Prior airway exposure to allergen increases virus-induced airway hyperresponsiveness Mika J Mäkelä, MD, Ralph Tripp, PhD, Azzeddine Dakhama, PhD, Jun-Won.

Slides:

Advertisements

Similar presentations

Dual effects of vitamin D–induced alteration of TH1/TH2 cytokine expression Victor Matheu, MD, Ove Bäck, MD, PhD, Emma Mondoc, BSc, Shohreh Issazadeh-Navikas,

Advertisements

Toll-like receptor 2 ligands promote chronic atopic dermatitis through IL-4–mediated suppression of IL-10 Susanne Kaesler, PhD, Thomas Volz, MD, Yuliya.

Exposure to allergen and diesel exhaust particles potentiates secondary allergen- specific memory responses, promoting asthma susceptibility Eric B. Brandt,

Glucagon-like peptide 1 receptor signaling attenuates respiratory syncytial virus– induced type 2 responses and immunopathology Melissa H. Bloodworth,

Maternal immune response to helminth infection during pregnancy determines offspring susceptibility to allergic airway inflammation Kathrin Straubinger,

IL-4 induces IL-13–independent allergic airway inflammation

Effective prevention and therapy of experimental allergic asthma using a GATA-3– specific DNAzyme Serdar Sel, MD, Michael Wegmann, PhD, Tanja Dicke, MSc,

CD4 T-helper cells engineered to produce IL-10 prevent allergen-induced airway hyperreactivity and inflammation Jae-Won Oh, MD, PhD, Christine M. Seroogy,

Essential role of dendritic cell CD80/CD86 costimulation in the induction, but not reactivation, of TH2 effector responses in a mouse model of asthma

Virus-specific IgE enhances airway responsiveness on reinfection with respiratory syncytial virus in newborn mice Azzeddine Dakhama, PhD, Young-Mok Lee,

Allergy prevention starts before conception: Maternofetal transfer of tolerance protects against the development of asthma Tobias Polte, PhD, Christian.

Local administration of antisense phosphorothioate oligonucleotides to the c-kit ligand, stem cell factor, suppresses airway inflammation and IL-4 production.

Innate IL-13–producing nuocytes arise during allergic lung inflammation and contribute to airways hyperreactivity Jillian L. Barlow, PhD, Agustin Bellosi,

Expression of IL-4 receptor α on smooth muscle cells is not necessary for development of experimental allergic asthma Frank Kirstein, PhD, William G.C.

Frank Kirstein, PhD, Natalie E

Innate immune responses during respiratory tract infection with a bacterial pathogen induce allergic airway sensitization Nicolas W.J. Schröder, MD,

Enteric helminth-induced type I interferon signaling protects against pulmonary virus infection through interaction with the microbiota Amanda J. McFarlane,

Exposure to allergen and diesel exhaust particles potentiates secondary allergen- specific memory responses, promoting asthma susceptibility Eric B. Brandt,

Nazanin Farhadi, MSc, Laura Lambert, BA, Chiara Triulzi, PhD, Peter J

Pentraxin 3 deletion aggravates allergic inflammation through a TH17-dominant phenotype and enhanced CD4 T-cell survival Jyoti Balhara, MSc, Lianyu Shan,

Compartmentalized chemokine-dependent regulatory T-cell inhibition of allergic pulmonary inflammation Roshi Afshar, PhD, James P. Strassner, BS, Edward.

IL-33 dysregulates regulatory T cells and impairs established immunologic tolerance in the lungs Chien-Chang Chen, PhD, Takao Kobayashi, PhD, Koji Iijima,

Restoration of T-box–containing protein expressed in T cells protects against allergen- induced asthma Jung Won Park, MD, Hyun Jung Min, MS, Jung Ho Sohn,

Β-Glucan exacerbates allergic asthma independent of fungal sensitization and promotes steroid-resistant TH2/TH17 responses Zhonghua Zhang, MD, Jocelyn.

Allergic airway disease is unaffected by the absence of IL-4Rα–dependent alternatively activated macrophages Natalie E. Nieuwenhuizen, PhD, Frank Kirstein,

Responsiveness to respiratory syncytial virus in neonates is mediated through thymic stromal lymphopoietin and OX40 ligand Junyan Han, PhD, Azzeddine.

Pediatric severe asthma with fungal sensitization is mediated by steroid-resistant IL-33 Susana Castanhinha, MD, Rebekah Sherburn, MSc, Simone Walker,

Eosinophils contribute to the resolution of lung-allergic responses following repeated allergen challenge Katsuyuki Takeda, MD, PhD, Yoshiki Shiraishi,

Lung dendritic cells induce TH17 cells that produce TH2 cytokines, express GATA-3, and promote airway inflammation Marianne Raymond, PhD, Vu Quang Van,

CD4+CD25+ regulatory T cells reverse established allergic airway inflammation and prevent airway remodeling Jennifer Kearley, PhD, Douglas S. Robinson,

Experimental gastrointestinal allergy enhances pulmonary responses to specific and unrelated allergens Eric B. Brandt, PhD, Troy A. Scribner, MD, Hiroko.

