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© Matteo Bonazzi, Edith Gouin
Observation en immunofluorescence d'une cellule infectée par Listeria monocytogenes. En bleu: marquage des protéines de surface de Listeria qui permet de visualiser les bactéries. En rouge et vert: marquage de l'actine, une protéine qui forme le cytosquelette des cellules. Les Listeria utilisent l'actine cellulaire pour former des "comêtes" et se déplacer à l'intérieur des cellules qu'elles infectent. Cell infected by Listeria monocytogenes. The surface proteins (in blue) of Listeria enable us to view the bacteria. Actin, a constituent protein of cells, is shown in red and green.
Publication : The Journal of clinical investigation

Mouse and human neutrophils induce anaphylaxis

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of clinical investigation - 23 Mar 2011

Jönsson F, Mancardi DA, Kita Y, Karasuyama H, Iannascoli B, Van Rooijen N, Shimizu T, Daëron M, Bruhns P

Link to Pubmed [PMID] – 21436586

J. Clin. Invest. 2011 Apr;121(4):1484-96

Anaphylaxis is a life-threatening hyperacute immediate hypersensitivity reaction. Classically, it depends on IgE, FcεRI, mast cells, and histamine. However, anaphylaxis can also be induced by IgG antibodies, and an IgG1-induced passive type of systemic anaphylaxis has been reported to depend on basophils. In addition, it was found that neither mast cells nor basophils were required in mouse models of active systemic anaphylaxis. Therefore, we investigated what antibodies, receptors, and cells are involved in active systemic anaphylaxis in mice. We found that IgG antibodies, FcγRIIIA and FcγRIV, platelet-activating factor, neutrophils, and, to a lesser extent, basophils were involved. Neutrophil activation could be monitored in vivo during anaphylaxis. Neutrophil depletion inhibited active, and also passive, systemic anaphylaxis. Importantly, mouse and human neutrophils each restored anaphylaxis in anaphylaxis-resistant mice, demonstrating that neutrophils are sufficient to induce anaphylaxis in mice and suggesting that neutrophils can contribute to anaphylaxis in humans. Our results therefore reveal an unexpected role for IgG, IgG receptors, and neutrophils in anaphylaxis in mice. These molecules and cells could be potential new targets for the development of anaphylaxis therapeutics if the same mechanism is responsible for anaphylaxis in humans.

http://www.ncbi.nlm.nih.gov/pubmed/21436586