Differential Mononuclear Leukocyte Attracting Chemokine Production after Stimulation with Active and Inactivated Influenza A Virus

Bussfeld, Delia; Kaufmann, Andreas M.; Meyer, Ralf G.; Gemsa, Diethard; Sprenger, Hans

doi:10.1006/cimm.1998.1295

Cited by 61 publications

(39 citation statements)

References 39 publications

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“…Titered, active influenza A virus was diluted in PBS (1/4). For some experiments, the virus was partially inactivated using UV light at 209 mW/cm for 5-10 min or was fully inactivated by boiling at 100°C for 15 min (14).…”

Section: Influenza Virusmentioning

confidence: 99%

Autocrine Type I IFN and Contact with Endothelium Promote the Presentation of Influenza A Virus by Monocyte-Derived APC

Moran

Randolph

2003

The Journal of Immunology

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Purified monocytes infected with influenza A virus do not become mature dendritic cells (DCs) and they present viral peptides poorly to autologous memory T cells. In this study, we investigated whether influenza A-infected monocytes matured to DCs with a high capacity to stimulate T cells when they were infected with influenza A virus in a model tissue setting wherein they were cocultured with endothelium grown on a type I collagen matrix. Intercellular interactions with endothelium strongly promoted the Ag-presenting capacity of monocyte-derived cells infected with influenza A virus, and the heterologous coculture system also enhanced production of IFN-α by monocytes in the absence of plasmacytoid cells. Production of IFN-α in the presence of endothelium correlated with monocyte differentiation to mature DCs and their ability to stimulate proliferation and IFN-γ production by autologous T cells. Monocyte-derived cells that developed into migratory DCs promoted proliferation of influenza A virus-specific CD4+ and CD8+ cells, whereas those that developed into macrophages promoted proliferation of CD8+ T cells only. This onset of APC activity could be partially blocked with Ab to the IFN-αβ receptor when monocytes were infected with UV-treated virus, but neutralizing this pathway was inconsequential when monocytes were infected with live virus. Thus, type I IFN and direct contact with endothelium promote development of influenza A virus-presenting activity in monocyte-derived cells in a setting in which this differentiation does not depend on plasmacytoid cells. However, when infected with live influenza virus, the role of type I IFN in mediating differentiation and Ag-presenting capacity is expendable, apparently due to other mechanisms of virus-mediated activation.

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Section: Influenza Virusmentioning

confidence: 99%

Autocrine Type I IFN and Contact with Endothelium Promote the Presentation of Influenza A Virus by Monocyte-Derived APC

Moran

Randolph

2003

The Journal of Immunology

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“…Monocytes and pDCs produce proinflammatory cytokines, such as interferon α (IFN-α), and chemokines, such as IFN-γ-inducible protein 10 (IP-10) and MIP-1β. IP-10 and MIP-1β recruit and activate immune effector cells such as neutrophils, CD8 + T cells, and NK cells, promoting influenza A virus clearance [8,9]. In one study, PBMCs from pregnant women produced less IFN-α and IFN-λ that did PBMCs from nonpregnant women in response to influenza A virus [10].…”

mentioning

confidence: 99%

Increased Proinflammatory Responses of Monocytes and Plasmacytoid Dendritic Cells to Influenza A Virus Infection During Pregnancy

Gars¹,

Kay²,

Bayless³

et al. 2016

J Infect Dis.

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Pregnancy-induced alterations in immunity may contribute to the increased morbidity associated with influenza A virus infection during pregnancy. We characterized the immune response of monocytes and plasmacytoid dendritic cells ( pDCs) to influenza A virus infection in 21 pregnant and 21 nonpregnant women. In pregnant women, monocytes and pDCs exhibit an exaggerated proinflammatory immune response to 2 strains of influenza A virus, compared with nonpregnant women, characterized by increased expression of major histocompatibility complex class II (approximately 2.0-fold), CD69 (approximately 2.2-fold), interferon γ-induced protein 10 (approximately 2.0-fold), and macrophage inflammatory protein 1β (approximately 1.5-fold). This enhanced innate inflammatory response during pregnancy could contribute to pulmonary inflammation following influenza A virus infection.

