Novel effect of methionine enkephalin against influenza A virus infection through inhibiting TLR7-MyD88-TRAF6-NF-?B p65 signaling pathway

The morbidity and mortality associated with influenza A virus infections, have stimulated the search for novel prophylactic and therapeutic drugs. The purpose of this study was to investigate the prophylactic and therapeutic effect of synthetic methionine enkephalin (MENK) on mice infected by A/PR/8...

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Published inInternational immunopharmacology Vol. 55; p. 38
Main Authors Tian, Jing, Jiao, Xue, Wang, Xiaonan, Geng, Jin, Wang, Reizhe, Liu, Ning, Gao, Xinhua, Griffin, Noreen, Shan, Fengping
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier BV 01.02.2018
Subjects
Antiviral drugs
Drug therapy
Enkephalins
Infections
Influenza
Influenza A
Interleukin 6
Intranasal administration
Lungs
Methionine
Mice
Mode of action
Morbidity
MyD88 protein
Narcotics
NF-κB protein
Opioid receptors
Receptors
Rodents
Signal transduction
Signaling
T cell receptors
TLR7 protein
Toll-like receptors
TRAF6 protein
Tumor necrosis factor-α
Viruses
α-Interferon
β-Interferon
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Summary:The morbidity and mortality associated with influenza A virus infections, have stimulated the search for novel prophylactic and therapeutic drugs. The purpose of this study was to investigate the prophylactic and therapeutic effect of synthetic methionine enkephalin (MENK) on mice infected by A/PR/8/34 influenza virus (H1N1) in vivo. The results showed that MENK could exert both prophylactic and therapeutic influences on infected mice, significantly improve the survival rate, relieve acute lung injury and decrease cytokine (IFN-α, IFN-β, TNF-α, IL-6, and IL-1β) levels. MENK also inhibited virus replication on day 4 post infection (p.i.) through upregulating opioid receptors (MOR, DOR) and suppressing TLR7-MyD88-TRAF6-NF-κB p65 signaling pathways. These results suggest that MENK, given via intranasal administration, could provide a novel drug with a new mode of action as a nonspecific anti-influenza agent or vaccine adjuvant.
ISSN:1567-5769
1878-1705