Comparison of influenza A virus and formyl-methionyl-leucyl- phenylalanine activation of the human neutrophil

Hartshorn, KL; Daigneault, DE; White, MR; Tuvin, M; Tauber, JL; Tauber, AI

doi:10.1182/blood.v79.4.1049.bloodjournal7941049

Cited by 12 publications

(6 citation statements)

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“…To date, information on virus-neutrophil interactions has come mainly from studies performed with the influenza A virus: which cannot only bind to the surface of neutrophils and activate these cells, but also render them dysfunctional.22. 23 Until recently, EBV target cell tropism was believed to be limited to epithelial cells of the oropharynx as well as to B lymphocytes. Growing evidence suggests that T lymphocytes may also be subjected to EBV targeting in vivo.24 Furthermore, interaction of this virus with monocytes has also been clearly shown.…”

Section: Discussionmentioning

confidence: 99%

Epstein-Barr virus modulates de novo protein synthesis in human neutrophils

Beaulieu

Paquin

Gosselin

1995

Blood

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Neutrophils and macrophages represent the first line of defense against microbial invaders. However, the role of phagocytes in host response to viral infection is poorly understood. We have previously shown that Epstein-Barr virus (EBV) interacts with human monocytes and modulates cytokine production in this cell type, but its effects on neutrophils are still unknown. In the present study, we investigated the presence of EBV receptor (CR2 or CD21) on neutrophils by cytofluorometry using five different anti-CD21 monoclonal antibodies (MoAbs), as well as fluoroscein isothiocyanate-EBV (FITC-EBV). Whereas no significant amount of neutrophils reacted with anti-CD21 MoAbs, studies with FITC-EBV indicated that viral particles bind to 30% of cells (in some individuals, EBV binds to more than 50% of neutrophils). This interaction is specific as it was completely inhibited by nonconjugated virus or with labeled virus preincubated with neutralizing MoAbs. After EBV treatment, cellular aggregation was observed in neutrophil cultures, an indication that neutrophils were activated. Although EBV did not induce respiratory burst activity in neutrophils, pretreatment with infectious particles enhanced (priming effect) the fMLP-induced O2-release in neutrophils. Instead of restricting our analysis to specific cytokine genes, we investigated the effects of EBV on neutrophil transcriptional events in general. The effect of this virus on de novo synthesis of total cellular RNA was first investigated by measuring the incorporation of [5–3H] uridine into total RNA. The results showed that RNA synthesis in neutrophils was significantly increased (2.3- to 21.3-fold) by EBV compared with the unstimulated controls. Live and UV-inactivated virus markedly induced RNA synthesis, whereas heat-inactivated virus lost this ability. Induction of RNA transcription was EBV specific, as an EBV-neutralizing antiserum abolished this effect. Induction of protein synthesis was also studied by measuring the incorporation of [35S] methionine and [35S] cysteine into secreted and intracellular proteins in neutrophils incubated with EBV. The synthesis of both secreted and cytoplasmic proteins was induced by EBV. One- and two-dimensional gel electrophoresis analysis showed that EBV modulates protein synthesis, because activation of the synthesis of certain proteins was accompanied by the inhibition of others. Interleukin-1 beta (IL-1 beta) and IL-1 receptor antagonist (IL-1Ra) synthesis was found to be induced by EBV. Therefore, modulation of host-response proteins such as IL-1Ra could be one of the many mechanisms by which this virus avoids rejection.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Discussionmentioning

confidence: 99%

Epstein-Barr virus modulates de novo protein synthesis in human neutrophils

Beaulieu

Paquin

Gosselin

1995

Blood

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“…H 2 O 2 production was measured by assessing reduction in scopoletin fluorescence as previously described. 24,25 In brief, neutrophils were added to a mixture of scopoletin, sodium azide, and horseradish peroxidase, which were previously shown to maximize detection of H 2 O 2 .…”

Section: Measurement Of Neutrophil H 2 O 2 Productionmentioning

confidence: 99%

Histone H4 directly stimulates neutrophil activation through membrane permeabilization

