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Airway Innervation

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Axel Fischer – One of the best experts on this subject based on the ideXlab platform.

  • i
    , 2016
    Co-Authors: Clin J. Invest, Axel Fischer, Gerard P. Mcgregor, Alois Saria, Wolfgang Kummer
    Abstract:

    Substance P (SP), neurokinin A (NKA), and calcitonin gene-related peptide (CGRP) have potent proinflammatory effects in the Airways. They are released from sensory nerve endings originating in jugular and dorsal root ganglia. How-ever, the major sensory supply to the Airways originates from the nodose ganglion. In this study, we evaluated changes in neuropeptide biosynthesis in the sensory Airway Innervation of ovalbumin-sensitized and-challenged guinea pigs at the mRNA and peptide level. In the Airways, a three-to fourfold increase of SP, NKA, and CGRP, was seen 24 h following allergen challenge. Whereas no evidence of local tachykinin biosynthesis was found 12 h after challenge, in-creased levels of preprotachykinin (PPT)-A mRNA (encod-ing SP and NKA) were found in nodose ganglia. Quantita-tive in situ hybridization indicated that this increase could be accounted for by de novo induction of PPT-A mRNA in nodose ganglion neurons. Quantitative immunohistochem-istry showed that 24 h after challenge, the number of tachy-kinin-immunoreactive nodose ganglion neurons had in-creased by 25%. Their projection to the Airways was shown. Changes in other sensory ganglia innervating the Airways were not evident. These findings suggest that an induction of sensory neuropeptides in nodose ganglion neurons is cru-cially involved in the increase of Airway hyperreactivity in the late response to allergen challenge.

  • Neuronal plasticity in persistent perennial allergic rhinitis.
    Journal of occupational and environmental medicine, 2005
    Co-Authors: Axel Fischer, W. Heppt, C. Peiser, Q. Thai Dinh, M. Zweng, Anke Wussow, Annette Cryer, Bernd Schmeck, Oliver Noga, D.a. Groneberg
    Abstract:

    Persistent perennial allergic rhinitis belongs to the most frequent diseases in occupational and environmental medicine. Because the Innervation may play a role in the pathogenesis of the disease, the present study analyzed nasal mucosal nerve profiles. Neuropeptide-containing nerve fibers were examined using immunohistochemistry and related to eosinophil and mast cell numbers. In contrast to constant numbers of mast cells, there was a significant increase in the number of eosinophils. Immunohistochemistry for calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptpeptide (VIP), and neuropeptide tyrosine (NPY) revealed abundant staining of mucosal nerves. Semiquantitative assessment of nerve fiber neuropeptide density demonstrated a significant increase of VIP-positive fibers in rhinitis tissues. The present data indicate a differential regulation of neuropeptide-containing nerve fibers with increased numbers of VIPergic fibers suggesting a modulatory role of the upper Airway Innervation in perennial allergic rhinitis.

  • Phenotypic alteration of neuropeptide‐containing nerve fibres in seasonal intermittent allergic rhinitis
    Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2004
    Co-Authors: W. Heppt, Axel Fischer, C. Peiser, Q. Thai Dinh, M. Zweng, Christian Witt, Annette Cryer, Oliver Noga, M. Melvan, D.a. Groneberg
    Abstract:

    Allergic rhinitis (AR) is the most common allergic disease affecting the respiratory tract. Next to inflammatory changes, the Airway Innervation plays an important modulatory role in the pathogenesis of the disease. To examine the participation of different neuropeptides in the human nasal mucosa of intermittent (seasonal) AR tissues in the allergic season. Immunohistochemistry for substance P (SP), calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP) and neuropeptide tyrosine (NPY) was related to the characterization of inflammatory cells in tissues of patients with seasonal AR (n=18). While there was a significant increase in the number of eosinophils present if compared with a control group, no changes occurred in mast cell numbers. Immunostaining was abundantly found in different nerve fibre populations of both groups. SP expression was significantly increased in mucosal nerve fibres of patients with intermittent (seasonal) AR. Also, significantly increased numbers of VIP- and NPY-immunoreactive nerve fibres were found in biopsies of rhinitis patients in comparison with sections of normal human nasal mucosa. In contrast, CGRP expression did not change significantly. The increase of neuropeptide expression in mucosal nerve fibres indicates a major role of the autonomous mucosal Innervation in the pathophysiology of intermittent (seasonal) AR.

