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Lorcan Mcgarvey - One of the best experts on this subject based on the ideXlab platform.

  • rhinovirus upregulates transient receptor potential channels in a human Neuronal Cell Line implications for respiratory virus induced cough reflex sensitivity
    Thorax, 2014
    Co-Authors: Haniah Abdullah, Liam G Heaney, S L Cosby, Lorcan Mcgarvey
    Abstract:

    Background The mechanism underlying respiratory virus-induced cough hypersensitivity is unknown. Upregulation of airway Neuronal receptors responsible for sensing physical and chemical stimuli is one possibility, and the transient receptor potential (TRP) channel family are potential candidates. We have used an in vitro model of sensory neurons and human rhinovirus (HRV-16) to study the effect of virus infection on TRP expression. Methods IMR-32 neuroblastoma Cells were differentiated in culture to express three TRP channels: TRPV1, TRPA1 and TRPM8. Flow cytometry and qRT-PCR were used to measure TRP channel protein and mRNA levels following inoculation with live virus, inactivated virus, virus-induced soluble factors or pelleted virus particles. Multiplex bioassay was used to determine nerve growth factor (NGF), interleukin (IL)-1β, IL-6 and IL-8 levels in response to infection. Results Early upregulation of TRPA1 and TRPV1 expression occurred 2–4 h post infection. This was independent of replicating virus as virus-induced soluble factors alone were sufficient to increase channel expression 50-fold and 15-fold, respectively. NGF, IL-6 and IL-8 levels, increased in infected Cell supernatants, represent possible candidates. In contrast, TRPM8 expression was maximal at 48 h (9.6-fold) and required virus replication rather than soluble factors. Conclusions We show for the first time that rhinovirus can infect Neuronal Cells. Furthermore, infection causes upregulation of TRP channels by channel-specific mechanisms. The increase in TRPA1 and TRPV1 levels can be mediated by soluble factors induced by infection whereas TRPM8 requires replicating virus. TRP channels may be novel therapeutic targets for controlling virus-induced cough.

  • rhinovirus upregulates transient receptor potential channels in a human Neuronal Cell Line implications for respiratory virus induced cough reflex sensitivity
    Thorax, 2014
    Co-Authors: Haniah Abdullah, Liam G Heaney, S L Cosby, Lorcan Mcgarvey
    Abstract:

    Background The mechanism underlying respiratory virus-induced cough hypersensitivity is unknown. Upregulation of airway Neuronal receptors responsible for sensing physical and chemical stimuli is one possibility, and the transient receptor potential (TRP) channel family are potential candidates. We have used an in vitro model of sensory neurons and human rhinovirus (HRV-16) to study the effect of virus infection on TRP expression. Methods IMR-32 neuroblastoma Cells were differentiated in culture to express three TRP channels: TRPV1, TRPA1 and TRPM8. Flow cytometry and qRT-PCR were used to measure TRP channel protein and mRNA levels following inoculation with live virus, inactivated virus, virus-induced soluble factors or pelleted virus particles. Multiplex bioassay was used to determine nerve growth factor (NGF), interleukin (IL)-1β, IL-6 and IL-8 levels in response to infection. Results Early upregulation of TRPA1 and TRPV1 expression occurred 2–4 h post infection. This was independent of replicating virus as virus-induced soluble factors alone were sufficient to increase channel expression 50-fold and 15-fold, respectively. NGF, IL-6 and IL-8 levels, increased in infected Cell supernatants, represent possible candidates. In contrast, TRPM8 expression was maximal at 48 h (9.6-fold) and required virus replication rather than soluble factors. Conclusions We show for the first time that rhinovirus can infect Neuronal Cells. Furthermore, infection causes upregulation of TRP channels by channel-specific mechanisms. The increase in TRPA1 and TRPV1 levels can be mediated by soluble factors induced by infection whereas TRPM8 requires replicating virus. TRP channels may be novel therapeutic targets for controlling virus-induced cough.

Haniah Abdullah - One of the best experts on this subject based on the ideXlab platform.