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“…These studies have shown that influenza A virus stimulated the release of IL-6, IL-8, and RANTES from cultured primary human bronchial epithelial cells (2). Influenza A virus-infected monocytes/macrophages secrete macrophage inflammatory protein 1␣ (MIP-1␣), MIP-1␤, RANTES, monocyte chemotactic peptide 1 (MCP-1), MCP-3, MIP-3␣, and interferon-inducible protein 10 (IP-10), whereas the production of IL-8 appears to be limited (7,27,36). S. pneumoniae stimulates tumor necrosis factor alpha (TNF-␣) and IL-10 production by human monocytes, whereas S. pneumoniae is a less potent inducer of IL-8 and MIP-1␣ production in human peripheral blood neutrophils (19,43).…”

mentioning

confidence: 99%

Expression of Cytokine and Chemokine Genes by Human Middle Ear Epithelial Cells Induced by Influenza A Virus andStreptococcus pneumoniaeOpacity Variants

et al. 2003

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Real-time PCR and enzyme-linked immunosorbent assay were used to evaluate the ability of influenza A virus and Streptococcus pneumoniae opacity variants, either alone or in combination, to induce cytokine and chemokine genes in primary cultures of human middle ear epithelial (HMEE) cells. Following treatment with influenza A virus, the induction of gene expression, which occurred in a dose-and time-dependent manner, was strong for macrophage inflammatory protein 1␣ (MIP-1␣) and MIP-1␤; moderate for tumor necrosis factor alpha (TNF-␣), interleukin-6 (IL-6), and IL-8; and weak for IL-1␤ and monocyte chemotactic peptide 1 (MCP-1). Except for TNF-␣, all the gene products were detected in the cell culture supernatants. In contrast, infection of HMEE cells with S. pneumoniae alone induced low levels of mRNA expression of MIP-1␣ and MIP-1␤ and did not significantly induce the transcription of the other cytokines and chemokines examined. However, both S. pneumoniae opacity variants increased mRNA expression of MIP-1␣, MIP-1␤, IL-6, and MCP-1 in HMEE cells activated by a prior influenza A virus infection compared to levels in cells treated with either agent alone. Up-regulation of IL-6, IL-8, and MCP-1 mRNA expression and production by the virus in combination with opaque S. pneumoniae was two-to threefold higher than that induced by the virus combined with the transparent S. pneumoniae variant. These data indicate that the activation of HMEE cells by influenza A virus enhances the induction of cytokine and chemokine gene transcripts by S. pneumoniae and that this effect appears to be most pronounced when S. pneumoniae is in the opaque phase.Streptococcus pneumoniae is the primary bacterial pathogen associated with otitis media (OM), accounting for 30% of the cases of this disease (5). The process whereby S. pneumoniae becomes established in the human nasopharynx and effects the transition from a colonized to a disease state in the middle ear has been the focus of intense investigation for years. S. pneumoniae-induced OM is characterized by the presence of numerous bacteria, inflammatory cells, middle ear effusion, and middle ear epithelial cell injury. It is widely accepted that the middle ear epithelium plays a crucial role, serving as a first line of defense in the interaction with invasive pathogens during OM (25). Innate proinflammatory responses induced in host cells by S. pneumoniae infection that may contribute to the OM pathology include the synthesis and release of cytokines, chemokines, and other inflammatory mediators. Extensive evidence suggests that the middle ear epithelium not only is a physical barrier but also has the potential to synthesize a variety of cytokines, including interleukin-1 (IL-1), IL-6, IL-8, and IL-10, which are recognized as being important local mediators in acute inflammation in various animal models of OM (20,28,33). Activation of host epithelial and endothelial cells by cytokines results in a shift in S. pneumoniae adherence to new receptors, particularly the platelet-activating fa...

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Differential Mononuclear Leukocyte Attracting Chemokine Production after Stimulation with Active and Inactivated Influenza A Virus

Cited by 61 publications

References 39 publications

Autocrine Type I IFN and Contact with Endothelium Promote the Presentation of Influenza A Virus by Monocyte-Derived APC

Autocrine Type I IFN and Contact with Endothelium Promote the Presentation of Influenza A Virus by Monocyte-Derived APC

Increased Proinflammatory Responses of Monocytes and Plasmacytoid Dendritic Cells to Influenza A Virus Infection During Pregnancy

Expression of Cytokine and Chemokine Genes by Human Middle Ear Epithelial Cells Induced by Influenza A Virus andStreptococcus pneumoniaeOpacity Variants

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