Kent E. Pinkerton – One of the best experts on this subject based on the ideXlab platform.

  • perinatal environmental tobacco smoke exposure alters the immune response and Airway Innervation in infant primates
    The Journal of Allergy and Clinical Immunology, 2008
    Co-Authors: Xiaomu Zheng, Janice L. Peake, Jesse P. Joad, Kent E. Pinkerton
    Abstract:

    Background Epidemiologic studies associate environmental tobacco smoke (ETS) exposure with childhood asthma. Objective To investigate whether specific pathophysiological alterations that contribute to asthma development in human beings can be induced in infant monkeys after perinatal ETS exposure. Methods Rhesus macaque fetuses/infants were exposed to ETS at 1 mg/m3 of total suspended particulate matter from 50 days gestational age to 2.5 months postnatal age. Inflammatory and neural responses to ETS exposure were measured in the infant monkeys. Results Perinatal ETS exposure could induce systemic and local responses, which include significant elevation of plasma levels of C5a and brain-derived neurotrophic factor, as well as significant increases in pulmonary expression of proinflammatory cytokine TNF-α and TH2 cytokine IL-5, chemokine monocyte chemoattractant protein 1, and the density of substance P–positive nerves along the bronchial epithelium. Perinatal ETS exposure also significantly increased the numbers of mast cells, eosinophils, monocytes, and lymphocytes in the lungs of infant monkeys. In addition, ex vivo measurements showed significantly increased levels of IL-4 and brain-derived neurotrophic factor in the culture supernatant of PBMCs. Interestingly, as an important component of cigarette smoke, LPS was detected in the plasma of infant monkeys subjected to perinatal exposure to ETS. In contrast, an inhibitory effect of perinatal ETS exposure was also observed, which is associated with decreased phagocytic activity of alveolar macrophages and a significantly decreased level of nerve growth factor in the bronchoalveolar lavalavageid. Conclusion Perinatal ETS exposure can induce a TH2-biased inflammatory response and alter Airway Innervation in infant monkeys.

  • Perinatal environmental tobacco smoke exposure alters the immune response and Airway Innervation in infant primates.
    The Journal of allergy and clinical immunology, 2008
    Co-Authors: Xiaomu Zheng, Janice L. Peake, Jesse P. Joad, Kent E. Pinkerton
    Abstract:

    Epidemiologic studies associate environmental tobacco smoke (ETS) exposure with childhood asthma. To investigate whether specific pathophysiological alterations that contribute to asthma development in human beings can be induced in infant monkeys after perinatal ETS exposure. Rhesus macaque fetuses/infants were exposed to ETS at 1 mg/m(3) of total suspended particulate matter from 50 days gestational age to 2.5 months postnatal age. Inflammatory and neural responses to ETS exposure were measured in the infant monkeys. Perinatal ETS exposure could induce systemic and local responses, which include significant elevation of plasma levels of C5a and brain-derived neurotrophic factor, as well as significant increases in pulmonary expression of proinflammatory cytokine TNF-alpha and T(H)2 cytokine IL-5, chemokine monocyte chemoattractant protein 1, and the density of substance P-positive nerves along the bronchial epithelium. Perinatal ETS exposure also significantly increased the numbers of mast cells, eosinophils, monocytes, and lymphocytes in the lungs of infant monkeys. In addition, ex vivo measurements showed significantly increased levels of IL-4 and brain-derived neurotrophic factor in the culture supernatant of PBMCs. Interestingly, as an important component of cigarette smoke, LPS was detected in the plasma of infant monkeys subjected to perinatal exposure to ETS. In contrast, an inhibitory effect of perinatal ETS exposure was also observed, which is associated with decreased phagocytic activity of alveolar macrophages and a significantly decreased level of nerve growth factor in the bronchoalveolar lavalavageid. Perinatal ETS exposure can induce a T(H)2-biased inflammatory response and alter Airway Innervation in infant monkeys.

