Amb a 1–linked CpG oligodeoxynucleotides reverse established airway hyperresponsiveness in a murine model of asthma  Joanna V. Santeliz, MDa, Gary Van.

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

Epoxyeicosatrienoic acids are involved in the C70 fullerene derivative–induced control of allergic asthma  Sarah K. Norton, PhD, Dayanjan S. Wijesinghe,
Heat-killed Lactobacillus plantarum L-137 suppresses naturally fed antigen–specific IgE production by stimulation of IL-12 production in mice  Shinji.
IL-4 induces IL-13–independent allergic airway inflammation
Weiguo Chen, PhD, Umasundari Sivaprasad, PhD, Aaron M
CD4 T-helper cells engineered to produce IL-10 prevent allergen-induced airway hyperreactivity and inflammation  Jae-Won Oh, MD, PhD, Christine M. Seroogy,
Local administration of antisense phosphorothioate oligonucleotides to the c-kit ligand, stem cell factor, suppresses airway inflammation and IL-4 production.
Interferon response factor 3 is essential for house dust mite–induced airway allergy  Thomas Marichal, DVM, Denis Bedoret, DVM, PhD, Claire Mesnil, DVM,
Cigarette smoke extract induces thymic stromal lymphopoietin expression, leading to TH2-type immune responses and airway inflammation  Yuki Nakamura,
Pentraxin 3 deletion aggravates allergic inflammation through a TH17-dominant phenotype and enhanced CD4 T-cell survival  Jyoti Balhara, MSc, Lianyu Shan,
IL-33 dysregulates regulatory T cells and impairs established immunologic tolerance in the lungs  Chien-Chang Chen, PhD, Takao Kobayashi, PhD, Koji Iijima,
Antigen-specific effector CD8 T cells regulate allergic responses via IFN-γ and dendritic cell function  Yafang Tang, BSc, Shou Ping Guan, BSc, Benson.
Thomas F. Tedder, PhD, Takashi Matsushita, MD, PhD 
Prostaglandin E2 control of T cell cytokine production is functionally related to the reduced lymphocyte proliferation in atopic dermatitis  Sai Chan,
Lung dendritic cells induce TH17 cells that produce TH2 cytokines, express GATA-3, and promote airway inflammation  Marianne Raymond, PhD, Vu Quang Van,
Activin A and TGF-β promote TH9 cell–mediated pulmonary allergic pathology  Carla P. Jones, PhD, Lisa G. Gregory, PhD, Benjamin Causton, BSc, Gaynor A.
Pathophysiology of severe asthma
CD4+CD25+ regulatory T cells reverse established allergic airway inflammation and prevent airway remodeling  Jennifer Kearley, PhD, Douglas S. Robinson,
Inhibition of house dust mite–induced allergic airways disease by antagonism of microRNA-145 is comparable to glucocorticoid treatment  Adam Collison,
Inhibition of the IL-4/IL-13 receptor system prevents allergic sensitization without affecting established allergy in a mouse model for allergic asthma 
Specific epicutaneous immunotherapy prevents sensitization to new allergens in a murine model  Lucie Mondoulet, PhD, Vincent Dioszeghy, PhD, Emilie Puteaux,
Requirements for allergen-induced airway inflammation and hyperreactivity in CD4- deficient and CD4-sufficient HLA-DQ transgenic mice  Svetlana P. Chapoval,
A specific sphingosine kinase 1 inhibitor attenuates airway hyperresponsiveness and inflammation in a mast cell–dependent murine model of allergic asthma 
Selective early increases of bronchoalveolar CD8+ lymphocytes in a LEW rat model of hypersensitivity pneumonitis  Hal B. Richerson, MD, J.Daniel Coon,
CpG-oligodeoxynucleotides inhibit airway remodeling in a murine model of chronic asthma  Vipul V. Jain, MDa, Kunihiko Kitagaki, PhDa, Thomas Businga,
Prostaglandin E2 suppresses allergic sensitization and lung inflammation by targeting the E prostanoid 2 receptor on T cells  Zbigniew Zasłona, PhD, Katsuhide.
Regulation of allergic airway inflammation by class I–restricted allergen presentation and CD8 T-cell infiltration  James W. Wells, PhD, Christopher J.
Jesús Merayo-Lloves, MD, Tong Z. Zhao, MD, James E. Dutt, BA, C
A novel allergen-specific therapy with CD40-silenced B cells and dendritic cells  Motohiko Suzuki, MD, PhD, Makoto Yokota, MD, PhD, Yoshihisa Nakamura,
Prostaglandin E2 suppresses allergic sensitization and lung inflammation by targeting the E prostanoid 2 receptor on T cells  Zbigniew Zasłona, PhD, Katsuhide.
