Pathways of anaphylaxis in the mouse

Slides:

Advertisements

Similar presentations

Yvan Boutin, PhD, Jacques Hébert, MD

Advertisements

Fig. 1. TLR4 expression is much greater on macrophages than on DCs

IgE antibodies, FcεRIα, and IgE-mediated local anaphylaxis can limit snake venom toxicity Philipp Starkl, PhD, Thomas Marichal, DVM, PhD, Nicolas Gaudenzio,

IgG subclasses determine pathways of anaphylaxis in mice

Selective ablation of mast cells or basophils reduces peanut-induced anaphylaxis in mice Laurent L. Reber, PhD, Thomas Marichal, DVM, PhD, Kaori Mukai,

Histamine H4 receptor antagonists are superior to traditional antihistamines in the attenuation of experimental pruritus Paul J. Dunford, MSc, Kacy N.

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

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

Odelya E. Pagovich, MD, Bo Wang, MD, Maria J

The sphingosine-1-phosphate/sphingosine-1-phosphate receptor 2 axis regulates early airway T-cell infiltration in murine mast cell–dependent acute allergic.

Oral immunotherapy induces IgG antibodies that act through FcγRIIb to suppress IgE- mediated hypersensitivity Oliver T. Burton, PhD, Stephanie L. Logsdon,

Protective role of nuclear factor of activated T cells 2 in CD8+ long-lived memory T cells in an allergy model Roman Karwot, PhD, Joachim H. Maxeiner,

Ramipril and metoprolol intake aggravate human and murine anaphylaxis: Evidence for direct mast cell priming Maria Nassiri, MS, Magda Babina, PhD, Sabine.

Allergen-induced IgE-dependent gut inflammation in a human PBMC–engrafted murine model of allergy Benno Weigmann, PhD, Nadja Schughart, MSc, Christian.

Odelya E. Pagovich, MD, Bo Wang, MD, Maria J

Activated glycoprotein A repetitions predominant (GARP)–expressing regulatory T cells inhibit allergen-induced intestinal inflammation in humanized mice

Badrul A. Chowdhury, MD, PhD

Investigation of peanut oral immunotherapy with CpG/peanut nanoparticles in a murine model of peanut allergy Kamal D. Srivastava, PhD, Alyssa Siefert,

Dominique Velin, Daniel Bachmann, Hanifa Bouzourene, Pierre Michetti

Pharmacologic inhibition of Notch signaling suppresses food antigen–induced mucosal mast cell hyperplasia Asuka Honjo, MD, Nobuhiro Nakano, PhD, Susumu.

Circadian clock gene Period2 regulates a time-of-day–dependent variation in cutaneous anaphylactic reaction Yuki Nakamura, Daisuke Harama, Naomi Shimokawa,

Differential roles for the IL-9/IL-9 receptor α-chain pathway in systemic and oral antigen–induced anaphylaxis Heather Osterfeld, BSc, Richard Ahrens,

Induction of IgE antibodies in mice and rhesus monkeys with recombinant birch pollen allergens: Different allergenicity of Bet v 1 and Bet v 2 Susanne.

Oliver T. Burton, PhD, Jaciel M. Tamayo, PhD, Amanda J

Volume 8, Issue 2, Pages (February 1998)

Peanuts can contribute to anaphylactic shock by activating complement

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

Persistent protective effect of heat-killed Escherichia coli producing “engineered,” recombinant peanut proteins in a murine model of peanut allergy

Ellen Mueller Fox, PhD, Marina N

Oral immunotherapy induces local protective mechanisms in the gastrointestinal mucosa Stephanie A. Leonard, MD, Gustavo Martos, PhD, Wei Wang, MD, Anna.