D.a. Groneberg – One of the best experts on this subject based on the ideXlab platform.

  • Neuronal plasticity in persistent perennial allergic rhinitis.
    Journal of occupational and environmental medicine, 2005
    Co-Authors: Axel Fischer, W. Heppt, C. Peiser, Q. Thai Dinh, M. Zweng, Anke Wussow, Annette Cryer, Bernd Schmeck, Oliver Noga, D.a. Groneberg
    Abstract:

    Persistent perennial allergic rhinitis belongs to the most frequent diseases in occupational and environmental medicine. Because the Innervation may play a role in the pathogenesis of the disease, the present study analyzed nasal mucosal nerve profiles. Neuropeptide-containing nerve fibers were examined using immunohistochemistry and related to eosinophil and mast cell numbers. In contrast to constant numbers of mast cells, there was a significant increase in the number of eosinophils. Immunohistochemistry for calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptide (VIP), and neuropeptide tyrosine (NPY) revealed abundant staining of mucosal nerves. Semiquantitative assessment of nerve fiber neuropeptide density demonstrated a significant increase of VIP-positive fibers in rhinitis tissues. The present data indicate a differential regulation of neuropeptide-containing nerve fibers with increased numbers of VIPergic fibers suggesting a modulatory role of the upper Airway Innervation in perennial allergic rhinitis.

  • Phenotypic alteration of neuropeptide‐containing nerve fibres in seasonal intermittent allergic rhinitis
    Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2004
    Co-Authors: W. Heppt, Axel Fischer, C. Peiser, Q. Thai Dinh, M. Zweng, Christian Witt, Annette Cryer, Oliver Noga, M. Melvan, D.a. Groneberg
    Abstract:

    Allergic rhinitis (AR) is the most common allergic disease affecting the respiratory tract. Next to inflammatory changes, the Airway Innervation plays an important modulatory role in the pathogenesis of the disease. To examine the participation of different neuropeptides in the human nasal mucosa of intermittent (seasonal) AR tissues in the allergic season. Immunohistochemistry for substance P (SP), calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP) and neuropeptide tyrosine (NPY) was related to the characterization of inflammatory cells in tissues of patients with seasonal AR (n=18). While there was a significant increase in the number of eosinophils present if compared with a control group, no changes occurred in mast cell numbers. Immunostaining was abundantly found in different nerve fibre populations of both groups. SP expression was significantly increased in mucosal nerve fibres of patients with intermittent (seasonal) AR. Also, significantly increased numbers of VIP- and NPY-immunoreactive nerve fibres were found in biopsies of rhinitis patients in comparison with sections of normal human nasal mucosa. In contrast, CGRP expression did not change significantly. The increase of neuropeptide expression in mucosal nerve fibres indicates a major role of the autonomous mucosal Innervation in the pathophysiology of intermittent (seasonal) AR.

  • Aspirin-sensitive rhinitis-associated changes in upper Airway Innervation
    The European respiratory journal, 2003
    Co-Authors: D.a. Groneberg, W. Heppt, P. Welker, C. Peiser, Q. Thai Dinh, A. Cryer, M. Zweng, Christian Witt, Axel Fischer
    Abstract:

    Aspirin-sensitive rhinitis is the manifestation of aspirin intolerance in the upper respiratory tract. The disease represents a pseudoallergy against aspirin or related nonsteroidal anti-inflammatory drugs. As a major immunomodulatory role for Airway Innervation has been proposed in Airway inflammatory diseases, the present study assessed changes in human nasal mucosa Innervation in patients with aspirin-sensitive rhinitis in comparison to a control group. Immunohistochemistry for protein gene product 9.5, tachykinins, calcitonin gene-related peptide, vasoactive intestinal peptpeptide (VIP) and neuropeptide tyrosine was performed on cryostats sections of nasal mucosa and neuropeptide containing nerves were examined independently using a score grading. In comparison to the control, the aspirin-sensitive rhinitis group had a significant increase of VIP-like immunoreactivity in mucosal nerve fibres. In contrast to constant numbers of mast cells, highly significant increases in the numbers of eosinophils were found in the group of aspirin-sensitive rhinitis patients. In summary, the present quantification of neuropeptide-immunoreactivity of mucosal nerves demonstrated differences in the human nasal mucosa Innervation between nonrhinitic and aspirin-sensitive rhinitic individuals. These differences may reflect a pathophysiological role of upper Airway Innervation in pseudoallergic reactions.

