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Barney S Graham - One of the best experts on this subject based on the ideXlab platform.

  • respiratory syncytial virus infection does not increase allergen induced type 2 cytokine production yet increases airway hyperresponsiveness in mice
    Journal of Medical Virology, 2001
    Co-Authors: Stokes R Peebles, James R Sheller, Robert D Collins, Kasia A Jarzecka, Daphne B Mitchell, Robert A Parker, Barney S Graham
    Abstract:

    Severe respiratory syncytial virus (RSV)-induced disease is associated with childhood asthma and atopy. We combined murine models of allergen-sensitization and RSV infection to explore the interaction of allergic and virus-induced airway inflammation and its impact on airway hyperresponsiveness (AHR). We found that RSV infection during Ova-sensitization (Ova/RSV) increased and prolonged AHR compared to mice only RSV-infected (RSV) or Ova-sensitized (Ova). AHR is known to be associated with an increase in Type 2 cytokines (IL-4, IL-5, and IL-13) in allergen-sensitized mice. Therefore, we hypothesized that RSV-induced enhancement of AHR was a result of potentiating the Type 2 cytokine profile promoted by Ova-sensitization. Surprisingly, we found that Type 2 cytokines induced by Ova-sensitization were not increased by RSV infection despite the increase in AHR, and in some cases were diminished. RNAse protection assay revealed no difference in IL-4 and IL-5 mRNA levels between the Ova and Ova/RSV groups, and IL-13 mRNA was significantly decreased in the Ova/RSV mice compared to the Ova group. Flow cytometric analysis of Type 2 cytokines demonstrated the same frequency of IL-4 and IL-5 production in lung-derived T lymphocytes from the Ova/RSV and Ova groups. Direct cytokine ELISA measurements of lung supernatant showed the level of IL-13 was significantly decreased in the Ova/RSV group compared to Ova mice, while there was no difference in either IL-4 or IL-5 between these two groups. These data indicate that the enhanced and prolonged AHR caused by the interaction of allergic airway inflammation and virus-induced immune responses is a complex process that can not be explained simply by augmented production of Type 2 cytokines.

  • respiratory syncytial virus infection prolongs methacholine induced airway hyperresponsiveness in Ovalbumin sensitized mice
    Journal of Medical Virology, 1999
    Co-Authors: Stokes R Peebles, James R Sheller, Daphne B Mitchell, Joyce E Johnson, Barney S Graham
    Abstract:

    Severe respiratory syncytial virus (RSV)-induced disease is associated with childhood asthma and atopy. We combined models of allergen sensitization and RSV infection to begin exploring the immunologic interactions between allergic and virus-induced airway inflammation and its impact on airway hypersensitivity. Airway resistance was measured after methacholine challenge in tracheally intubated mice by whole body plethysmography. Lung inflammation was assessed by bronchoalveolar lavage (BAL) and histopathology. RSV infection alone did not cause significant airway hyperresponsiveness (AHR) to methacholine. Ovalbumin (Ova)-induced AHR lasted only a few days past the discontinuance of Ova aerosol in mice that were Ovalbumin sensitized and mock infected. In contrast, Ova-sensitized mice infected with RSV during the Ova aerosol treatments (Ova/RSV) had AHR for more than 2 weeks after infection. However, 2 weeks after either RSV or mock infection, Ova/RSV mice had significantly more lymphocytes found during BAL than Ova mice, whereas the Ova and Ova/RSV groups had the same number of eosinophils. Histopathologic analysis confirmed an increased inflammation in the lungs of Ova/RSV mice compared with Ova mice. In addition, Ova/RSV mice had a more widespread distribution of mucus in their airways with increased amounts of intraluminal mucus pools compared with the other groups. Thus, prolonged AHR in RSV-infected mice during Ovalbumin-sensitization correlates with increased numbers of lymphocytes in BAL fluid, increased lung inflammation, and mucus deposition in the airways, but not with airway eosinophilia. A further understanding of the immunologic consequences of combined allergic and virus-induced airway inflammation will impact the management of diseases associated with airway hyperreactivity.

Stokes R Peebles - One of the best experts on this subject based on the ideXlab platform.

