Remission of chronic fungal asthma in the absence of CCR8

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Remission of chronic fungal asthma in the absence of CCR8 Karen F. Buckland, PhD, Erica C. O'Connor, BA, Eilish M. Coleman, BSc, Sergio A. Lira, MD, PhD, Nicholas W. Lukacs, PhD, Cory M. Hogaboam, PhD  Journal of Allergy and Clinical Immunology  Volume 119, Issue 4, Pages 997-1004 (April 2007) DOI: 10.1016/j.jaci.2006.12.660 Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 1 Detailed examination of the features of allergic airways disease at day 3 after conidia challenge. Representative photomicrographs of hematoxylin and eosin–stained histologic lung sections from CCR8+/+(A) and CCR8−/−(B) mice; original magnification ×200. C, Serum IgE and IgG2A. D, Quantification of BAL leukocytes. E, AHR after methacholine provocation; statistical significance is compared with baseline values. F, Cytokine protein content in the lung tissue and BAL. G, Cytokine mRNA in the lung, n = 5. ∗P ≤ .05; ∗∗P ≤ .01 compared with baseline airway hyperresponsiveness in wild type; ##P ≤ .01 compared with baseline airway hyperresponsiveness in CCR8−/−. Journal of Allergy and Clinical Immunology 2007 119, 997-1004DOI: (10.1016/j.jaci.2006.12.660) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 2 Examination of the features of allergic airways disease at day 7 after conidia challenge. Giant cells are depicted by arrows in photomicrographs of Gomori Methenamine Silver–stained histologic lung sections from CCR8+/+(A) and CCR8−/−(B) mice; original magnification ×200, representative of n = 5. C, Serum IgE and IgG2A. D, Quantification of BAL leukocytes, n = 5. E, AHR after methacholine provocation; statistical significance is compared with baseline values, n = 3-4. F, Cytokine protein content in the lung tissue and BAL, n = 5. G, Cytokine protein content in lung tissue, n = 5. ∗P ≤ .05; ∗∗P ≤ .01 compared with baseline airway hyperresponsiveness in wild type; ##P ≤ .01 compared with baseline airway hyperresponsiveness in CCR8−/−. Journal of Allergy and Clinical Immunology 2007 119, 997-1004DOI: (10.1016/j.jaci.2006.12.660) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 3 Reduced physiological and remodeling parameters of allergic airways disease at day 14 postconidial challenge. Representative photomicrographs of periodic acid-Schiff–stained histologic lung sections from CCR8+/+(A) and CCR8−/−(B) mice; original magnification ×200. C, Serum IgE and IgG2A. D, Measurement of AHR after methacholine provocation; statistical significance is compared with baseline values. E, MUC5A mRNA detected in the lung, n = 5. ∗P ≤ .05; ∗∗P ≤ .01 compared with baseline airway hyperresponsiveness in wild type; #P ≤ .05 compared with baseline airway hyperresponsiveness in CCR8−/−. Journal of Allergy and Clinical Immunology 2007 119, 997-1004DOI: (10.1016/j.jaci.2006.12.660) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Fig 4 Cytokine production by antigen-restimulated splenocytes. Cytokine production by whole spleen cell populations from A fumigatus–sensitized CCR8−/−(open bars) and CCR8+/+(closed bars) mice before (ie, day 0) and at days 2 or 7 after conidia cultured for 24 hours with Con A (10 μg/mL) or A fumigatus antigens (1 μg/mL); data shown are means ± SEMs from 3 replicate wells of cells pooled from 5 mice. ∗P ≤ .05; ∗∗P ≤ .01. Journal of Allergy and Clinical Immunology 2007 119, 997-1004DOI: (10.1016/j.jaci.2006.12.660) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions