The adjuvant activity of diesel exhaust particles and carbon black on systemic IgE production to ovalbumin in mice after intranasal instillation

Nilsen, Asbjørn Magne; Hagemann, Randi; Eide, Ingvar

doi:10.1016/s0300-483x(97)00150-9

Cited by 39 publications

(26 citation statements)

References 18 publications

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“…The DEP quality was the same as that used by Nilsen et al [29]and Lovik et al [30]. DEP particle size was approximately 0.03 µm, as determined by transmission electron microscope, and specific surface area was 64 m 2 /g according to the Braunauer-Emmet-Teller (BET) method [31].…”

Section: Methodsmentioning

confidence: 99%

“…IL-4, IL-5, IL-6, IL-10 and IL-13 mRNA expression was significantly enhanced, while that of IFNγ was significantly reduced when DEP were instilled with the allergen. Numerous independent observations have supported the view that DEP may act as an exacerbating adjuvant in IgE-based airway inflammation [5, 29]. However, the mechanisms of this effect are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

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Reduction of IL-12 p40 Production in Activated Monocytes after Exposure to Diesel Exhaust Particles

Nilsen

Hagemann²,

Eikås³

et al. 2003

Int Arch Allergy Immunol

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Background: A reduction of IL-12 production by lung macrophages may partly explain the presumed adjuvant effect of diesel exhaust particles (DEP) in allergy and asthma. IL-12 stimulates T helper type 1 (Th1) lymphocytes, which inhibit Th2 cells via Th1-specific cytokines. The aim of this study was to investigate the influence of DEP on the production of IL-12 p40 in lipopolysaccharide (LPS)-activated monocytes. Methods: The human monocytic cell line Mono-Mac-6 was stimulated with LPS (200 ng/ml) and grown with DEP (0–200 µg/ml) for 0, 6 or 24 h. IL-12 p40 and the pro-inflammatory cytokine TNF were analysed in the cell supernatants by ELISA and a cell assay, respectively. Results: Levels of IL-12 p40 correlated inversely with the DEP exposure concentrations, whereas TNF increased in parallel to the DEP concentrations. At a DEP concentration of 200 µg/ml, the amount of IL-12 p40 was 35% of that observed without DEP. The corresponding TNF value was 230% of the control. Reduced viability, binding of cytokines to DEP or endotoxin in the DEP samples cannot fully explain the changes in the concentrations of these two cytokines. Conclusion: DEP seem to inhibit the production of IL-12 p40 and stimulate that of TNF in activated monocytes. This may partly explain the presumed adjuvant effect of DEP in atopy; by altering the Th1/Th2 balance via down-regulation of IL-12, the Th2 response characteristic of allergy and asthma may be favoured.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Reduction of IL-12 p40 Production in Activated Monocytes after Exposure to Diesel Exhaust Particles

Nilsen

Hagemann²,

Eikås³

et al. 2003

Int Arch Allergy Immunol

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“…In order to elucidate whether the carbon core of the DEPs or the adsorbed organic substance is responsible for the effect [60], mice were immunized four times with either OA, OA with DEPs or OA with carbon black (carbon black). Speci®c IgE for OA was then analysed.…”

Section: In Vivo Studiesmentioning

confidence: 99%

Health effects of diesel exhaust emissions

et al. 2001

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Epidemiological studies have demonstrated an association between different levels of air pollution and various health outcomes including mortality, exacerbation of asthma, chronic bronchitis, respiratory tract infections, ischaemic heart disease and stroke. Of the motor vehicle generated air pollutants, diesel exhaust particles account for a highly significant percentage of the particles emitted in many towns and cities. This review is therefore focused on the health effects of diesel exhaust, and especially the particular matter components.Acute effects of diesel exhaust exposure include irritation of the nose and eyes, lung function changes, respiratory changes, headache, fatigue and nausea. Chronic exposures are associated with cough, sputum production and lung function decrements. In addition to symptoms, exposure studies in healthy humans have documented a number of profound inflammatory changes in the airways, notably, before changes in pulmonary function can be detected. It is likely that such effects may be even more detrimental in asthmatics and other subjects with compromised pulmonary function.There are also observations supporting the hypothesis that diesel exhaust is one important factor contributing to the allergy pandemic. For example, in many experimental systems, diesel exhaust particles can be shown to act as adjuvants to allergen and hence increase the sensitization response.Much of the research on adverse effects of diesel exhaust, bothin vivoandin vitro, has however been conducted in animals. Questions remain concerning the relevance of exposure levels and whether findings in such models can be extrapolated into humans. It is therefore imperative to further assess acute and chronic effects of diesel exhaust in mechanistic studies with careful consideration of exposure levels. Whenever possible and ethically justified, studies should be carried out in humans.

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“…However, many of these studies show a diversity of routes of administration. The intraperitoneal (Miyabara et al, 1998;Suzuki et al, 1993;Heo et al, 2001), intranasal (Takafuji et al, 1987;Fujimaki et al, 1997;Nilsen et al, 1997), aerosol Goldsmith et al, 2002), intratracheal Al Humadi et al, 2002), and subcutaneous (van Zijverden et al, 2000;Lovik et al, 1997) routes of administration and their combinations have all been used.…”

Section: In Comparison With Responses Observed By Intraperitoneal (Ipmentioning

confidence: 99%

Optimization of Route of Administration for Coexposure to Ovalbumin and Particle Matter to Induce Adjuvant Activity in Respiratory Allergy in the Mouse

Steerenberg

Dalen

Withagen

et al. 2003

Inhalation Toxicology

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Epidemiological and experimental studies have not only shown that air pollution induces increased pulmonary morbidity, and mortality, but also that air pollution components may potentiate allergic responses. The respiratory allergy model to ovalbumin in the mouse has been shown a useful tool to characterize the adjuvant potency of air pollution components. However, the choice for the most effective route of administration for testing small amounts of air pollution component is hampered by the diversity of routes of administration used. To test the adjuvant activity of airborne particles (Ottawa dust EHC-93), we studied the optimal route of respiratory administration: intranasally (in) and aerosol (aero) in comparison with responses observed by intraperitoneal (ip) with diesel exhaust particles (DEP) as a positive control. Our results show that the combination of in/aero with ovalbumin caused almost similar immunoglobulin (Ig)E and inflammatory responses compared to the ip/aero. In/in application induced less responses for IgE, less inflammation in the lung, and less increased numbers of eosinophils in the bronchoalveolar lavage (BAL). This response increased dramatically when ovalbumin was coadministered with DEP. Subsequently, EHC-93, which is made up of airborne particles, was tested via the in/in route of administration. EHC-93 induced similar IgE responses, inflammation, and eosinophilic response in BAL compared to DEP. In addition, EHC-93 increased the airway responsiveness of the ovalbumin-sensitized mice measured in unrestrained condition and not in nonsensitized control mice. It is concluded that intranasal sensitization with intranasal challenge with airborne particles (EHC-93) is an effective route of administration to show potency of adjuvant activity of airborne particles.

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The adjuvant activity of diesel exhaust particles and carbon black on systemic IgE production to ovalbumin in mice after intranasal instillation

Cited by 39 publications

References 18 publications

Reduction of IL-12 p40 Production in Activated Monocytes after Exposure to Diesel Exhaust Particles

Reduction of IL-12 p40 Production in Activated Monocytes after Exposure to Diesel Exhaust Particles

Health effects of diesel exhaust emissions

Optimization of Route of Administration for Coexposure to Ovalbumin and Particle Matter to Induce Adjuvant Activity in Respiratory Allergy in the Mouse

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