Mast cell degranulation and histamine release during A/H5N1 influenza infection in influenza-sensitized mice

Desheva, Yulia; Mamontov, A S; Petkova, Nadezhda; Карев, В. Е.; Nazarov, Peter G.

doi:10.1016/j.lfs.2020.118230

Cited by 8 publications

(5 citation statements)

References 37 publications

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“…We next sought to identify the sites that contributed most strongly to PC1 and found that the genes mapped to the top 200 sites were enriched in mast cell activation involved in immune responses. Our finding supports previous work that demonstrated that mast cells influence the response to influenza virus infection in mice 27 . We also mapped significant differentially methylated CpG sites post-vaccination to proximal genes and performed gene ontology enrichment analysis.…”

Section: Discussionsupporting

confidence: 93%

Longitudinal analysis of influenza vaccination implicates regulation of RIG-I signaling by DNA methylation

Fu,

Pickering,

Rubbi

et al. 2024

Sci Rep

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Influenza virus infection alters the promoter DNA methylation of key immune response-related genes, including type-1 interferons and proinflammatory cytokines. However, less is known about the effect of the influenza vaccine on the epigenome. We utilized a targeted DNA methylation approach to study the longitudinal effects (day 0 pre-vaccination and day 28 post-vaccination) on influenza vaccination responses in peripheral blood mononuclear cells. We found that baseline, pre-vaccination methylation profiles are associated with pre-existing, protective serological immunity. Additionally, we identified 481 sites that were differentially methylated between baseline and day 28 post-vaccination. These were enriched for genes involved in the regulation of the RIG-I signaling pathway, an important regulator of viral responses. Our results suggest that DNA methylation changes to components of the RIG-I pathway are associated with vaccine effectiveness. Therefore, immunization strategies that target this pathway may improve serological responses to influenza vaccination.

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Section: Discussionsupporting

confidence: 93%

Longitudinal analysis of influenza vaccination implicates regulation of RIG-I signaling by DNA methylation

Fu,

Pickering,

Rubbi

et al. 2024

Sci Rep

View full text Add to dashboard Cite

show abstract

“…We next sought to identify the sites that contributed most strongly to PC1 and found that the genes mapped to the top 200 sites were enriched in mast cell activation involved in immune responses. Our nding supports previous work that demonstrated that mast cells in uence the response to in uenza virus infection in mice (19). We also mapped signi cant differentially methylated CpG sites post-vaccination to proximal genes and performed gene ontology enrichment analysis.…”

Section: Discussionsupporting

confidence: 88%

Longitudinal analysis of influenza vaccination implicates regulation of RIG-I signaling by DNA methylation

Pickering

Rubbi

Ross³

et al. 2022

Preprint

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Background Influenza virus infection alters the promoter DNA methylation of key immune response-related genes, including type-1 interferons and proinflammatory cytokines. However, less is known about the effect of the influenza vaccine on the epigenome. We utilized a targeted DNA methylation approach to study the longitudinal effects (day 0 pre-vaccination and day 28 post-vaccination) on influenza vaccination responses in peripheral blood mononuclear cells. Results We found that baseline, pre-vaccination methylation profiles are associated with pre-existing, protective serological immunity. Additionally, we identified 481 sites that were differentially methylated between baseline and day 28 post-vaccination. These were enriched for genes involved in the regulation of the RIG-I signaling pathway, an important regulator of viral responses. Conclusions Our results suggest that DNA methylation changes to components of the RIG-I pathway are associated with vaccine effectiveness. Therefore, immunization strategies that target this pathway may improve serological responses to influenza vaccination.

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“…To block the action of histamine in experiments on mice, we used a mixture of H1 and H2 blockers (although the main type of receptors on cells responsible for the anaphylactogenic effects of histamine are H1 receptors). Our previous data indicate that the introduction of histamine receptor blockers decreased in lethality after A/H5N1 infection of vaccinated mice (31). In the present study, it was shown that after challenge with the A/H1N1 virus, protection reached 90% of the immunized animals and the administration of antihistamines did not make an additional contribution to improving survival.…”

Section: Discussionsupporting

confidence: 47%

Study of Antibody-Dependent Reactions of Mast Cells In Vitro and in a Model of Severe Influenza Infection in Mice

et al. 2021

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We investigated the reaction of mouse peritoneal mast cells (MCs) in vitro after IgG-containing immune complex introduction using A/H5N1 and A/H1N1pdm09 influenza viruses as antigens. The sera of immune mice served as a source of IgG antibodies. The concentration of histamine in the supernatants was determined at 4 hours after incubation with antisera and virus. We compared the contribution of MCs to the pathogenesis of post-immunization influenza infection with A/H5N1 and A/H1N1 influenza viruses in mice. The mice were immunized parenterally with inactivated viruses and challenged with lethal doses of drift A/H5N1 and A/H1N1 influenza viruses on the 14th day after immunization. Simultaneously, half of the mice were injected intraperitoneally with a mixture of histamine receptor blockers (chloropyramine and quamatel). In in vitro experiments, the immune complex formed by A/H5N1 virus and antiserum caused a significant increase in the histamine release compared to immune serum or the virus alone. With regard to the A/H1N1 virus, such an increase was not significant. A/H1N1 immunization caused detectable HI response in mice at 12th day after immunization, in contrast to the A/H5N1 virus. After challenge of A/H5N1-immunized mice, administration of antihistamines increased the survival rate by up to 90%. When infecting the A/H1N1-immunized mice, 90% of the animals were already protected from lethal infection by day 14; the administration of histamine receptor blockers did not increase survival. Histological examination of the lungs has shown that toluidine blue staining allows to estimate the degree of MC degranulation. The possibility of in vitro activation of murine MCs by IgG-containing immune complexes has been shown. In a model of influenza infection, it was shown that the administration of histamine receptor blockers increased survival. When the protection was formed faster due to the earlier production of HI antibodies, the administration of histamine receptor blockers did not significantly affect the course of the infection. These data allow to propose that even if there are antibody-dependent MC reactions, they can be easily stopped by the administration of histamine receptor blockers.

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Mast cell degranulation and histamine release during A/H5N1 influenza infection in influenza-sensitized mice

Cited by 8 publications

References 37 publications

Longitudinal analysis of influenza vaccination implicates regulation of RIG-I signaling by DNA methylation

Longitudinal analysis of influenza vaccination implicates regulation of RIG-I signaling by DNA methylation

Longitudinal analysis of influenza vaccination implicates regulation of RIG-I signaling by DNA methylation

Study of Antibody-Dependent Reactions of Mast Cells In Vitro and in a Model of Severe Influenza Infection in Mice

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