Targeting complement anaphylatoxin C5a receptor in hyperoxic lung injury in mice

Receptor binding of complement anaphylatoxin C5a results in proinflammatory activation of numerous diseases, but the role of receptor-mediated action during hyperoxic lung injury has, to the best of our knowledge, not yet been investigated. The contribution of the C5a receptor (C5aR) to hyperoxic lu...

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Veröffentlicht in:	Molecular medicine reports 2014-10, Vol.10 (4), p.1786-1792
Hauptverfasser:	XU, YING, TIAN, ZHE, XIE, PEIYU
Format:	Artikel
Sprache:	eng
Schlagworte:	Alveoli Animals Antigens, CD - genetics Antigens, CD - metabolism Antigens, Differentiation, Myelomonocytic - genetics Antigens, Differentiation, Myelomonocytic - metabolism Body weight Bronchoalveolar Lavage Fluid - cytology Bronchus Chemokine CCL2 - genetics Chemokine CCL2 - metabolism Chemokines Complement activation complement anaphylatoxin C5a Complement component C5a Complement receptors Cytokines Enzyme-linked immunosorbent assay Flow cytometry Gene expression Hyperoxia hyperoxic lung injury Inflammation Interleukin 6 Interleukin-6 - genetics Interleukin-6 - metabolism Leukocytes (neutrophilic) Lung - metabolism Lung diseases Lung Injury - metabolism Lung Injury - pathology Lungs Lymphocytes Lymphocytes - cytology macrophage Macrophages Macrophages - cytology Mice Mice, Inbred BALB C Monocyte chemoattractant protein 1 Morphology Neutrophils Neutrophils - cytology Oxygen Peroxidase Peroxidase - metabolism Physiological aspects Polymerase chain reaction receptor antagonist Receptor, Anaphylatoxin C5a - antagonists & inhibitors Receptor, Anaphylatoxin C5a - genetics Receptor, Anaphylatoxin C5a - metabolism Reverse transcription RNA, Messenger - metabolism Rodents Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α Ventilation
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