  • rhinovirus upregulates transient receptor potential channels in a human Neuronal Cell Line implications for respiratory virus induced cough reflex sensitivity
    Thorax, 2014
    Co-Authors: Haniah Abdullah, Liam G Heaney, S L Cosby, Lorcan Mcgarvey
    Abstract:

    Background The mechanism underlying respiratory virus-induced cough hypersensitivity is unknown. Upregulation of airway Neuronal receptors responsible for sensing physical and chemical stimuli is one possibility, and the transient receptor potential (TRP) channel family are potential candidates. We have used an in vitro model of sensory neurons and human rhinovirus (HRV-16) to study the effect of virus infection on TRP expression. Methods IMR-32 neuroblastoma Cells were differentiated in culture to express three TRP channels: TRPV1, TRPA1 and TRPM8. Flow cytometry and qRT-PCR were used to measure TRP channel protein and mRNA levels following inoculation with live virus, inactivated virus, virus-induced soluble factors or pelleted virus particles. Multiplex bioassay was used to determine nerve growth factor (NGF), interleukin (IL)-1β, IL-6 and IL-8 levels in response to infection. Results Early upregulation of TRPA1 and TRPV1 expression occurred 2–4 h post infection. This was independent of replicating virus as virus-induced soluble factors alone were sufficient to increase channel expression 50-fold and 15-fold, respectively. NGF, IL-6 and IL-8 levels, increased in infected Cell supernatants, represent possible candidates. In contrast, TRPM8 expression was maximal at 48 h (9.6-fold) and required virus replication rather than soluble factors. Conclusions We show for the first time that rhinovirus can infect Neuronal Cells. Furthermore, infection causes upregulation of TRP channels by channel-specific mechanisms. The increase in TRPA1 and TRPV1 levels can be mediated by soluble factors induced by infection whereas TRPM8 requires replicating virus. TRP channels may be novel therapeutic targets for controlling virus-induced cough.

  • rhinovirus upregulates transient receptor potential channels in a human Neuronal Cell Line implications for respiratory virus induced cough reflex sensitivity
    Thorax, 2014
    Co-Authors: Haniah Abdullah, Liam G Heaney, S L Cosby, Lorcan Mcgarvey
    Abstract:

    Background The mechanism underlying respiratory virus-induced cough hypersensitivity is unknown. Upregulation of airway Neuronal receptors responsible for sensing physical and chemical stimuli is one possibility, and the transient receptor potential (TRP) channel family are potential candidates. We have used an in vitro model of sensory neurons and human rhinovirus (HRV-16) to study the effect of virus infection on TRP expression. Methods IMR-32 neuroblastoma Cells were differentiated in culture to express three TRP channels: TRPV1, TRPA1 and TRPM8. Flow cytometry and qRT-PCR were used to measure TRP channel protein and mRNA levels following inoculation with live virus, inactivated virus, virus-induced soluble factors or pelleted virus particles. Multiplex bioassay was used to determine nerve growth factor (NGF), interleukin (IL)-1β, IL-6 and IL-8 levels in response to infection. Results Early upregulation of TRPA1 and TRPV1 expression occurred 2–4 h post infection. This was independent of replicating virus as virus-induced soluble factors alone were sufficient to increase channel expression 50-fold and 15-fold, respectively. NGF, IL-6 and IL-8 levels, increased in infected Cell supernatants, represent possible candidates. In contrast, TRPM8 expression was maximal at 48 h (9.6-fold) and required virus replication rather than soluble factors. Conclusions We show for the first time that rhinovirus can infect Neuronal Cells. Furthermore, infection causes upregulation of TRP channels by channel-specific mechanisms. The increase in TRPA1 and TRPV1 levels can be mediated by soluble factors induced by infection whereas TRPM8 requires replicating virus. TRP channels may be novel therapeutic targets for controlling virus-induced cough.

S L Cosby - One of the best experts on this subject based on the ideXlab platform.

  • rhinovirus upregulates transient receptor potential channels in a human Neuronal Cell Line implications for respiratory virus induced cough reflex sensitivity
    Thorax, 2014
    Co-Authors: Haniah Abdullah, Liam G Heaney, S L Cosby, Lorcan Mcgarvey
    Abstract:

    Background The mechanism underlying respiratory virus-induced cough hypersensitivity is unknown. Upregulation of airway Neuronal receptors responsible for sensing physical and chemical stimuli is one possibility, and the transient receptor potential (TRP) channel family are potential candidates. We have used an in vitro model of sensory neurons and human rhinovirus (HRV-16) to study the effect of virus infection on TRP expression. Methods IMR-32 neuroblastoma Cells were differentiated in culture to express three TRP channels: TRPV1, TRPA1 and TRPM8. Flow cytometry and qRT-PCR were used to measure TRP channel protein and mRNA levels following inoculation with live virus, inactivated virus, virus-induced soluble factors or pelleted virus particles. Multiplex bioassay was used to determine nerve growth factor (NGF), interleukin (IL)-1β, IL-6 and IL-8 levels in response to infection. Results Early upregulation of TRPA1 and TRPV1 expression occurred 2–4 h post infection. This was independent of replicating virus as virus-induced soluble factors alone were sufficient to increase channel expression 50-fold and 15-fold, respectively. NGF, IL-6 and IL-8 levels, increased in infected Cell supernatants, represent possible candidates. In contrast, TRPM8 expression was maximal at 48 h (9.6-fold) and required virus replication rather than soluble factors. Conclusions We show for the first time that rhinovirus can infect Neuronal Cells. Furthermore, infection causes upregulation of TRP channels by channel-specific mechanisms. The increase in TRPA1 and TRPV1 levels can be mediated by soluble factors induced by infection whereas TRPM8 requires replicating virus. TRP channels may be novel therapeutic targets for controlling virus-induced cough.

  • rhinovirus upregulates transient receptor potential channels in a human Neuronal Cell Line implications for respiratory virus induced cough reflex sensitivity
    Thorax, 2014
    Co-Authors: Haniah Abdullah, Liam G Heaney, S L Cosby, Lorcan Mcgarvey
    Abstract:

    Background The mechanism underlying respiratory virus-induced cough hypersensitivity is unknown. Upregulation of airway Neuronal receptors responsible for sensing physical and chemical stimuli is one possibility, and the transient receptor potential (TRP) channel family are potential candidates. We have used an in vitro model of sensory neurons and human rhinovirus (HRV-16) to study the effect of virus infection on TRP expression. Methods IMR-32 neuroblastoma Cells were differentiated in culture to express three TRP channels: TRPV1, TRPA1 and TRPM8. Flow cytometry and qRT-PCR were used to measure TRP channel protein and mRNA levels following inoculation with live virus, inactivated virus, virus-induced soluble factors or pelleted virus particles. Multiplex bioassay was used to determine nerve growth factor (NGF), interleukin (IL)-1β, IL-6 and IL-8 levels in response to infection. Results Early upregulation of TRPA1 and TRPV1 expression occurred 2–4 h post infection. This was independent of replicating virus as virus-induced soluble factors alone were sufficient to increase channel expression 50-fold and 15-fold, respectively. NGF, IL-6 and IL-8 levels, increased in infected Cell supernatants, represent possible candidates. In contrast, TRPM8 expression was maximal at 48 h (9.6-fold) and required virus replication rather than soluble factors. Conclusions We show for the first time that rhinovirus can infect Neuronal Cells. Furthermore, infection causes upregulation of TRP channels by channel-specific mechanisms. The increase in TRPA1 and TRPV1 levels can be mediated by soluble factors induced by infection whereas TRPM8 requires replicating virus. TRP channels may be novel therapeutic targets for controlling virus-induced cough.

Liam G Heaney - One of the best experts on this subject based on the ideXlab platform.

  • rhinovirus upregulates transient receptor potential channels in a human Neuronal Cell Line implications for respiratory virus induced cough reflex sensitivity
    Thorax, 2014
    Co-Authors: Haniah Abdullah, Liam G Heaney, S L Cosby, Lorcan Mcgarvey
    Abstract:

    Background The mechanism underlying respiratory virus-induced cough hypersensitivity is unknown. Upregulation of airway Neuronal receptors responsible for sensing physical and chemical stimuli is one possibility, and the transient receptor potential (TRP) channel family are potential candidates. We have used an in vitro model of sensory neurons and human rhinovirus (HRV-16) to study the effect of virus infection on TRP expression. Methods IMR-32 neuroblastoma Cells were differentiated in culture to express three TRP channels: TRPV1, TRPA1 and TRPM8. Flow cytometry and qRT-PCR were used to measure TRP channel protein and mRNA levels following inoculation with live virus, inactivated virus, virus-induced soluble factors or pelleted virus particles. Multiplex bioassay was used to determine nerve growth factor (NGF), interleukin (IL)-1β, IL-6 and IL-8 levels in response to infection. Results Early upregulation of TRPA1 and TRPV1 expression occurred 2–4 h post infection. This was independent of replicating virus as virus-induced soluble factors alone were sufficient to increase channel expression 50-fold and 15-fold, respectively. NGF, IL-6 and IL-8 levels, increased in infected Cell supernatants, represent possible candidates. In contrast, TRPM8 expression was maximal at 48 h (9.6-fold) and required virus replication rather than soluble factors. Conclusions We show for the first time that rhinovirus can infect Neuronal Cells. Furthermore, infection causes upregulation of TRP channels by channel-specific mechanisms. The increase in TRPA1 and TRPV1 levels can be mediated by soluble factors induced by infection whereas TRPM8 requires replicating virus. TRP channels may be novel therapeutic targets for controlling virus-induced cough.

