Ozone-Induced Stimulation of Pulmonary Sympathetic Fibers: A Protective Mechanism against Edema

Delaunois, Annie; Segura, Patricia; Dessy-Doize, C.; Ansay, Michel; Montaño, Luis M.; Vargas, Mario H.; Gustin, Pascal

doi:10.1006/taap.1997.8266

Cited by 8 publications

(5 citation statements)

References 35 publications

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“…Experiments utilizing residual oil fly ash (Veronesi and Oortgiesen 2001) have demonstrated that afferent neural fibers play a crucial role in mediating a variety of inflammatory mechanisms following airborne pollutant exposure. Additional studies have indicated that these nerves are sensitive to many air pollutants, such as ozone (Jimba et al 1995;Delaunois et al 1997), SO 2 (Long et al 1999), NO 2 (Lucchini et al 1996;Joad et al 1997), and cigarette smoke (Bonham et al 1996). However, molecular tachykinergic mechanisms are relatively unknown in the pathogenesis of DE-induced inflammatory responses.…”

Section: Introductionmentioning

confidence: 97%

Tachykinin substance P signaling involved in diesel exhaust-induced bronchopulmonary neurogenic inflammation in rats

Wong

Sun

Keith

et al. 2003

Archives of Toxicology

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This study characterizes the molecular neurotoxicity of diesel exhaust (DE) on the tachykinin substance P (SP) signaling system in the lungs. A total of 96 female Fischer 344/NH rats (approximately 175 g, approximately 4 weeks old) were randomly assigned to eight groups in a 2 x4 factorial design: capsaicin versus non-capsaicin (vehicle) pretreatment, and filtered room air versus two exposure levels of DE with diesel engine room control. The rats were exposed nose-only to room air or low (35.3 micro g/m(3)) and high concentrations (669.3 micro g/m(3)) particulates directly from a Cummins N14 research engine at 75% throttle for 4 h/day, 5 days/week, for 3 weeks. The findings showed that exposure to DE dose-dependently induced bronchopulmonary neurogenic inflammation, both in capsaicin- and vehicle-pretreated rats, as measured by plasma extravasation, edema, and inflammatory cells. DE inhalation affected the SP signaling processes, including stored SP depletion and the gene/protein overexpression for neurokinin-1 receptor. DE also significantly reduced the activity of neutral endopeptidase, a main degradation enzyme for SP. Consequently, these changes may be regarded as critical factors that switched neurogenic pulmonary responses from their protective functions to a detrimental role that perpetuates lung inflammation. These changes may possibly be associated with the mass concentration of DE particles due to their physico-chemical characteristics. Moreover, capsaicin-pretreated rats had more sensitivity to these levels of DE exposure due to stimulation of bronchopulmonary C-fibers. However, the effects of capsaicin treatment were not consistent and apparent in this study. Taken together, our findings suggest that neurokininergic mechanisms may possibly be involved in DE-induced lung inflammation, but that bronchopulmonary C-fibers did not dominate DE-induced inflammatory abnormalities.

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Section: Introductionmentioning

confidence: 97%

Tachykinin substance P signaling involved in diesel exhaust-induced bronchopulmonary neurogenic inflammation in rats

Wong

Sun

Keith

et al. 2003

Archives of Toxicology

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“…This "inhibitory" effect of O 3 , which appeared rather surprising since the gas is a well-known pulmonary edema inducer (Alpert et al, 1973;Plopper et al, 1973), has been interpreted as a stress response of the organism, partly involving pulmonary sympathetic fiber activation with subsequent release of catecholamines and neuropeptide Y (Delaunois et al, 1997). However, the involvement of other mechanisms, in particular depending on CYP450, was not investigated in this work.…”

mentioning

confidence: 76%

“…After exposure to 0.4 ppm O 3 for 4 h, the increase in K f,c induced by ACh (Figure 1) but also by substance P (Delaunois et al, 1997) in isolated rabbit lungs was completely inhibited. This "protective" effect of O 3 against pulmonary edema appears rather surprising, Since O 3 is a wellknown edema inducer (Alpert et al, 1973;Plopper et al, 1973).…”

Section: Figurementioning

confidence: 89%

“…Alterations of Clara cells and alveolar type II pneumocytes, which have been reported to contain high amounts of CYP450 (Boyd, 1977;Devereux, 1984), could also be involved. However, electron microscopy studies performed on lung tissue isolated from rabbits immediately after their exposure to O 3 did not reveal damage in these cells (Delaunois et al, 1997).…”