Janice L. Peake – One of the best experts on this subject based on the ideXlab platform.

  • perinatal environmental tobacco smoke exposure alters the immune response and Airway Innervation in infant primates
    The Journal of Allergy and Clinical Immunology, 2008
    Co-Authors: Xiaomu Zheng, Janice L. Peake, Jesse P. Joad, Kent E. Pinkerton
    Abstract:

    Background Epidemiologic studies associate environmental tobacco smoke (ETS) exposure with childhood asthma. Objective To investigate whether specific pathophysiological alterations that contribute to asthma development in human beings can be induced in infant monkeys after perinatal ETS exposure. Methods Rhesus macaque fetuses/infants were exposed to ETS at 1 mg/m3 of total suspended particulate matter from 50 days gestational age to 2.5 months postnatal age. Inflammatory and neural responses to ETS exposure were measured in the infant monkeys. Results Perinatal ETS exposure could induce systemic and local responses, which include significant elevation of plasma levels of C5a and brain-derived neurotrophic factor, as well as significant increases in pulmonary expression of proinflammatory cytokine TNF-α and TH2 cytokine IL-5, chemokine monocyte chemoattractant protein 1, and the density of substance P–positive nerves along the bronchial epithelium. Perinatal ETS exposure also significantly increased the numbers of mast cells, eosinophils, monocytes, and lymphocytes in the lungs of infant monkeys. In addition, ex vivo measurements showed significantly increased levels of IL-4 and brain-derived neurotrophic factor in the culture supernatant of PBMCs. Interestingly, as an important component of cigarette smoke, LPS was detected in the plasma of infant monkeys subjected to perinatal exposure to ETS. In contrast, an inhibitory effect of perinatal ETS exposure was also observed, which is associated with decreased phagocytic activity of alveolar macrophages and a significantly decreased level of nerve growth factor in the bronchoalveolar lavage fluid. Conclusion Perinatal ETS exposure can induce a TH2-biased inflammatory response and alter Airway Innervation in infant monkeys.

  • Perinatal environmental tobacco smoke exposure alters the immune response and Airway Innervation in infant primates.
    The Journal of allergy and clinical immunology, 2008
    Co-Authors: Xiaomu Zheng, Janice L. Peake, Jesse P. Joad, Kent E. Pinkerton
    Abstract:

    Epidemiologic studies associate environmental tobacco smoke (ETS) exposure with childhood asthma. To investigate whether specific pathophysiological alterations that contribute to asthma development in human beings can be induced in infant monkeys after perinatal ETS exposure. Rhesus macaque fetuses/infants were exposed to ETS at 1 mg/m(3) of total suspended particulate matter from 50 days gestational age to 2.5 months postnatal age. Inflammatory and neural responses to ETS exposure were measured in the infant monkeys. Perinatal ETS exposure could induce systemic and local responses, which include significant elevation of plasma levels of C5a and brain-derived neurotrophic factor, as well as significant increases in pulmonary expression of proinflammatory cytokine TNF-alpha and T(H)2 cytokine IL-5, chemokine monocyte chemoattractant protein 1, and the density of substance P-positive nerves along the bronchial epithelium. Perinatal ETS exposure also significantly increased the numbers of mast cells, eosinophils, monocytes, and lymphocytes in the lungs of infant monkeys. In addition, ex vivo measurements showed significantly increased levels of IL-4 and brain-derived neurotrophic factor in the culture supernatant of PBMCs. Interestingly, as an important component of cigarette smoke, LPS was detected in the plasma of infant monkeys subjected to perinatal exposure to ETS. In contrast, an inhibitory effect of perinatal ETS exposure was also observed, which is associated with decreased phagocytic activity of alveolar macrophages and a significantly decreased level of nerve growth factor in the bronchoalveolar lavage fluid. Perinatal ETS exposure can induce a T(H)2-biased inflammatory response and alter Airway Innervation in infant monkeys.

