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Deprecated: Implicit conversion from float 300.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Antiviral+Res 2014 ; 106 (ä): 95-104 Nephropedia Template TP
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Anti-inflammatory and antiviral effects of indirubin derivatives in influenza A (H5N1) virus infected primary human peripheral blood-derived macrophages and alveolar epithelial cells #MMPMID24717263
Mok CK; Kang SS; Chan RW; Yue PY; Mak NK; Poon LL; Wong RN; Peiris JS; Chan MC
Antiviral Res 2014[Jun]; 106 (ä): 95-104 PMID24717263show ga
Human disease caused by highly pathogenic avian influenza A (HPAI) (H5N1) is associated with fulminant viral pneumonia and mortality rates in excess of 60%. Acute respiratory syndrome (ARDS) has been found to be the most severe form of acute lung injury caused by H5N1 virus infection while cytokine dysregulation and viral replication are thought to contribute to its pathogenesis. In this study, the antiviral and anti-inflammatory effects of two indirubin derivatives: indirubin-3'-oxime (IM) and E804 on primary human peripherial blood-derived macrophages and type-I like pneumocytes (human alveolar epithelial cells) during influenza A (H5N1) virus infection were investigated. We found that both of the indirubin derivatives strongly suppress the pro-inflammatory cytokines including IP-10 (CXCL10), one of the key factors which contribute to the lung inflammation during H5N1 virus infection. In addition, we also demonstrated that the indirubin derivative delays the virus replication in the primary cell culture models. Our results showed that indirubin derivatives have a potential to be used as an adjunct to antiviral therapy for the treatment of severe human H5N1 disease.
|Anti-Inflammatory Agents/*pharmacology[MESH]
|Antiviral Agents/*pharmacology[MESH]
|Cells, Cultured[MESH]
|Cytokines/antagonists & inhibitors[MESH]
|Epithelial Cells/*drug effects/virology[MESH]
|Humans[MESH]
|Indoles/pharmacology[MESH]
|Influenza A Virus, H5N1 Subtype/*drug effects/growth & development/*immunology[MESH]