Frank Kirstein, PhD, Natalie E

Inhibition of house dust mite–induced allergic airways disease by antagonism of microRNA-145 is comparable to glucocorticoid treatment Adam Collison,

Requirements for allergen-induced airway inflammation and hyperreactivity in CD4- deficient and CD4-sufficient HLA-DQ transgenic mice Svetlana P. Chapoval,

IL-2–inducible T-cell kinase modulates TH2-mediated allergic airway inflammation by suppressing IFN-γ in naive CD4+ T cells Arun K. Kannan, MS, Nisebita.

Exaggerated IL-17 response to epicutaneous sensitization mediates airway inflammation in the absence of IL-4 and IL-13 Rui He, MD, PhD, Hye Young Kim,

Regulation of allergic airway inflammation by class I–restricted allergen presentation and CD8 T-cell infiltration James W. Wells, PhD, Christopher J.

Janus kinase 1/3 signaling pathways are key initiators of TH2 differentiation and lung allergic responses Shigeru Ashino, PhD, Katsuyuki Takeda, MD,

Prophylactic and therapeutic inhibition of allergic airway inflammation by probiotic Escherichia coli O83 Christian Zwicker, MSc, Priya Sarate, MSc,

Epigenetic regulation in murine offspring as a novel mechanism for transmaternal asthma protection induced by microbes Stephanie Brand, PhD, René Teich,

Sarita Sehra, PhD, Weiguo Yao, PhD, Evelyn T. Nguyen, MS, Nicole L

Animal shed Bacillus licheniformis spores possess allergy-protective as well as inflammatory properties Kay Vogel, MSc, Nicole Blümer, PhD, Melanie Korthals,

Programmed cell death ligand 2 regulates TH9 differentiation and induction of chronic airway hyperreactivity Jerome Kerzerho, PhD, Hadi Maazi, PhD, Anneliese.

Effects of established allergen sensitization on immune and airway responses after secondary allergen sensitization Katharina Blumchen, MD, Kerstin Gerhold,

Recombinant basic fibroblast growth factor inhibits the airway hyperresponsiveness, mucus production, and lung inflammation induced by an allergen challenge

IFN-τ inhibits IgE production in a murine model of allergy and in an IgE-producing human myeloma cell line Mustafa G. Mujtaba, PhDa, Lorelie Villarete,

Staphylococcal enterotoxin A–activated regulatory T cells promote allergen-specific TH2 response to intratracheal allergen inoculation Wei-ping Zeng,

Susceptibility to allergic lung disease regulated by recall responses of dual-receptor memory T cells∗ Mark A. Aronica, MD, Shadi Swaidani, MS, Yan H.

Inhibiting pollen reduced nicotinamide adenine dinucleotide phosphate oxidase–induced signal by intrapulmonary administration of antioxidants blocks allergic.

IL-35 production by inducible costimulator (ICOS)–positive regulatory T cells reverses established IL-17–dependent allergic airways disease Gregory S.

Stephanie A. Shore, PhD, Raya D

IL-10–treated dendritic cells decrease airway hyperresponsiveness and airway inflammation in mice Toshiyuki Koya, MD, PhD, Hiroyuki Matsuda, MD, PhD,

Protection by budesonide and fluticasone on allergen-induced airway responses after discontinuation of therapy Padmaja Subbarao, MD, MSc, Sandra C. Dorman,

Duy Pham, PhD, Sarita Sehra, PhD, Xin Sun, PhD, Mark H. Kaplan, PhD

No defect in T-cell priming, secondary response, or tolerance induction in response to inhaled antigens in Fms-like tyrosine kinase 3 ligand–deficient.

Toll-like receptor 2 ligands promote chronic atopic dermatitis through IL-4–mediated suppression of IL-10 Susanne Kaesler, PhD, Thomas Volz, MD, Yuliya.

DNA methylation of TH1/TH2 cytokine genes affects sensitization and progress of experimental asthma Stephanie Brand, PhD, Dörthe Andrea Kesper, PhD,

Effects of diesel exhaust on allergic airway inflammation in mice

IL-22 attenuates IL-25 production by lung epithelial cells and inhibits antigen-induced eosinophilic airway inflammation Kentaro Takahashi, MD, Koichi.

Inhibition of allergic airways inflammation and airway hyperresponsiveness in mice by dexamethasone: Role of eosinophils, IL-5, eotaxin, and IL-13 Seok-Yong.

MicroRNA-155 is essential for TH2-mediated allergen-induced eosinophilic inflammation in the lung Carina Malmhäll, BSc, Sahar Alawieh, BSc, You Lu, PhD,

TH17 cells mediate pulmonary collateral priming

IL-4–independent pathways exacerbate methacholine-induced airway hyperreactivity during mycoplasma respiratory disease Matthew D. Woolard, PhD, R. Doug.

The extra domain A of fibronectin is essential for allergen-induced airway fibrosis and hyperresponsiveness in mice Martin Kohan, MSc, Andres F. Muro,

Local treatment with IL-12 is an effective inhibitor of airway hyperresponsiveness and lung eosinophilia after airway challenge in sensitized mice Jürgen.