Sarita Sehra, PhD, Weiguo Yao, PhD, Evelyn T. Nguyen, MS, Nicole L
Mycobacterium bovis BCG killed by extended freeze-drying reduces airway hyperresponsiveness in 2 animal models  Micheline Lagranderie, PhD, Mohammad Abolhassani,
Production and Pharmacologic Modulation of the Granulocyte-Associated Allergic Responses to Ovalbumin in Murine Skin Models Induced by Injecting Ovalbumin-
The relative contribution of IL-4 and IL-13 to human IgE synthesis induced by activated CD4+ or CD8+ T cells  Juha Punnonen, MD, PhD, Hans Yssel, PhD,
Mukesh Kumar, PhDa, Aruna K. Behera, PhDa, Jianan Hu, MDa, Richard F
Effects of established allergen sensitization on immune and airway responses after secondary allergen sensitization  Katharina Blumchen, MD, Kerstin Gerhold,
Recruitment of T cells to the lung in response to antigen challenge
Kirthana Ganeshan, BS, Colleen V
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,
IL-12 affects Dermatophagoides farinae–induced IL-4 production by T cells from pediatric patients with mite-sensitive asthma  Takeshi Noma, MD, PhD, Izumi.
Diesel exhaust particles exert acute effects on airway inflammation and function in murine allergen provocation models  Minqi Hao, MD, PhD, Stephania.
Genetic susceptibility to food allergy is linked to differential TH2-TH1 responses in C3H/HeJ and BALB/c mice  Vivian Morafo, PhD*, Kamal Srivastava,
Antigen-specific and nonspecific determinants of cytokine production during topical sensitization of mice to chemical allergens  Artin Moussavi, PhDa,
Protective effect of Schistosoma mansoni infection on allergic airway inflammation depends on the intensity and chronicity of infection  Hermelijn H.
Effect of rush immunotherapy on airway inflammation and airway hyperresponsiveness after bronchoprovocation with allergen in asthma  Yasurou Kohno, MDa,
IL-10–treated dendritic cells decrease airway hyperresponsiveness and airway inflammation in mice  Toshiyuki Koya, MD, PhD, Hiroyuki Matsuda, MD, PhD,
Antibody to very late activation antigen 4 prevents interleukin-5–induced airway hyperresponsiveness and eosinophil infiltration in the airways of guinea.
Harald Renz, MD, Chaya Brodie, PhD, Katherine Bradley, BS, Donald Y. M
Inhibition of human allergic T-cell responses by IL-10–treated dendritic cells: Differences from hydrocortisone-treated dendritic cells  Iris Bellinghausen,
Duy Pham, PhD, Sarita Sehra, PhD, Xin Sun, PhD, Mark H. Kaplan, PhD 
The steroidogenic enzyme Cyp11a1 is essential for development of peanut-induced intestinal anaphylaxis  Meiqin Wang, MD, PhD, Julita Ramirez, DVM, PhD,
IL-13 induces eosinophil recruitment into the lung by an IL-5– and eotaxin-dependent mechanism  Samuel M. Pope, BAa,b, Eric B. Brandt, PhDa, Anil Mishra,
Qianli Zhuang, MD, PhD, Bruce Mazer, MD 
Viswanath P. Kurup, PhDa, Brian W. P
Chemical constituents of diesel exhaust particles induce IL-4 production and histamine release by human basophils  Gilles Devouassoux, MDa, Andrew Saxon,
13-Hydroxy-linoleic acid induces airway hyperresponsiveness to histamine and methacholine in guinea pigs in vivo  Paul A.J. Henricks, PhDa, Ferdi Engels,
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.
Blocking IL-25 prevents airway hyperresponsiveness in allergic asthma
MicroRNA-155 is essential for TH2-mediated allergen-induced eosinophilic inflammation in the lung  Carina Malmhäll, BSc, Sahar Alawieh, BSc, You Lu, PhD,
Anti-IgE efficacy in murine asthma models is dependent on the method of allergen sensitization  Daniel B. Tumas, DVM, PhDa, Betty Chan, BSb, Winifred.
Therapeutic efficacy of an anti–IL-5 monoclonal antibody delivered into the respiratory tract in a murine model of asthma  Felix R. Shardonofsky, MD,
DNA-based vaccination reduces the risk of lethal anaphylactic hypersensitivity in mice  Anthony A. Horner, MDa, Minh-Duc Nguyen, BAa, Arash Ronaghy, BAa,
Tatiana Zavorotinskaya, Adrian Tomkinson, John E Murphy 
Local treatment with IL-12 is an effective inhibitor of airway hyperresponsiveness and lung eosinophilia after airway challenge in sensitized mice  Jürgen.