Innate immune system plays a critical role in determining the progression and severity of acetaminophen hepatotoxicity Zhang-Xu Liu, Sugantha Govindarajan,

Rapid polyclonal desensitization with antibodies to IgE and FcεRIα

Food Allergy Herbal Formula-2 silences peanut-induced anaphylaxis for a prolonged posttreatment period via IFN-γ–producing CD8+ T cells Kamal D. Srivastava,

Serum IgE response to orally ingested antigen: A novel IgE response model with allergen-specific T-cell receptor transgenic mice Kan Shida a,b, Satoshi.

IL-33 promotes food anaphylaxis in epicutaneously sensitized mice by targeting mast cells Claire Galand, PhD, Juan Manuel Leyva-Castillo, PhD, Juhan.

Iván López-Expósito, PhD, Ying Song, MD, Kirsi M

3-Methyl-4-nitrophenol triggers nasal allergy by modulating dendritic cell properties Xiao-Yu Liu, PhD, Yong-Jin Wu, MD, PhD, Li-Juan Song, MD, Xian-Hai.

Estrogen increases the severity of anaphylaxis in female mice through enhanced endothelial nitric oxide synthase expression and nitric oxide production

IgE-class–specific immunosuppression in offspring by administration of anti-IgE to pregnant mice Hideaki Morita, MD, PhD, Masato Tamari, MD, PhD, Masako.

Rapid desensitization of mice with anti-FcγRIIb/FcγRIII mAb safely prevents IgG- mediated anaphylaxis Marat V. Khodoun, PhD, Zeynep Yesim Kucuk, MD, Richard.

Mycobacterium bovis BCG killed by extended freeze-drying reduces airway hyperresponsiveness in 2 animal models Micheline Lagranderie, PhD, Mohammad Abolhassani,

Orally administered TGF-β is biologically active in the intestinal mucosa and enhances oral tolerance Takashi Ando, MD, PhD, Kyosuke Hatsushika, MD,

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

Histamine H4 receptor antagonists are superior to traditional antihistamines in the attenuation of experimental pruritus Paul J. Dunford, MSc, Kacy N.

Kirthana Ganeshan, BS, Colleen V

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,

Identification of IgE Journal of Allergy and Clinical Immunology

Volume 28, Issue 4, Pages (April 2008)

IL-12 affects Dermatophagoides farinae–induced IL-4 production by T cells from pediatric patients with mite-sensitive asthma Takeshi Noma, MD, PhD, Izumi.

Genetic susceptibility to food allergy is linked to differential TH2-TH1 responses in C3H/HeJ and BALB/c mice Vivian Morafo, PhD*, Kamal Srivastava,

Dietary medium-chain triglycerides promote oral allergic sensitization and orally induced anaphylaxis to peanut protein in mice Jianing Li, MS, Yu Wang,

TH1-promoting DNA immunization against allergens modulates the ratio of IgG1/IgG2a but does not affect the anaphylactic potential of IgG1 antibodies

Case report: Streptomycin-induced anaphylactic shock during oocyte retrieval procedures for in vitro fertilization Motoyasu Iikura, MD, PhDa, Masao Yamaguchi,

Sarbjit S. Saini, MDa, Jennifer J

Antibody to very late activation antigen 4 prevents interleukin-5–induced airway hyperresponsiveness and eosinophil infiltration in the airways of guinea.

Ligation of IgE receptors causes an anaphylactic response and neutrophil infiltration but does not induce eosinophilic inflammation in mice Masayuki.