  • rhinovirus upregulates transient receptor potential channels in a human Neuronal Cell Line implications for respiratory virus induced cough reflex sensitivity
    Thorax, 2014
    Co-Authors: Haniah Abdullah, Liam G Heaney, S L Cosby, Lorcan Mcgarvey
    Abstract:

    Background The mechanism underlying respiratory virus-induced cough hypersensitivity is unknown. Upregulation of airway Neuronal receptors responsible for sensing physical and chemical stimuli is one possibility, and the transient receptor potential (TRP) channel family are potential candidates. We have used an in vitro model of sensory neurons and human rhinovirus (HRV-16) to study the effect of virus infection on TRP expression. Methods IMR-32 neuroblastoma Cells were differentiated in culture to express three TRP channels: TRPV1, TRPA1 and TRPM8. Flow cytometry and qRT-PCR were used to measure TRP channel protein and mRNA levels following inoculation with live virus, inactivated virus, virus-induced soluble factors or pelleted virus particles. Multiplex bioassay was used to determine nerve growth factor (NGF), interleukin (IL)-1β, IL-6 and IL-8 levels in response to infection. Results Early upregulation of TRPA1 and TRPV1 expression occurred 2–4 h post infection. This was independent of replicating virus as virus-induced soluble factors alone were sufficient to increase channel expression 50-fold and 15-fold, respectively. NGF, IL-6 and IL-8 levels, increased in infected Cell supernatants, represent possible candidates. In contrast, TRPM8 expression was maximal at 48 h (9.6-fold) and required virus replication rather than soluble factors. Conclusions We show for the first time that rhinovirus can infect Neuronal Cells. Furthermore, infection causes upregulation of TRP channels by channel-specific mechanisms. The increase in TRPA1 and TRPV1 levels can be mediated by soluble factors induced by infection whereas TRPM8 requires replicating virus. TRP channels may be novel therapeutic targets for controlling virus-induced cough.

Israel Steiner - One of the best experts on this subject based on the ideXlab platform.

  • herpes simplex virus type 1 latency associated transcripts suppress viral replication and reduce immediate early gene mrna levels in a Neuronal Cell Line
    Journal of Virology, 1998
    Co-Authors: Nurith Mador, Daniel Goldenberg, Oren Cohen, Amos Panet, Israel Steiner
    Abstract:

    During herpes simplex virus type 1 (HSV-1) latent infection in human dorsal root ganglia, limited viral transcription, which has been linked to HSV-1 reactivation ability, takes place. To study the involvement of this transcription in HSV-1 replication in Neuronal Cells and consequently in viral latency, we constructed stably transfected Neuronal Cell Lines containing (i) the entire HSV-1 latency transcriptionally active DNA fragment, (ii) the same DNA sequence with deletions of the latency-associated transcript (LAT) promoters, or (iii) the DNA coding sequence of the LAT domain. Replication of HSV-1 or a LAT-negative mutant was markedly repressed in the LAT-expressing Cells, a phenomenon mediated by the LATs. To study the mechanism responsible for this effect, we examined LAT influence upon expression of HSV-1 immediate-early (IE) genes ICP0, ICP4, and ICP27, by Northern blot analysis. Following infection of a LAT-expressing Neuronal Cell Line with a LAT-negative mutant, the steady-state levels of all three IE mRNAs were reduced compared to those for control Cells. Transient transfections into a Neuronal Cell Line indicated that the LAT suppressive effect upon ICP0 mRNA was mediated directly and was not due to the LAT effect upon the ICP0 promoter. We therefore propose that the LATs may repress viral replication in Neuronal Cells by reducing IE gene mRNA levels and thus facilitate the establishment of HSV-1 latency in nervous tissue.