Jay E. Slater, MDa, Elizabeth J. Paupore, BSa, Michael R
Recombinant basic fibroblast growth factor inhibits the airway hyperresponsiveness, mucus production, and lung inflammation induced by an allergen challenge 
TNF can contribute to multiple features of ovalbumin-induced allergic inflammation of the airways in mice  Susumu Nakae, PhD, Carolina Lunderius, PhD,
Presentation transcript:

Amb a 1–linked CpG oligodeoxynucleotides reverse established airway hyperresponsiveness in a murine model of asthma  Joanna V. Santeliz, MDa, Gary Van Nest, PhDb, Paula Traquina, MScb, Elizabeth Larsen, BSb, Marsha Wills-Karp, PhDc  Journal of Allergy and Clinical Immunology  Volume 109, Issue 3, Pages 455-462 (March 2002) DOI: 10.1067/mai.2002.122156 Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 1 Experimental protocol. BALB/cj mice were sensitized by means of an intraperitoneal injection of RWP in alum on days 0 and 3. On day 10, mice were challenged intratracheally with RWP or PBS as a control. On days 14 and 21, mice were injected intradermally with 10 μg of either Amb a 1 alone, Amb a 1-ISS conjugate, or Amb a 1-non-ISS control conjugate. On day 28, mice were rechallenged intratracheally with either RWP or PBS. Characterization of the allergic phenotype was performed 72 hours after the second antigen challenge. Journal of Allergy and Clinical Immunology 2002 109, 455-462DOI: (10.1067/mai.2002.122156) Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 2 A, Amb a 1-ISS treatment inhibits ragweed-induced AHR. AHR was defined by the time-integrated change in peak airway pressure (airway pressure-time index [APTI] ; in centimeters of water times seconds). Values shown are means ± SE of 8 to 10 animals per group. *P < .0001 compared with PBS control; **P = .03 compared with the RWP-sensitized and RWP-challenged group; and +P = .0005 compared with the RWP-sensitized and RWP-challenged group. B , Administration of Amb a 1-non-ISS did not suppress ragweed-induced AHR. Protocol is as described in Fig 1. Values shown are means ± SE of 8 to 10 animals per group. *P < .0001 compared with PBS control. Journal of Allergy and Clinical Immunology 2002 109, 455-462DOI: (10.1067/mai.2002.122156) Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 3 Effects of ragweed sensitization and challenge on cellular infiltration and mucus-containing cells in the airway wall. Ten-micrometer lung sections were fixed in formalin and stained with hematoxylin, eosin, and periodic acid-Schiff. Representative sections were obtained from the following treatment groups: A , PBS/PBS control group with few mucus-containing cells and no interstitial inflammatory cells; B , RWP/PBS group with ragweed-induced marked increases in interstitial inflammatory cells and intense periodic acid-Schiff staining in airway epithelium; C , RWP/Amb a 1; D , RWP/Amb a 1-ISS with inflammatory infiltrates and mucus-containing cells; E , high-power view (40×) of section from RWP/PBS; and F , high-power view of section from RWP/Amb a 1-ISS with no significant suppression of ragweed-induced inflammatory cells or mucus-containing cells. Journal of Allergy and Clinical Immunology 2002 109, 455-462DOI: (10.1067/mai.2002.122156) Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 4 A, Amb a 1-ISS treatment increases IFN-γ-productive capacity of murine splenocytes stimulated in vitro with Amb a 1. Spleens were harvested 72 hours after antigen challenge, and splenocytes from individual mice were cultured for 96 hours in the presence of 25 μg of Amb a 1. Values shown are means ± SE of 8 to 10 animals per group. *P < .005 compared with the RWP/PBS and RWP/Amb a 1 groups. B , Splenocytes stimulated in vitro with PMA show similar IFN-γ responses. Splenocytes from individual mice were cultured for 96 hours in the presence of 10 ng/mL PMA. C , In vivo Amb a 1-ISS treatment of ragweed-sensitized mice does not suppress the IL-5-productive capacity of their splenocytes when stimulated with Amb a 1 in vitro. IL-5 levels in supernatants were measured by means of ELISA. *P < .04 versus PBS/PBS and +P = .001 versus PBS/PBS. Journal of Allergy and Clinical Immunology 2002 109, 455-462DOI: (10.1067/mai.2002.122156) Copyright © 2002 Mosby, Inc. Terms and Conditions