Mechanisms of allergen-specific desensitization

Eric B. Brandt, PhD, Ariel Munitz, PhD, Tatyana Orekov, MS, Melissa K

Ellen Mueller Fox, PhD, Marina N

Qianli Zhuang, MD, PhD, Bruce Mazer, MD

Anaphylaxis after initial ingestion of rambutan, a tropical fruit

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

Suplatast tosilate inhibits goblet-cell metaplasia of airway epithelium in sensitized mice Jae Jeong Shim, MD, Karim Dabbagh, PhD, Kiyoshi Takeyama, MD,

Systemic and localized seminal plasma hypersensitivity patients exhibit divergent immunologic characteristics Debajyoti Ghosh, PhD, Jonathan A. Bernstein,

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

Hapten-Specific Tolerance Promoted by Calcitonin Gene-Related Peptide

DNA-based vaccination reduces the risk of lethal anaphylactic hypersensitivity in mice Anthony A. Horner, MDa, Minh-Duc Nguyen, BAa, Arash Ronaghy, BAa,

Jay E. Slater, MDa, Elizabeth J. Paupore, BSa, Michael R

Presentation transcript:

Pathways of anaphylaxis in the mouse Richard T. Strait, MDa, Suzanne C. Morris, PhDc, Mingyan Yang, MDc, Xiao-Wu Qu, PhDd, Fred D Finkelman, MDb,c Journal of Allergy and Clinical Immunology Volume 109, Issue 4, Pages 658-668 (April 2002) DOI: 10.1067/mai.2002.123302 Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 1 Challenge with antigen or anti-IgE mAb induces similar decreases in activity and body temperature in GaMD-primed mice. BALB/c mice (10 per group) were injected intravenously with GaMD and then intravenously challenged 14 days later with 100 μg of anti-IgE mAb or GIgG. Rectal temperatures and activity levels were serially determined for 2 hours after challenge. Means and SEs for rectal temperatures (left panel) and means for activity level (middle panel) are shown. In a separate experiment GaMD-primed mice (5 per group) were challenged intravenously with 1, 10, or 100 μg of either anti-IgE mAb or GIgG. Means and SEs of lowest rectal temperature after challenge are shown for each dose (right panel) . A repeat of all experiments provided similar results. Journal of Allergy and Clinical Immunology 2002 109, 658-668DOI: (10.1067/mai.2002.123302) Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 2 Different Ig isotypes and Fc receptors are involved in antigen- and anti-IgE mAb–induced anaphylaxis. Mice in all experiments were primed with GaMD and intravenously challenged 14 days later with antigen or anti-IgE mAb. Upper panels , BALB/c mice (5 per group) were injected intraperitoneally 24 hours before challenge (day 13) with 100 μg of anti-IgE mAb, 500 μg of anti-FcγRII/III mAb, or an isotype-matched control mAb. Mice were challenged intravenously with 100 μg of anti-IgE mAb or GIgG. Middle panels , IgE−/− and wild-type mice (5 per group) on the same FVBN background were challenged intravenously with 100 μg of anti-IgE mAb or 10 mg of GIgG. (A much higher dose of antigen is required to induce anaphylaxis in GaMD-primed FVBN mice than in BALB/c mice.) Lower panels , FcϵRIα−/− and wild-type mice on the same BALB/c background (5 per group) were challenged with 100 μg of anti-IgE mAb or GIgG. Rectal temperatures (means and SEMs) are shown. Control mAbs had no effect on anaphylaxis (data not shown). A repeat of all experiments provided similar results. Journal of Allergy and Clinical Immunology 2002 109, 658-668DOI: (10.1067/mai.2002.123302) Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 3 Mast cell dependence of anaphylaxis. Upper panels , Mast cell–deficient, W/Wv, and wild-type litter mates (5 per group) were primed with GaMD and challenged intravenously with GIgG (left panel) , anti-IgE mAb (middle panel) , or anti-FcγRII/RIII mAb (right panel) 14 days later. Rectal temperatures (means and SEs) are shown. Repeat experiments provided similar results. Lower panel , BALB/c mice (5 per group) were left unprimed or primed with GaMD and challenged 14 days later as indicated. MMCP-1 levels in sera obtained 2 hours after challenge were determined by means of ELISA. MMCP-1 levels in anti-IgE mAb–challenged mice were higher than those in any other group (P < .01), and MMCP-1 levels in GIgG-challenged mice were higher than those in unchallenged or anti-FcγRII/III mAb–challenged groups (P < .02). Journal of Allergy and Clinical Immunology 2002 109, 658-668DOI: (10.1067/mai.2002.123302) Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 4 Cell types involved in anaphylaxis. BALB/c mice (5 per group) were primed intravenously with GaMD and challenged intravenously 14 days later with either anti-IgE mAb (upper panels) or GIgG (lower panels) . Some mice were pretreated with gadolinium (left panels) , anti-granulocyte mAb (middle panels) , or anti-platelet antiserum (right panels) . Mean rectal temperatures and SEs are shown. Repeat experiments provided similar results. Normal rabbit serum and rat IgG2b mAb were used as controls and had no effect on anaphylaxis (data not shown). Journal of Allergy and Clinical Immunology 2002 109, 658-668DOI: (10.1067/mai.2002.123302) Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 5 Platelets are not required for antigen-induced anaphylaxis. BALB/c mice (5 per group) were primed with GaMD and challenged with GIgG 14 days later. Some mice were injected daily with anti-platelet antiserum for 3 days before challenge (left panel) or 24 hours before challenge with neuraminidase (right panel) . Means and SEs of rectal temperatures after challenge are shown. Normal rabbit serum had no effect on anaphylaxis (data not shown). Journal of Allergy and Clinical Immunology 2002 109, 658-668DOI: (10.1067/mai.2002.123302) Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 6 Mediators involved in anti-IgE and antigen-induced anaphylaxis. BALB/c mice (5 per group) were GaMD primed and then challenged 14 days later with either GIgG (upper panels) or anti-IgE mAb (lower panels) . Where indicated, mice were desensitized before challenge with an antihistamine (triprolidine), a PAF antagonist (CV6209), or a 5-HT antagonist (metergoline). Rectal temperatures (means and SEs) are shown for 2 hours after challenge. Repeat experiments provided similar results. Experiments that substituted the 5-HT antagonist ketanserin for metergoline provided similar results. Combinations of antagonists (eg, CV6209 and triprolidine, metergoline and CV6209, or metergoline and triprolidine) did not consistently have greater inhibitory effects than the most potent antagonist given alone (data not shown). Journal of Allergy and Clinical Immunology 2002 109, 658-668DOI: (10.1067/mai.2002.123302) Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 7 Histamine and PAF responses to anti-IgE mAb and antigen challenge. BALB/c mice were primed with GaMD and challenged 14 days later with either antigen or anti-IgE mAb. Mice (5 per group) were bled 2 minutes after challenge, and plasma histamine levels were determined by means of ELISA. Other groups were killed 15 minutes after challenge, and spleens were immediately removed and flash frozen in liquid nitrogen. Splenic PAF levels were determined as described in the “Methods” section. Means and SEMs are shown. Histamine levels differ significantly between anti-IgE mAb–challenged and all other groups (P < .01) and between antigen-challenged and all other groups (P < .01). PAF levels differ significantly between the unchallenged group and each of the 2 challenged groups (P < .01). Journal of Allergy and Clinical Immunology 2002 109, 658-668DOI: (10.1067/mai.2002.123302) Copyright © 2002 Mosby, Inc. Terms and Conditions

Fig. 8 Anti-IgE mAb–induced anaphylaxis temporarily desensitizes mice to antigen-induced anaphylaxis. Mast cell–deficient W/Wv mice (3 or 4 per group) or wild-type mice (4 or 5 per group) on the same genetic background were primed with GaMD and received no further treatment or were injected 14 days later intraperitoneally with anti-IgE mAb. Four hours after anti-IgE mAb injection, all mice were challenged intravenously with GIgG. Rectal temperatures (means and SEs) after GIgG challenge are shown. Journal of Allergy and Clinical Immunology 2002 109, 658-668DOI: (10.1067/mai.2002.123302) Copyright © 2002 Mosby, Inc. Terms and Conditions