Xiaomu Zheng – One of the best experts on this subject based on the ideXlab platform.

  • perinatal environmental tobacco smoke exposure alters the immune response and Airway Innervation in infant primates
    The Journal of Allergy and Clinical Immunology, 2008
    Co-Authors: Xiaomu Zheng, Janice L. Peake, Jesse P. Joad, Kent E. Pinkerton
    Abstract:

    Background Epidemiologic studies associate environmental tobacco smoke (ETS) exposure with childhood asthma. Objective To investigate whether specific pathophysiological alterations that contribute to asthma development in human beings can be induced in infant monkeys after perinatal ETS exposure. Methods Rhesus macaque fetuses/infants were exposed to ETS at 1 mg/m3 of total suspended particulate matter from 50 days gestational age to 2.5 months postnatal age. Inflammatory and neural responses to ETS exposure were measured in the infant monkeys. Results Perinatal ETS exposure could induce systemic and local responses, which include significant elevation of plasma levels of C5a and brain-derived neurotrophic factor, as well as significant increases in pulmonary expression of proinflammatory cytokine TNF-α and TH2 cytokine IL-5, chemokine monocyte chemoattractant protein 1, and the density of substance P–positive nerves along the bronchial epithelium. Perinatal ETS exposure also significantly increased the numbers of mast cells, eosinophils, monocytes, and lymphocytes in the lungs of infant monkeys. In addition, ex vivo measurements showed significantly increased levels of IL-4 and brain-derived neurotrophic factor in the culture supernatant of PBMCs. Interestingly, as an important component of cigarette smoke, LPS was detected in the plasma of infant monkeys subjected to perinatal exposure to ETS. In contrast, an inhibitory effect of perinatal ETS exposure was also observed, which is associated with decreased phagocytic activity of alveolar macrophages and a significantly decreased level of nerve growth factor in the bronchoalveolar lavage fluid. Conclusion Perinatal ETS exposure can induce a TH2-biased inflammatory response and alter Airway Innervation in infant monkeys.

  • Perinatal environmental tobacco smoke exposure alters the immune response and Airway Innervation in infant primates.
    The Journal of allergy and clinical immunology, 2008
    Co-Authors: Xiaomu Zheng, Janice L. Peake, Jesse P. Joad, Kent E. Pinkerton
    Abstract:

    Epidemiologic studies associate environmental tobacco smoke (ETS) exposure with childhood asthma. To investigate whether specific pathophysiological alterations that contribute to asthma development in human beings can be induced in infant monkeys after perinatal ETS exposure. Rhesus macaque fetuses/infants were exposed to ETS at 1 mg/m(3) of total suspended particulate matter from 50 days gestational age to 2.5 months postnatal age. Inflammatory and neural responses to ETS exposure were measured in the infant monkeys. Perinatal ETS exposure could induce systemic and local responses, which include significant elevation of plasma levels of C5a and brain-derived neurotrophic factor, as well as significant increases in pulmonary expression of proinflammatory cytokine TNF-alpha and T(H)2 cytokine IL-5, chemokine monocyte chemoattractant protein 1, and the density of substance P-positive nerves along the bronchial epithelium. Perinatal ETS exposure also significantly increased the numbers of mast cells, eosinophils, monocytes, and lymphocytes in the lungs of infant monkeys. In addition, ex vivo measurements showed significantly increased levels of IL-4 and brain-derived neurotrophic factor in the culture supernatant of PBMCs. Interestingly, as an important component of cigarette smoke, LPS was detected in the plasma of infant monkeys subjected to perinatal exposure to ETS. In contrast, an inhibitory effect of perinatal ETS exposure was also observed, which is associated with decreased phagocytic activity of alveolar macrophages and a significantly decreased level of nerve growth factor in the bronchoalveolar lavage fluid. Perinatal ETS exposure can induce a T(H)2-biased inflammatory response and alter Airway Innervation in infant monkeys.