  • respiratory syncytial virus infection does not increase allergen induced type 2 cytokine production yet increases airway hyperresponsiveness in mice
    Journal of Medical Virology, 2001
    Co-Authors: Stokes R Peebles, James R Sheller, Robert D Collins, Kasia A Jarzecka, Daphne B Mitchell, Robert A Parker, Barney S Graham
    Abstract:

    Severe respiratory syncytial virus (RSV)-induced disease is associated with childhood asthma and atopy. We combined murine models of allergen-sensitization and RSV infection to explore the interaction of allergic and virus-induced airway inflammation and its impact on airway hyperresponsiveness (AHR). We found that RSV infection during Ova-sensitization (Ova/RSV) increased and prolonged AHR compared to mice only RSV-infected (RSV) or Ova-sensitized (Ova). AHR is known to be associated with an increase in Type 2 cytokines (IL-4, IL-5, and IL-13) in allergen-sensitized mice. Therefore, we hypothesized that RSV-induced enhancement of AHR was a result of potentiating the Type 2 cytokine profile promoted by Ova-sensitization. Surprisingly, we found that Type 2 cytokines induced by Ova-sensitization were not increased by RSV infection despite the increase in AHR, and in some cases were diminished. RNAse protection assay revealed no difference in IL-4 and IL-5 mRNA levels between the Ova and Ova/RSV groups, and IL-13 mRNA was significantly decreased in the Ova/RSV mice compared to the Ova group. Flow cytometric analysis of Type 2 cytokines demonstrated the same frequency of IL-4 and IL-5 production in lung-derived T lymphocytes from the Ova/RSV and Ova groups. Direct cytokine ELISA measurements of lung supernatant showed the level of IL-13 was significantly decreased in the Ova/RSV group compared to Ova mice, while there was no difference in either IL-4 or IL-5 between these two groups. These data indicate that the enhanced and prolonged AHR caused by the interaction of allergic airway inflammation and virus-induced immune responses is a complex process that can not be explained simply by augmented production of Type 2 cytokines.

  • respiratory syncytial virus infection prolongs methacholine induced airway hyperresponsiveness in Ovalbumin sensitized mice
    Journal of Medical Virology, 1999
    Co-Authors: Stokes R Peebles, James R Sheller, Daphne B Mitchell, Joyce E Johnson, Barney S Graham
    Abstract:

    Severe respiratory syncytial virus (RSV)-induced disease is associated with childhood asthma and atopy. We combined models of allergen sensitization and RSV infection to begin exploring the immunologic interactions between allergic and virus-induced airway inflammation and its impact on airway hypersensitivity. Airway resistance was measured after methacholine challenge in tracheally intubated mice by whole body plethysmography. Lung inflammation was assessed by bronchoalveolar lavage (BAL) and histopathology. RSV infection alone did not cause significant airway hyperresponsiveness (AHR) to methacholine. Ovalbumin (Ova)-induced AHR lasted only a few days past the discontinuance of Ova aerosol in mice that were Ovalbumin sensitized and mock infected. In contrast, Ova-sensitized mice infected with RSV during the Ova aerosol treatments (Ova/RSV) had AHR for more than 2 weeks after infection. However, 2 weeks after either RSV or mock infection, Ova/RSV mice had significantly more lymphocytes found during BAL than Ova mice, whereas the Ova and Ova/RSV groups had the same number of eosinophils. Histopathologic analysis confirmed an increased inflammation in the lungs of Ova/RSV mice compared with Ova mice. In addition, Ova/RSV mice had a more widespread distribution of mucus in their airways with increased amounts of intraluminal mucus pools compared with the other groups. Thus, prolonged AHR in RSV-infected mice during Ovalbumin-sensitization correlates with increased numbers of lymphocytes in BAL fluid, increased lung inflammation, and mucus deposition in the airways, but not with airway eosinophilia. A further understanding of the immunologic consequences of combined allergic and virus-induced airway inflammation will impact the management of diseases associated with airway hyperreactivity.

Jianxun J. Song - One of the best experts on this subject based on the ideXlab platform.

  • 91-OR: Stem Cell-Derived Tissue-Associated Regulatory T Cells Suppress the Activity of Pathogenic Immune Cells in Autoimmune Diabetes
    Diabetes, 2019
    Co-Authors: Jianxun J. Song
    Abstract:

    The auto antigen (Ag)-specific regulatory T cells (Tregs) from pluripotent stem cells (PSCs), i.e., PSC-Tregs, have the ability to suppress autoimmunity. PSC-Tregs can be programmed to be tissue-associated and to infiltrate into local inflamed tissues to suppress autoimmune responses after adoptive transfer. Nevertheless, the mechanisms by which the auto Ag-specific PSC-Tregs suppress the autoimmune response remain to be fully elucidated. In this study, we generated the functional auto Ag-specific Tregs from the induced PSC (iPSCs), i.e., iPSC-Tregs, and investigated the underlying mechanisms of autoimmunity suppression by these Tregs in a type 1 diabetes (T1D) murine model. A double transgenic (Tg) mouse model of T1D was established in F1 mice in which the first generation of RIP-mOva Tg mice that were crossed with OT-I T cell receptor (TCR) Tg mice was challenged with vaccinia viruses expressing Ova (VACV-Ova). We show that adoptive transfer of Ova-specific iPSC-Tregs greatly suppressed autoimmunity in the animal model and prevented the insulin-secreting pancreatic β cells from destruction. Further, we demonstrate that the adoptive transfer significantly reduced the expression of ICAM-1 in the diabetic pancreas and inhibited the migration of pathogenic CD8+ T cells and the production of the pro-inflammatory IFN-γ in the pancreas. These results indicate that the stem cell-derived tissue-associated Tregs can robustly accumulate in the diabetic pancreas, and through down-regulating the expression of ICAM-1 in the local inflamed tissues and inhibiting the production of pro-inflammatory cytokine IFN-γ, suppress the migration and activity of the pathogenic immune cells that cause T1D. Disclosure J.J. Song: None. Funding American Diabetes Association (1-16-IBS-281); National Institutes of Health (R01AI121180, R21AI109239)

Daphne B Mitchell - One of the best experts on this subject based on the ideXlab platform.

  • respiratory syncytial virus infection does not increase allergen induced type 2 cytokine production yet increases airway hyperresponsiveness in mice
    Journal of Medical Virology, 2001
    Co-Authors: Stokes R Peebles, James R Sheller, Robert D Collins, Kasia A Jarzecka, Daphne B Mitchell, Robert A Parker, Barney S Graham
    Abstract:

    Severe respiratory syncytial virus (RSV)-induced disease is associated with childhood asthma and atopy. We combined murine models of allergen-sensitization and RSV infection to explore the interaction of allergic and virus-induced airway inflammation and its impact on airway hyperresponsiveness (AHR). We found that RSV infection during Ova-sensitization (Ova/RSV) increased and prolonged AHR compared to mice only RSV-infected (RSV) or Ova-sensitized (Ova). AHR is known to be associated with an increase in Type 2 cytokines (IL-4, IL-5, and IL-13) in allergen-sensitized mice. Therefore, we hypothesized that RSV-induced enhancement of AHR was a result of potentiating the Type 2 cytokine profile promoted by Ova-sensitization. Surprisingly, we found that Type 2 cytokines induced by Ova-sensitization were not increased by RSV infection despite the increase in AHR, and in some cases were diminished. RNAse protection assay revealed no difference in IL-4 and IL-5 mRNA levels between the Ova and Ova/RSV groups, and IL-13 mRNA was significantly decreased in the Ova/RSV mice compared to the Ova group. Flow cytometric analysis of Type 2 cytokines demonstrated the same frequency of IL-4 and IL-5 production in lung-derived T lymphocytes from the Ova/RSV and Ova groups. Direct cytokine ELISA measurements of lung supernatant showed the level of IL-13 was significantly decreased in the Ova/RSV group compared to Ova mice, while there was no difference in either IL-4 or IL-5 between these two groups. These data indicate that the enhanced and prolonged AHR caused by the interaction of allergic airway inflammation and virus-induced immune responses is a complex process that can not be explained simply by augmented production of Type 2 cytokines.

  • respiratory syncytial virus infection prolongs methacholine induced airway hyperresponsiveness in Ovalbumin sensitized mice
    Journal of Medical Virology, 1999
    Co-Authors: Stokes R Peebles, James R Sheller, Daphne B Mitchell, Joyce E Johnson, Barney S Graham
    Abstract:

    Severe respiratory syncytial virus (RSV)-induced disease is associated with childhood asthma and atopy. We combined models of allergen sensitization and RSV infection to begin exploring the immunologic interactions between allergic and virus-induced airway inflammation and its impact on airway hypersensitivity. Airway resistance was measured after methacholine challenge in tracheally intubated mice by whole body plethysmography. Lung inflammation was assessed by bronchoalveolar lavage (BAL) and histopathology. RSV infection alone did not cause significant airway hyperresponsiveness (AHR) to methacholine. Ovalbumin (Ova)-induced AHR lasted only a few days past the discontinuance of Ova aerosol in mice that were Ovalbumin sensitized and mock infected. In contrast, Ova-sensitized mice infected with RSV during the Ova aerosol treatments (Ova/RSV) had AHR for more than 2 weeks after infection. However, 2 weeks after either RSV or mock infection, Ova/RSV mice had significantly more lymphocytes found during BAL than Ova mice, whereas the Ova and Ova/RSV groups had the same number of eosinophils. Histopathologic analysis confirmed an increased inflammation in the lungs of Ova/RSV mice compared with Ova mice. In addition, Ova/RSV mice had a more widespread distribution of mucus in their airways with increased amounts of intraluminal mucus pools compared with the other groups. Thus, prolonged AHR in RSV-infected mice during Ovalbumin-sensitization correlates with increased numbers of lymphocytes in BAL fluid, increased lung inflammation, and mucus deposition in the airways, but not with airway eosinophilia. A further understanding of the immunologic consequences of combined allergic and virus-induced airway inflammation will impact the management of diseases associated with airway hyperreactivity.

