Signal Immune Reactions of #Macrophages Differentiated from THP-1 #Monocytes to #Infection with #Pandemic #H1N1pdm09 Virus and #H5N2 and #H9N2 #Avian #Influenza A Virus (Bull Exp Biol Med., abstract)

[Source: US National Library of Medicine, full page: (LINK). Abstract, edited.]

Bull Exp Biol Med. 2018 Mar 26. doi: 10.1007/s10517-018-4048-3. [Epub ahead of print]

Signal Immune Reactions of Macrophages Differentiated from THP-1 Monocytes to Infection with Pandemic H1N1PDM09 Virus and H5N2 and H9N2 Avian Influenza A Virus.

Sokolova TM1, Poloskov VV2, Shuvalov AN2, Rudneva IA3, Timofeeva TA3.

Author information: 1 Subdivision of D. I. Ivanovsky Research Institute of Virology, N. F. Gamaleya Research Center of Epidemiology and Microbiology, Ministry of Health of Russian Federation, Moscow, Russia. tmsokolovavir@mail.ru. 2 Department of Interferons, Laboratory of Physiology of Viruses, Moscow, Russia. 3 Subdivision of D. I. Ivanovsky Research Institute of Virology, N. F. Gamaleya Research Center of Epidemiology and Microbiology, Ministry of Health of Russian Federation, Moscow, Russia.

 

Abstract

In culture of THP-1 cells differentiated into macrophages with PMA (THP-PMA macrophages) infected with influenza viruses of subtypes H1, H5 and H9, we measured the expression of TLR7 and RIG1 receptor genes, sensors of viral RNA and ribonucleoprotein, and the levels of production of inflammatory cytokines IL-1β, TNFα, IL-10, and IFNα. The sensitivity and inflammatory response of THP-PMA macrophages to pandemic influenza A virus H1N1pdm09 and avian influenza H5N2 and H9N2 viruses correlate with the intracellular level of their viral RNA and activation of the RIG1 gene. Abortive infection is accompanied by intensive macrophage secretion of TNFα, IL-1β, and toxic factors inducing cell death. Activity of endosomal TLR7 receptor gene changed insignificantly in 24 h after infection and significantly decreased in 48 and 72 h under the action of H5N2 and H9N2, which correlated with manifestation of the cytopathogenic effect of these viruses. H5N2 and H9N2 avian viruses in THP-PMA macrophages are strong activators of the expression of the gene of the cytoplasmic RIG1 receptor 24 and 48 h after infection, and the pandemic virus H1N1pdm09 is a weak stimulator of RIG1 gene. Avian influenza H5N2 and H9N2 viruses are released by rapid induction of the inflammatory response in macrophages. At the late stages of infection, we observed a minor increase in IL-10 secretion in macrophages and, probably, the polarization of a part of the population in type M2. The studied influenza A viruses are weak inductors of IFN in THP-PMA macrophages. In the culture medium of THP-PMA macrophages infected with H9N2 and H5N2 viruses, MTT test revealed high levels of toxic factors causing the death of Caco-2 cells. In contrast to avian viruses, pandemic virus H1N1pdm09 did not induce production of toxic factors.

KEYWORDS: cytokines; genes TLR7, RIG1; influenza A viruses; macrophages

PMID: 29577197 DOI: 10.1007/s10517-018-4048-3

Keywords: Avian Influenza; Seasonal Influenza; H1N1pdm09; H5N2; H9N2; Cytokines.

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Giuseppe Michieli

I am an Italian blogger, active since 2005 with main focus on emerging infectious diseases such as avian influenza, SARS, antibiotics resistance, and many other global Health issues. Other fields of interest are: climate change, global warming, geological and biological sciences. My activity consists mainly in collection and analysis of news, public services updates, confronting sources and making decision about what are the 'signals' of an impending crisis (an outbreak, for example). When a signal is detected, I follow traces during the entire course of an event. I started in 2005 my blog ''A TIME'S MEMORY'', now with more than 40,000 posts and 3 millions of web interactions. Subsequently I added an Italian Language blog, then discontinued because of very low traffic and interest. I contributed for seven years to a public forum (FluTrackers.com) in the midst of the Ebola epidemic in West Africa in 2014, I left the site to continue alone my data tracking job.