Hsieh

Deluna

White

et al. 2020

Journal of Leukocyte Biology

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Extracellular histones have been implicated as a cause of tissue inflammatory injury in a variety of disorders including sepsis, lung, and liver diseases. However, little is known about their interactions with neutrophils and how this might contribute to injury. Here, it is shown that histone H4 acts as neutrophil activator by inducing hydrogen peroxide production, degranulation, cell adhesion, and IL-8 generation. Histone H4 caused permeabilization of the neutrophil membrane (a phenomenon described in other cell types) leading to accelerated cell death. H4 caused sustained rise in neutrophil intracellular calcium that is necessary for respiratory burst activation and degranulation. Convincing evidence was not found for TLRs or ATP receptors in H4 mediated activation. However, pertussis toxin and wortmannin (inhibitors of G protein and PI3K) inhibited H4-induced hydrogen peroxide production and degranulation. These studies suggest that release of histone H4 in sites of infection or inflammation may potentiate neutrophil activation and promote additional inflammatory responses. These studies may provide a better basis for developing novel therapeutic strategies to block neutrophil extracellular trap (NET) and H4-related pathology in sepsis and various forms of lung injury including that induced by viruses like influenza or SAR-CoV2.

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“…Activation of PKC and Ras/Raf/MEK/ERK signaling cascade inhibits MLCP and enhances MLC phosphorylation [ 28 ]. Meanwhile, influenza infection also leads to an influx in intracellular calcium (Ca 2+ ) and actin polymerization [ 29 – 33 ]. These studies suggest that Ras/Raf/MEK/ERK, PKC, RhoA/ROCK pathways are activated after influenza infection and involved in influenza-induced actin cytoskeleton remodeling and permeability increase by phosphorylation of MLC.…”

Section: Discussionmentioning

confidence: 99%

Screening differential miRNAs responsible for permeability increase in HUVECs infected with influenza A virus

Zhang

Xuan

et al. 2017

PLoS ONE

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Severe influenza infections are featured by acute lung injury, a syndrome of increased pulmonary microvascular permeability. A growing number of evidences have shown that influenza A virus induces cytoskeletal rearrangement and permeability increase in endothelial cells. Although miRNA’s involvement in the regulation of influenza virus infection and endothelial cell (EC) function has been well documented, little is known about the miRNA profiles in influenza-infected endothelial cells. Using human umbilical vein endothelial cells (HUVECs) as cell models, the present study aims to explore the differential miRNAs in influenza virus-infected ECs and analyze their target genes involved in EC permeability regulation. As the results showed, permeability increased and F-actin cytoskeleton reorganized after HUVECs infected with influenza A virus (CA07 or PR8) at 30 MOI. MicroRNA microarray revealed a multitude of miRNAs differentially expressed in HUVECs after influenza virus infection. Through target gene prediction, we found that a series of miRNAs were involved in PKC, Rho/ROCK, HRas/Raf/MEK/ERK, and Ca2+/CaM pathways associated with permeability regulation, and most of these miRNAs were down-regulated after flu infection. It has been reported that PKC, Rho/ROCK, HRas/Raf/MEK/ERK, and Ca2+/CaM pathways are activated by flu infection and play important roles in permeability regulation. Therefore, the cumulative effects of these down-regulated miRNAs which synergistically enhanced activation of PKC, Rho/ROCK, Ras/Raf/MEK/ERK, and Ca2+/CaM pathways, can eventually lead to actin rearrangement and hyperpermeability in flu-infected HUVECs.

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Comparison of influenza A virus and formyl-methionyl-leucyl- phenylalanine activation of the human neutrophil

Cited by 12 publications

References 0 publications

Epstein-Barr virus modulates de novo protein synthesis in human neutrophils

Epstein-Barr virus modulates de novo protein synthesis in human neutrophils

Histone H4 directly stimulates neutrophil activation through membrane permeabilization

Screening differential miRNAs responsible for permeability increase in HUVECs infected with influenza A virus

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