Corticosteroids enhance CD8+ T cell–mediated airway hyperresponsiveness and allergic inflammation by upregulating leukotriene B4 receptor 1 Hiroshi Ohnishi,

Recombinant basic fibroblast growth factor inhibits the airway hyperresponsiveness, mucus production, and lung inflammation induced by an allergen challenge

Asthma is induced by intranasal coadministration of allergen and natural killer T-cell ligand in a mouse model Jae-Ouk Kim, PhD, Dong-Hyeon Kim, MS,

TNF can contribute to multiple features of ovalbumin-induced allergic inflammation of the airways in mice Susumu Nakae, PhD, Carolina Lunderius, PhD,

IL-2–inducible T-cell kinase modulates TH2-mediated allergic airway inflammation by suppressing IFN-γ in naive CD4+ T cells Arun K. Kannan, MS, Nisebita.

Presentation transcript:

Prior airway exposure to allergen increases virus-induced airway hyperresponsiveness Mika J Mäkelä, MD, Ralph Tripp, PhD, Azzeddine Dakhama, PhD, Jun-Won Park, MD, Toshihide Ikemura, PhD, Anthony Joetham, BSc, Matti Waris, PhD, Larry J Anderson, MD Journal of Allergy and Clinical Immunology Volume 112, Issue 5, Pages 861-869 (November 2003) DOI: 10.1016/S0091-6749(03)02020-7

FIG 1 RSV-induced airway responsiveness to inhaled MCh is enhanced by prior allergen airway exposure. BALB/c mice were exposed to aerosolized OVA or PBS exclusively through the airways for 30 minutes daily on 10 consecutive days. On day 11, mice were either sham-inoculated or RSV-infected. Airway responsiveness to inhaled MCh was assessed on day 6 after RSV infection by barometric whole-body plethysmography. Data are expressed as percentage of baseline Penh values obtained after inhaled PBS challenge. PBS-sham, PBS-exposed; sham-inoculated, OVA-sham; OVA-exposed, sham-inoculated; PBS-RSV, PBS-exposed; RSV-infected, OVA-RSV; OVA-exposed, RSV-infected. There were no significant differences in baseline Penh values among groups. ∗Significantly different from PBS-sham; #significantly different from all other groups (P < .05). NS, Not significant. Journal of Allergy and Clinical Immunology 2003 112, 861-869DOI: (10.1016/S0091-6749(03)02020-7)

FIG 2 BAL cell composition. Same groups of mice as in Fig 1. ∗Significant differences compared with PBS-sham or OVA-sham (P < .05, ANOVA with Fisher PLSD tests for multiple comparisons). Journal of Allergy and Clinical Immunology 2003 112, 861-869DOI: (10.1016/S0091-6749(03)02020-7)

FIG 3 Lung histopathology. Formalin-fixed, paraffin-embedded lung tissue sections were stained with PAS reaction to detect mucus-producing goblet cells. Abbreviations as in Fig 1. Prior airway exposure to OVA increased RSV-induced airway tissue inflammation and markedly enhanced mucus production in central intrapulmonary airways (arrowheads). Journal of Allergy and Clinical Immunology 2003 112, 861-869DOI: (10.1016/S0091-6749(03)02020-7)

FIG 4 Frequency of TH1 and TH2 cytokine-producing T cells in the lung. Cytokine-producing T cells were detected in the lung digests obtained on day 4 (A) and day 7 (B) after infection by double immunostaining for surface expression of CD3 and intracellular expression of IL-4, IL-5, IL-12, or IFN-γ without restimulation of cells in vitro. ∗Significantly different from PBS group; #significantly different from all the other groups (P < .05, Kruskal-Wallis test). Journal of Allergy and Clinical Immunology 2003 112, 861-869DOI: (10.1016/S0091-6749(03)02020-7)

FIG 4 Frequency of TH1 and TH2 cytokine-producing T cells in the lung. Cytokine-producing T cells were detected in the lung digests obtained on day 4 (A) and day 7 (B) after infection by double immunostaining for surface expression of CD3 and intracellular expression of IL-4, IL-5, IL-12, or IFN-γ without restimulation of cells in vitro. ∗Significantly different from PBS group; #significantly different from all the other groups (P < .05, Kruskal-Wallis test). Journal of Allergy and Clinical Immunology 2003 112, 861-869DOI: (10.1016/S0091-6749(03)02020-7)

FIG 5 Ratio of TH1 to TH2 cytokine-expressing lung T cells. Data (mean ± SEM) reflect normalized ratio of IFN-γ to IL-4 cytokine-producing T-cell frequencies in the lung. Normalized ratio was obtained by using the formula [(frequency of IFN-γ + T cells/ frequency of IL-4+ T cells)−1], where 1 corresponds to equal frequencies for both cell populations. ∗Significantly different from PBS group; #significantly different from all the other groups (P < .05, ANOVA with Fisher PLSD tests for multiple comparisons). Journal of Allergy and Clinical Immunology 2003 112, 861-869DOI: (10.1016/S0091-6749(03)02020-7)