342DOI: (10.1016/j.jaci.2007.04.025) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 2 Proteinase activity, but not endotoxin, is required for allergic chemokine secretion and inflammation. RAG-1−/− mice were challenged intranasally once with OVA, FAP, proteinase-inactive FAP (FAP [i]), or a combination of TLR ligands (E coli LPS and CpG motif-containing deoxyoligonucleotides) prepared with OVA (TLR/OVA). CCL17 (A), CCL7 (B), and CXCL10 (C) levels were measured by means of ELISA from bronchoalveolar lavage fluid 18 hours later. D, Total lung IL-4– and IFN-γ–secreting cells were enumerated by means of ELISPOT from whole lungs of mice challenged with either OVA or TLR/OVA. Journal of Allergy and Clinical Immunology 2007 120, 334-342DOI: (10.1016/j.jaci.2007.04.025) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 3 Allergic chemokine secretion without STAT6 and C3. Wild-type, STAT6−/−, C3−/−, and C3a anaphylatoxin receptor−/− mice were challenged once intranasally with FAP or OVA, and CCL17 (A) and CCL7 (B) concentrations in bronchoalveolar lavage (BAL) were determined 18 hours later. BAL fluid was obtained from wild-type and C3−/− mice challenged once intranasally with saline or FAP, and the total numbers of eosinophils, macrophages, neutrophils, and lymphocytes were determined (C). Eosinophil data are re-expressed in panel D. Vehicle (saline)–challenged animals showed induction of no chemokines or airway inflammation. Representative of 2 independent experiments (n = 3 or 4 mice per group). Journal of Allergy and Clinical Immunology 2007 120, 334-342DOI: (10.1016/j.jaci.2007.04.025) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 4 Allergic lung inflammation without STAT6. Wild-type and STAT6−/− mice received CFSE-labeled T cells from FAP-sensitized wild-type mice or sham treatment and were challenged intranasally with FAP or vehicle daily for 3 days. A, Flow cytometric detection of labeled lung T cells from a representative mouse. Total lung CD4+/CFSE+ T cells (B), bronchoalveolar lavage eosinophils (C), and lung IL-4+ (D) and IFN-γ+ (E) cells isolated from the indicated groups are shown. ∗P < .05 compared with mice receiving T cells and vehicle. Representative of 4 independent experiments (n = 4-5 mice per group). Journal of Allergy and Clinical Immunology 2007 120, 334-342DOI: (10.1016/j.jaci.2007.04.025) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions