Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response

Hofmann, Peter; Sprenger, Hans; Kaufmann, Andreas M.; Bender, Armin; Hasse, C; Nain, Marianne; Gemsa, Diethard

doi:10.1002/jlb.61.4.408

Cited by 127 publications

(110 citation statements)

References 8 publications

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“…This virus is able to replicate not only in epithelial cells, but also in monocytes/macrophages (29). Replication of human influenza A virus in monocytes promotes viral spreading through a host body.…”

Section: Discussionmentioning

confidence: 99%

Agonists of Proteinase-Activated Receptor-2 Enhance IFN-γ-Inducible Effects on Human Monocytes: Role in Influenza A Infection

Feld¹,

Shpacovitch²,

Ehrhardt³

et al. 2008

The Journal of Immunology

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Proteinase-activated receptor-2 (PAR2) is expressed by different types of human leukocytes and involved in the development of inflammatory and infectious diseases. However, its precise role in the regulation of human monocyte and macrophage function during viral infection remains unclear. Also, the ability of PAR2 agonists to enhance the effects induced by immune mediators during infection or inflammation is still poorly investigated. Therefore, we investigated the ability of a PAR2 agonist to enhance IFN-γ-induced suppression of influenza A virus replication in human monocytes. We found that this effect correlates with an increased abundance of IκBα after costimulation of cells with PAR2 agonist and IFN-γ. Remarkably, coapplication of PAR2 agonist and IFN-γ also enhances the effects of IFN-γ on IFN-γ-inducible protein 10 kDa release, and CD64 and αVβ3 surface expression by human monocytes. Together, these findings indicate a potentially protective role of PAR2 activation during the progression of influenza A virus infection. This effect could be associated with the ability of PAR2 agonists to enhance IFN-γ-induced protective effects on human monocytes.

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Section: Discussionmentioning

confidence: 99%

Agonists of Proteinase-Activated Receptor-2 Enhance IFN-γ-Inducible Effects on Human Monocytes: Role in Influenza A Infection

Feld¹,

Shpacovitch²,

Ehrhardt³

et al. 2008

The Journal of Immunology

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“…The tumour necrosis factor (TNF) members, including the Fas ligand (FasL), TNF-a and TNF-related apoptosis-inducing ligand (TRAIL), and their receptors play key roles in the extrinsic apoptotic pathway in a variety of cell types. Influenza viruses induce apoptosis in the cells of various mammalian species (Fesq et al, 1994;Hinshaw et al, 1994;Hofmann et al, 1997;Morris et al, 1999Morris et al, , 2005Takizawa et al, 1993) and in chicken cells (Ito et al, 2002). Both intrinsic and extrinsic pathways can be involved in apoptosis, which presumably promotes infection and alters viral pathogenesis in the host (Brydon et al, 2005;Brydon et al, 2003;Hofmann et al, 1997;Lowy, 2003;Uiprasertkul et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Differential regulation of antiviral and proinflammatory cytokines and suppression of Fas-mediated apoptosis by NS1 of H9N2 avian influenza virus in chicken macrophages

Xing

Cardona

Adams

et al. 2009

Journal of General Virology

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The NS1 protein is known to suppress immune responses in influenza virus-infected hosts. However, the role of NS1 in apoptosis in infected cells is disputed. In this study, through the use of a mutant A/pheasant/California/2373/1998 (H9N2) avian influenza virus (AIV) with a truncated NS1, we have demonstrated that a functional NS1 protein suppresses the induction of interferons in chicken macrophages. However, NS1 appeared to be irrelevant to the regulation of cytokines interleukin (IL)-1β and IL-6, indicating that distinct mechanisms may be employed in the regulation of antiviral and proinflammatory cytokines in chicken immune cells. Our study also showed that this H9N2 AIV induced apoptosis extrinsically through the Fas/Fas ligand (FasL)-mediated pathway. We found that NS1 suppressed the apoptotic process through suppression of the induction of FasL, but not tumour necrosis factor-α or TNF-related apoptosis-inducing ligand. Furthermore, our data indicated that the disruption of a potential binding site for the p85β subunit of phosphoinositide 3-kinase in the carboxyl terminus of NS1, while having no effect on the regulation of IFN induction, may contribute to the suppression of Fas/FasL-mediated apoptosis. Therefore, suppression of Fas/FasL-mediated apoptosis by NS1 is one of the critical mechanisms necessary to increase infectivity in AIV-infected chicken macrophages.

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“…Infection with live influenza virus induces potent activation of innate responses including the production of pro-inflammatory and anti-viral cytokines [19,20]. TLR7 has been found to be involved in the intracellular sensing of single-stranded (ss) RNA of live influenza virus of the X31 strain by plasmacytoid DC [5].…”

Section: Introductionmentioning

confidence: 99%

Influenza H2 haemagglutinin activates B cells via a MyD88‐dependent pathway

et al. 2005

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Influenza viruses are serious respiratory pathogens, responsible for half a million deaths each year. The viral surface haemagglutinin (HA) protein has been shown to be an important determinant of viral pathogenicity. HA is the virion attachment and fusion protein, and the major target for neutralizing antibodies; however, it is also involved in triggering innate responses that may have an important impact on the disease course. We have examined the role of the toll-like receptor (TLR) family in innate responses to influenza virus and influenza HA. TLR7 has recently been found to mediate recognition of influenza RNA. Here, we show for the first time that influenza HA of the H2 subtype induces innate responses in murine B lymphocytes via a MyD88-dependent pathway distinct from that involved in sensing viral RNA. We also show that inactivated influenza virus induces activation of human B cells. Our findings suggest that the molecule mediating these responses may be a novel member of the TLR family.

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Susceptibility of mononuclear phagocytes to influenza A virus infection and possible role in the antiviral response

Abstract: Abstract:Among

Cited by 127 publications

References 8 publications

Agonists of Proteinase-Activated Receptor-2 Enhance IFN-γ-Inducible Effects on Human Monocytes: Role in Influenza A Infection

Agonists of Proteinase-Activated Receptor-2 Enhance IFN-γ-Inducible Effects on Human Monocytes: Role in Influenza A Infection

Differential regulation of antiviral and proinflammatory cytokines and suppression of Fas-mediated apoptosis by NS1 of H9N2 avian influenza virus in chicken macrophages

Influenza H2 haemagglutinin activates B cells via a MyD88‐dependent pathway

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