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2014 ; 193
(7
): 3769-78
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gab.com Text
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English Wikipedia
Protective actions of aspirin-triggered (17R) resolvin D1 and its analogue,
17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester, in C5a-dependent IgG
immune complex-induced inflammation and lung injury
#MMPMID25172497
Tang H
; Liu Y
; Yan C
; Petasis NA
; Serhan CN
; Gao H
J Immunol
2014[Oct]; 193
(7
): 3769-78
PMID25172497
show ga
Increasing evidence suggests that the novel anti-inflammatory and proresolving
mediators such as the resolvins play an important role during inflammation.
However, the functions of these lipid mediators in immune complex-induced lung
injury remain unknown. In this study, we determined the role of aspirin-triggered
resolvin D1 (AT-RvD1) and its metabolically stable analog,
17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester (p-RvD1), in IgG
immune complex-induced inflammatory responses in myeloid cells and injury in the
lung. We show that lung vascular permeability in the AT-RvD1- or p-RvD1-treated
mice was significantly reduced when compared with values in mice receiving
control vesicle during the injury. Furthermore, i.v. administration of either
AT-RvD1 or p-RvD1 caused significant decreases in the bronchoalveolar lavage
fluid contents of neutrophils, inflammatory cytokines, and chemokines. Of
interest, AT-RvD1 or p-RvD1 significantly reduced bronchoalveolar lavage fluid
complement C5a level. By EMSA, we demonstrate that IgG immune complex-induced
activation of NF-?B and C/EBP? transcription factors in the lung was
significantly inhibited by AT-RvD1 and p-RvD1. Moreover, AT-RvD1 dramatically
mitigates IgG immune complex-induced NF-?B and C/EBP activity in alveolar
macrophages. Also, secretion of TNF-?, IL-6, keratinocyte cell-derived chemokine,
and MIP-1? from IgG immune complex-stimulated alveolar macrophages or neutrophils
was significantly decreased by AT-RvD1. These results suggest a new approach to
the blocking of immune complex-induced inflammation.
|*Acute Lung Injury/chemically induced/immunology/pathology/prevention & control
[MESH]
|*Pneumonia/chemically induced/immunology/pathology/prevention & control
[MESH]