Ozone Exposure may Enhance Airway Smooth Muscle Contraction by Increasing Ca2+ Refilling of Sarcoplasmic Reticulum in Guinea Pig

Yoshida, Makoto; Aizawa, Hisamichi; Inoue, Hiromasa; Kojima, Hiroshi; Nakano, Hirofumi; Komori, Motofumi; Fukuyama, Satoru; Hara, Nobuyuki

doi:10.1006/pupt.2001.0324

Cited by 5 publications

(5 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We observed no baseline differences in bronchial ring contractile response in unexposed (Figure 7A) or LPS-exposed mindin –/– or C57BL/6J mice (Figure 7B). However, we did observe significant mindin-dependent differences in bronchial ring contractility to carbachol 24 hr after inhalation of ozone (Figure 7C), in agreement with previous data suggesting that inhalation of ozone may enhance airway smooth muscle contraction (Yoshida et al 2002). Together, these observations support that mindin contributes to airway smooth muscle contractility after inhalation of ozone but not at baseline or after inhalation of LPS.…”

Section: Resultssupporting

confidence: 92%

Retracted: The Role of the Extracellular Matrix Protein Mindin in AirwayResponse to Environmental Airways Injury

Frush

Potts

et al. 2011

Environ Health Perspect

View full text Add to dashboard Cite

Background: Our previous work demonstrated that the extracellular matrix protein mindin contributes to allergic airways disease. However, the role of mindin in nonallergic airways disease has not previously been explored.Objectives: We hypothesized that mindin would contribute to airways disease after inhalation of either lipopolysaccharide (LPS) or ozone.Methods: We exposed C57BL/6J and mindin-deficient (–/–) mice to aerosolized LPS (0.9 μg/m3 for 2.5 hr), saline, ozone (1 ppm for 3 hr), or filtered air (FA). All mice were evaluated 4 hr after LPS/saline  exposure or 24 hr after ozone/FA exposure. We characterized the physiological and biological responses by analysis of airway hyperresponsiveness (AHR) with a computer-controlled small-animal ventilator (FlexiVent), inflammatory cellular recruitment, total protein in bronchoalveolar lavage fluid (BALF), proinflammatory cytokine profiling, and ex vivo bronchial ring studies.Results: After inhalation of LPS, mindin–/– mice demonstrated significantly reduced total cell and neutrophil recruitment into the airspace compared with their wild-type counterparts. Mindin–/– mice also exhibited reduced proinflammatory cytokine production and lower AHR to methacholine challenge by FlexiVent. After inhalation of ozone, mice had no detectible differences in cellular inflammation or total BALF protein dependent on mindin. However, mindin–/– mice were protected from increased proinflammatory cytokine production and AHR compared with their C57BL/6J counterparts. After ozone exposure, bronchial rings derived from mindin–/– mice demonstrated reduced constriction in response to carbachol.Conclusions: These data demonstrate that the extracellular matrix protein mindin modifies the airway response to both LPS and ozone. Our data support a conserved role of mindin in production of proinflammatory cytokines and the development of AHR in two divergent models of reactive airways disease, as well as a role of mindin in airway smooth muscle contractility after exposure to ozone.

show abstract

Section: Resultssupporting

confidence: 92%

Retracted: The Role of the Extracellular Matrix Protein Mindin in AirwayResponse to Environmental Airways Injury

Frush

Potts

et al. 2011

Environ Health Perspect

View full text Add to dashboard Cite

show abstract

“…However, we did observe significant mindindependent differences in bronchial ring contractility to carbachol 24 hr after inhalation of ozone ( Figure 7C), in agreement with previous data suggesting that inhalation of ozone may enhance airway smooth muscle contraction (Yoshida et al 2002). Together, these observations support that mindin contributes to airway smooth muscle contractility after inhalation of ozone but not at baseline or after inhalation of LPS.…”

Section: Mindin-dependent Response To Inhaled Lpssupporting

confidence: 92%

The Role Of Extracellular Matrix Protein Mindin In Airway Response To Environmental Airways Injury

