Early Response of Lungs to Low Levels of Nitrogen Dioxide

Stephens, Robert J.; Freeman, Gustave; Evans, Michael J.

doi:10.1080/00039896.1972.10666066

Cited by 201 publications

(64 citation statements)

References 15 publications

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“…25 In animal studies, inhaled NO 2 at ϳ2 ppm affected alveolar development and surfactant production, altered the epithelial lining of the terminal bronchioles, and induced loss of cilia. 21,26,27 In human studies, inhaled NO 2 at ϳ2 ppm affected alveolar permeability 28 and increased airway responsiveness. 29 In another study in humans, alterations of airway reactivity have been reported at exposures as low as 1.5 ppm NO 2 .…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Delivery by Neonatal Noninvasive Respiratory Support Devices

et al. 2014

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Section: Discussionmentioning

confidence: 99%

Nitric Oxide Delivery by Neonatal Noninvasive Respiratory Support Devices

et al. 2014

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“…"Neurogenic switching is proposed to result when a sensory impulse from a site of activation is rerouted via the central nervous system to a distant location to produce neurogenic inflammation at the second location" (46). (20).…”

Section: Individual Ids Descriptionsmentioning

confidence: 99%

“…The range of physical action for tolerance includes multiple tolerance instances, mechanisms, and symptoms involving multiple organ systems (7,20,(47)(48)(49)(50)(51)(52)(53)(54)(55) (56).…”

Section: Individual Ids Descriptionsmentioning

confidence: 99%

“…If (20) and is followed by pathologic tissue changes; c) a child raised in an environment of severe abuse and neglect and without any caring adult support frequently will evolve a coping pattern that includes changes in, among other things, SR to aggressive situations, involving catecholamine, cortisol, serotonin, and endogenous opioid response changes (21).…”

Section: Ids Disease Production Model Typesmentioning

confidence: 99%

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Integrated Defense System Overlaps as a Disease Model: With Examples for Multiple Chemical Sensitivity

Rowat¹

1998

Environmental Health Perspectives

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“…The mechanisms underlying epithelial hyperfragility and cell loss are likely to encompass contributions from varied sources that range from physicochemical factors such as stress distortion caused by sub-epithelial hydrostatic pressure, to outright cellular necrosis caused by mediators released from inflammatory cells (Robinson, 1995) or caused by the direct effects of inhaled noxious chemicals (Stephens et al, 1972;Vai et al, 1980;Welsh et al, 1985). In asthma, eosinophils are thought to be significant participants in these injury processes as a consequence of their repertoire of potent inflammatory mediators and toxic, granule-derived proteins (Filley et al, 1982;Jeffery et al, 1989;Djukanovic et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Augmentation by eosinophils of gelatinase activity in the airway mucosa: comparative effects as a putative mediator of epithelial injury

Herbert

Arthur

Robinson

1996

British J Pharmacology

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We have studied the release of gelatin‐degrading enzymes from isolated sheets of bronchial mucosa in the presence and absence of eosinophils. Isolated sheets of bovine bronchial mucosa released gelatin‐degrading activity in similar amounts from both the apical and basolateral aspects of the tissue. Gelatinolytic activity could not be increased by treatment of the mucosal sheets with calcium ionophore, A23187. The activity of the released gelatinases could be inhibited by chelation of divalent cations or by the matrix metalloproteinase inhibitors, BB‐94 and BB‐250. However, inhibitors of serine proteinases, or of cysteine proteinases were without effect. In zymography, major bands of gelatin‐degrading activity consistent with gelatinases A and B were identified. Addition of guinea‐pig eosinophils to the basolateral aspect of bronchial mucosa for 60 min resulted in an increase in the gelatinolytic activity of the conditioned medium, irrespective of whether the eosinophils were stimulated with ionophore A23187 or not. However, only ionophore‐stimulated eosinophils reacted to produce sufficient tissue damage to increase the transepithelial flux of serum albumin. Purified eosinophils were a poor source of gelatinolytic activity, indicating that when interacting with the bronchial mucosa their effect is to increase the apparent release and/or activation of gelatinases derived from the airway mucosa. After organomercurial activation, recombinant human progelatinase A increased the permeability of the bronchial mucosa to mannitol. However, the activity of enzyme and duration of exposure required to do this were greater than the amounts of gelatinase activity detected during eosinophil‐mediated injury. Sheets of airway mucosa were also resistant to injury evoked by high concentrations of hydrogen peroxide or plasmin. Collectively, these results suggest that if gelatinases are involved in eosinophil‐mediated injury and repair of the bronchial mucosa, they require other mediators to act in concert to bring about outright epithelial cell detachment. This does not preclude the possibility that gelatinases are crucial in rendering the airway mucosa hyperfragile.

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Early Response of Lungs to Low Levels of Nitrogen Dioxide

Cited by 201 publications

References 15 publications

Nitric Oxide Delivery by Neonatal Noninvasive Respiratory Support Devices

Nitric Oxide Delivery by Neonatal Noninvasive Respiratory Support Devices

Integrated Defense System Overlaps as a Disease Model: With Examples for Multiple Chemical Sensitivity

Augmentation by eosinophils of gelatinase activity in the airway mucosa: comparative effects as a putative mediator of epithelial injury

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