NDLI: Platelet-driven leukotriene C4-mediated airway inflammation in mice is aspirin-sensitive and depends on T prostanoid receptors.

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Platelet-driven leukotriene C4-mediated airway inflammation in mice is aspirin-sensitive and depends on T prostanoid receptors.

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Platelet-driven leukotriene C4-mediated airway inflammation in mice is aspirin-sensitive and depends on T prostanoid receptors.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Katz, Howard Feng, Chunli Boyce, Joshua A. Lai, Juying Liu, Tao Garofalo, Denise Laidlaw, Tanya M.
Description	Author Affiliation: Liu T ( Department of Medicine, Harvard Medical School, Boston, MA 02115); Garofalo D ( Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA 02115); Feng C ( Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA 02115); Lai J ( Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA 02115); Katz H ( Department of Medicine, Harvard Medical School, Boston, MA 02115); Laidlaw TM ( Department of Medicine, Harvard Medical School, Boston, MA 02115); Boyce JA ( Department of Medicine, Harvard Medical School, Boston, MA 02115)
Abstract	Cysteinyl leukotrienes (cysLTs) are bronchoconstricting lipid mediators that amplify eosinophilic airway inflammation by incompletely understood mechanisms. We recently found that LTC4, the parent cysLT, potently activates platelets in vitro and induces airway eosinophilia in allergen-sensitized and -challenged mice by a platelet- and type 2 cysLT receptor-dependent pathway. We now demonstrate that this pathway requires production of thromboxane A2 and signaling through both hematopoietic and lung tissue-associated T prostanoid (TP) receptors. Intranasal administration of LTC4 to OVA-sensitized C57BL/6 mice markedly increased the numbers of eosinophils in the bronchoalveolar lavage fluid, while simultaneously decreasing the percentages of eosinophils in the blood by a TP receptor-dependent mechanism. LTC4 upregulated the expressions of ICAM-1 and VCAM-1 in an aspirin-sensitive and TP receptor-dependent manner. Both hematopoietic and nonhematopoietic TP receptors were essential for LTC4 to induce eosinophil recruitment. Thus, the autocrine and paracrine functions of thromboxane A2 act downstream of LTC4/type 2 cysLT receptor signaling on platelets to markedly amplify eosinophil recruitment through pulmonary vascular adhesion pathways. The findings suggest applications for TP receptor antagonists in cases of asthma with high levels of cysLT production.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1402959
Journal	The Journal of Immunology
Issue Number	11
Volume Number	194
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Aspirin Pharmacology Blood Platelets Immunology Cysteine Leukotriene C4 Leukotrienes Platelet Activation Allergens Animals Asthma Drug Therapy Bone Marrow Transplantation Bronchoalveolar Lavage Fluid Cytology Eosinophilia Blood Inflammation Intercellular Adhesion Molecule-1 Biosynthesis Leukotriene Antagonists Lung Mice Mice, Inbred C57bl Mice, Knockout Ovalbumin Receptors, Prostaglandin Genetics Metabolism Thromboxane A2 Vascular Cell Adhesion Molecule-1 Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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