Frush¹,

Li²,

Potts³

et al. 2011

A36. Early Exposures and Environmental Exposures That Influence Allergy and Lung Disease

View full text Add to dashboard Cite

This article is being retracted at the request of the authors because of concerns about the accuracy of the initial data from the animal physiology laboratory at Duke University. The authors re-exported source data from the animal ventilator (FlexiVent) and compared the output with the raw data originally received from the animal pulmonary physiology laboratory. The results from these initial comparisons suggested potential inconsistencies in the data, so the authors requested that an independent laboratory replicate the experiments of animal airway physiology presented in Figure 1 and Figure 4. The results of the replicated experiments validated the originally reported central role of mindin in airway hyper-responsiveness after exposure to either lipopolysaccharide (LPS) or ozone.Because the animal physiology laboratory at Duke University also analyzed cytokines, the authors had an independent laboratory replicate experiments to analyze the original role of cytokines reported in Figure 3 and Figure 6. In these replicate studies, which were limited in the number of animals and samples tested, the authors did not observe the same results and could not definitively determine whether or not the findings were valid.The inconsistent results led the authors to take a conservative approach, and they agreed to retract this paper. They regret any inconvenience to the scientific community.

show abstract

“…The mechanisms underlying this phenomenon are also documented in the literature, including O 3 -induced elevated oxidative products (33,34); increased cholinergic neurotransmission (30,35); and direct stimulation of the airway sensory nerve (36). Although worldwide agreement has been reached in that O 3 can increase the airway smooth muscle contraction of various species (37)(38)(39), it is not clear whether O 3 can similarly influence an "irritated" airway smooth muscle in an experimental asthma model. Kierstein, S. and colleagues exposed their Aspergillus fumigatus-sensitized/-challenged mice to 3 ppm O 3 for 3 h, 82 h after the last challenge, and found that O 3 increased the P enh reaction to the agonist in both the control and asthma groups, but exclusively enhanced the contractility of the tracheal smooth muscle ring of the latter.…”

Section: Discussionmentioning

confidence: 99%

Consequences of acute ozone exposure imposed on the culminated allergic pulmonary inflammation in an established murine model of asthma

Bao

Li²,

Li³

et al. 2013

Front Biosci

View full text Add to dashboard Cite

Asthma exacerbations are often triggered by air pollution, including O3, whereas how patients with asthma exacerbations react to high levels of ambient ozone remain unknown. Here, we investigated the manner in which acute ozone exposure affects the pathophysiological characteristics of an asthma model on the premise of culminated allergic airway inflammation. The asthma model was constructed in mice, and enhanced pause (Penh), total and differential cell number, soluble mediator concentration, histopathology, and Muc5ac mRNA expression in the mice were observed. The results showed that ozone could induce airway hyperresponsiveness (AHR) in controls and an additional enhancement of preexisting AHR in asthmatic mice. When exposed to ozone, the asthmatic mice expressed more neutrophils, TNF-α, IL-13, and hyaluronan in bronchoalveolar lavage than controls. The mice with asthma and the controls both showed decreased epithelial cell density in the proximal and distal airways. Ozone aggravated the increased mucus production and mucin gene expression in mice with asthma. These results show that subjects with asthma may react differently to the same high level of ambient ozone, especially for those with asthma exacerbations.

show abstract

Ozone Exposure may Enhance Airway Smooth Muscle Contraction by Increasing Ca2+ Refilling of Sarcoplasmic Reticulum in Guinea Pig

Cited by 5 publications

References 19 publications

Retracted: The Role of the Extracellular Matrix Protein Mindin in AirwayResponse to Environmental Airways Injury

Retracted: The Role of the Extracellular Matrix Protein Mindin in AirwayResponse to Environmental Airways Injury

The Role Of Extracellular Matrix Protein Mindin In Airway Response To Environmental Airways Injury

Consequences of acute ozone exposure imposed on the culminated allergic pulmonary inflammation in an established murine model of asthma

Contact Info

Product

Resources

About