James R Sheller - One of the best experts on this subject based on the ideXlab platform.

  • respiratory syncytial virus infection does not increase allergen induced type 2 cytokine production yet increases airway hyperresponsiveness in mice
    Journal of Medical Virology, 2001
    Co-Authors: Stokes R Peebles, James R Sheller, Robert D Collins, Kasia A Jarzecka, Daphne B Mitchell, Robert A Parker, Barney S Graham
    Abstract:

    Severe respiratory syncytial virus (RSV)-induced disease is associated with childhood asthma and atopy. We combined murine models of allergen-sensitization and RSV infection to explore the interaction of allergic and virus-induced airway inflammation and its impact on airway hyperresponsiveness (AHR). We found that RSV infection during Ova-sensitization (Ova/RSV) increased and prolonged AHR compared to mice only RSV-infected (RSV) or Ova-sensitized (Ova). AHR is known to be associated with an increase in Type 2 cytokines (IL-4, IL-5, and IL-13) in allergen-sensitized mice. Therefore, we hypothesized that RSV-induced enhancement of AHR was a result of potentiating the Type 2 cytokine profile promoted by Ova-sensitization. Surprisingly, we found that Type 2 cytokines induced by Ova-sensitization were not increased by RSV infection despite the increase in AHR, and in some cases were diminished. RNAse protection assay revealed no difference in IL-4 and IL-5 mRNA levels between the Ova and Ova/RSV groups, and IL-13 mRNA was significantly decreased in the Ova/RSV mice compared to the Ova group. Flow cytometric analysis of Type 2 cytokines demonstrated the same frequency of IL-4 and IL-5 production in lung-derived T lymphocytes from the Ova/RSV and Ova groups. Direct cytokine ELISA measurements of lung supernatant showed the level of IL-13 was significantly decreased in the Ova/RSV group compared to Ova mice, while there was no difference in either IL-4 or IL-5 between these two groups. These data indicate that the enhanced and prolonged AHR caused by the interaction of allergic airway inflammation and virus-induced immune responses is a complex process that can not be explained simply by augmented production of Type 2 cytokines.

  • respiratory syncytial virus infection prolongs methacholine induced airway hyperresponsiveness in Ovalbumin sensitized mice
    Journal of Medical Virology, 1999
    Co-Authors: Stokes R Peebles, James R Sheller, Daphne B Mitchell, Joyce E Johnson, Barney S Graham
    Abstract:

    Severe respiratory syncytial virus (RSV)-induced disease is associated with childhood asthma and atopy. We combined models of allergen sensitization and RSV infection to begin exploring the immunologic interactions between allergic and virus-induced airway inflammation and its impact on airway hypersensitivity. Airway resistance was measured after methacholine challenge in tracheally intubated mice by whole body plethysmography. Lung inflammation was assessed by bronchoalveolar lavage (BAL) and histopathology. RSV infection alone did not cause significant airway hyperresponsiveness (AHR) to methacholine. Ovalbumin (Ova)-induced AHR lasted only a few days past the discontinuance of Ova aerosol in mice that were Ovalbumin sensitized and mock infected. In contrast, Ova-sensitized mice infected with RSV during the Ova aerosol treatments (Ova/RSV) had AHR for more than 2 weeks after infection. However, 2 weeks after either RSV or mock infection, Ova/RSV mice had significantly more lymphocytes found during BAL than Ova mice, whereas the Ova and Ova/RSV groups had the same number of eosinophils. Histopathologic analysis confirmed an increased inflammation in the lungs of Ova/RSV mice compared with Ova mice. In addition, Ova/RSV mice had a more widespread distribution of mucus in their airways with increased amounts of intraluminal mucus pools compared with the other groups. Thus, prolonged AHR in RSV-infected mice during Ovalbumin-sensitization correlates with increased numbers of lymphocytes in BAL fluid, increased lung inflammation, and mucus deposition in the airways, but not with airway eosinophilia. A further understanding of the immunologic consequences of combined allergic and virus-induced airway inflammation will impact the management of diseases associated with airway hyperreactivity.