Section: Figurementioning

confidence: 98%

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INTERACTIONS BETWEEN CYTOCHROME P-450 ACTIVITIES AND OZONE-INDUCED MODULATORY EFFECTS ON ENDOTHELIAL PERMEABILITY IN RABBIT LUNGS: Influence of Gender

Delaunois

Florquin

Segura

et al. 1999

Inhalation Toxicology

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The effects of rabbit exposure to ozone (O(3)) (0.4 ppm for 4 h) on two different cytochrome P-450 (CYP450)-dependent activities were investigated. In turn, the role of CYP450 in the inhibitory effect of O(3) on acetylcholine (ACh)-evoked increase in endothelial permeability was also assessed. Immediately after the period of exposure, rabbits of both sexes were sacrificed and their lungs were extracted. Some lungs were used for preparation of microsomes and measurement of 7-ethoxyresorufin O-deethylase (EROD) and parathion oxidase activities. Other rabbit lungs were isolated and recirculatingly blood-free perfused. Arterial, venous pressures, and lung weight were continuously recorded. Capillary pressure was measured by applying the double occlusion method. Capillary filtration coefficient (K(f,c)) was evaluated by measuring the amount of fluid filtering through the endothelium when vascular pressures were suddenly increased. Dose-response curves to ACh were constructed in air- or O(3)-exposed rabbits. Some animals were pretreated with piperonyl butoxide (PBO), a well-known inhibitor of CYP450. O(3) significantly reduced both EROD and parathion oxidase lung microsomal activities in females, while it had no effect in males. Exposure to O(3) strongly inhibited the ACh-induced increase in K(f,c). Pretreatment with PBO reversed the modulatory effect of O(3) on endothelial permeability in male rabbits, but not in females. It was concluded (1) that inhibition of 2 different CYP450-dependent activities after exposure to 0.4 ppm O(3) for 4 h appears to be a gender-dependent phenomenon, and (2) that CYP450 is probably involved in the O(3)-evoked inhibitory mechanism against ACh-induced increase in endothelial permeability, but only in males.

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“…OT can reduce pain because ozone increases the synthesis of superoxide dismutase, malondialdehyde, catalase, and the local release of catecholamines. 26 Besides, interleukin-6 and tumor necrosis factor-α levels in the synovial liquid of the TMJ are reduced. 27 This represents an increase in the threshold and a reduction in the responsiveness at the peripheral sensory nerve fibers.…”

Section: Discussionmentioning

confidence: 99%

Ozone for the treatment of temporomandibular joint disorders: a systematic review and meta-analysis

et al. 2023

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Temporomandibular joint disorders (TMD) generate pain and difficulties for mouth opening affecting the patients’ quality of life. Ozone is an emerging therapy that has been proposed as a potential treatment, due to that, the evidence about its efficacy should be reviewed. Therefore, this work aimed to conduct a comprehensive systematic review to address the efficacy of ozone therapy for the treatment of pain and limited mouth opening in patients with TMD. The design of the included studies was clinical trials and observational studies, whereas, a series of cases, in vivo, and in vitro studies were excluded. The search was performed in PubMed, ClinicalTrials, Web of Science, and Scopus. Gray literature was searched at Google Scholar. Relevant data of all included studies were recorded. The risk of bias (using RoB 2) and the quality (using Grading of Recommendations Assessment, Development, and Evaluation) assessments were carried out. Meta-analyses using random-effects models of pain and maximal mouth opening data were performed. This review included 8 studies with 404 participants suffering limited function and pain related to TMD. At the overall bias of the studies, 25% exhibited some concerns and 75% had high risk; and the quality of the studies was low. The analysis of the included studies suggests that ozone therapy can diminish pain and improve the maximal mouth opening in TMD patients. However, there is no conclusive evidence of ozone therapy as a superior treatment for TMD compared with occlusal splint and pharmacotherapy.

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Ozone-Induced Stimulation of Pulmonary Sympathetic Fibers: A Protective Mechanism against Edema

Cited by 8 publications

References 35 publications

Tachykinin substance P signaling involved in diesel exhaust-induced bronchopulmonary neurogenic inflammation in rats

Tachykinin substance P signaling involved in diesel exhaust-induced bronchopulmonary neurogenic inflammation in rats

INTERACTIONS BETWEEN CYTOCHROME P-450 ACTIVITIES AND OZONE-INDUCED MODULATORY EFFECTS ON ENDOTHELIAL PERMEABILITY IN RABBIT LUNGS: Influence of Gender

Ozone for the treatment of temporomandibular joint disorders: a systematic review and meta-analysis

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