Inhaled chemicals may enhance allergic airway inflammation in ovalbumin-sensitised mice

Ban, M.; Langonné, Isabelle; Huguet, Nelly; Pépin, Elsa; Morel, G.

doi:10.1016/j.tox.2006.06.012

Cited by 22 publications

(10 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A recent study with latex NPs has shown the inability of NPs to increase eosinophilic lung inflammation in the OVA model of asthma [44]. Modulation of OVA-induced asthma in mouse model by TDI [45] or bakery flour has also been reported [46]. Particle exposure in the lung leads to macrophage recruitment and, during concomitant challenge with TDI, a significant augmentation of neutrophilic chemoattraction was observed.…”

Section: Discussionmentioning

confidence: 95%

Lung exposure to nanoparticles modulates an asthmatic response in a mouse model

Hussain¹,

Vanoirbeek²,

Luyts³

et al. 2010

Eur Respir J

147

110

View full text Add to dashboard Cite

The aim of this study was to investigate the modulation of an asthmatic response by titanium dioxide (TiO 2 ) or gold (Au) nanoparticles (NPs) in a murine model of diisocyanateinduced asthma.On days 1 and 8, BALB/c mice received 0.3% toluene diisocyanate (TDI) or the vehicle acetoneolive oil (AOO) on the dorsum of both ears (20 mL). On day 14, the mice were oropharyngeally dosed with 40 mL of a NP suspension (0.4 mg?mL -1 (,0.8 mg?kg -1 ) TiO 2 or Au). 1 day later (day 15), the mice received an oropharyngeal challenge with 0.01% TDI (20 mL). On day 16, airway hyperreactivity (AHR), bronchoalveolar lavage (BAL) cell and cytokine analysis, lung histology, and total serum immunoglobulin E were assessed. NP exposure in sensitised mice led to a two-(TiO 2 ) or three-fold (Au) increase in AHR, and a three-(TiO 2 ) or five-fold (Au) increase in BAL total cell counts, mainly comprising neutrophils and macrophages. The NPs taken up by BAL macrophages were identified by energy dispersive X-ray spectroscopy. Histological analysis revealed increased oedema, epithelial damage and inflammation.In conclusion, these results show that a low, intrapulmonary doses of TiO 2 or Au NPs can aggravate pulmonary inflammation and AHR in a mouse model of diisocyanate-induced asthma.

show abstract

Section: Discussionmentioning

confidence: 95%

Lung exposure to nanoparticles modulates an asthmatic response in a mouse model

Hussain¹,

Vanoirbeek²,

Luyts³

et al. 2010

Eur Respir J

147

110

View full text Add to dashboard Cite

show abstract

“…Apparently the dermal uptake is of greater importance than the inhalation dose alone; the estimated dermal contribution is even 80% (40). In an ovalbumin (OVA)‐sensitized mice model of asthma, exposure to chloroform inhalation during the sensitization period exacerbated the inflammatory reaction after allergen challenges (41). Even exposure to the chloroform alone, without concomitant sensitization, potentiated IL‐5 production by the lymph node cells (41).…”

Section: Swimmers Asthma – Example Of Complex Mechanismsmentioning

confidence: 99%

Mechanisms of asthma in Olympic athletes – practical implications

Haahtela

Malmberg

Moreira

2008

Allergy

View full text Add to dashboard Cite

Athletes’ symptoms may only occur in extreme conditions, which are far from normal. Exercise may increase ventilation up to 200 l/min for short periods in speed and power athletes, and for longer periods in endurance athletes such as swimmers and cross‐country skiers. Increasing proportions of young athletes are atopic, i.e. they show signs of IgE‐mediated allergy which is, along with the sport event (endurance sport), a major risk factor for asthma and respiratory symptoms. Mechanisms in the etiology and clinical phenotypes vary between disciplines and individuals, and it may be an oversimplification to discuss athlete’s asthma as a distinct and unambiguous disease. Nevertheless, the experience on Finnish Olympic athletes suggests at least two different clinical phenotypes, which may reflect different underlying mechanisms. The pattern of ‘classical asthma’ is characterized by early onset childhood asthma, methacholine responsiveness, atopy and signs of eosinophilic airway inflammation, reflected by increased exhaled nitric oxide levels. Another distinct phenotype includes late onset symptoms (during sports career), bronchial responsiveness to eucapnic hyperventilation test, but not necessarily to inhaled methacholine, and a variable association with atopic markers and nitric oxide. A mixed type of eosinophilic and neutrophilic airway inflammation seems to affect especially swimmers, ice‐hockey players, and cross‐country skiers. The inflammation may represent a multifactorial trauma, in which both allergic and irritant mechanisms play a role. There is a significant problem of both under‐ and overdiagnosing asthma in athletes and the need for objective testing is emphasized. Follow‐up studies are needed to assess the temporal relationship between asthma and competitive sporting, taking better into account individual disposition, environmental factors (exposure), intensity of training and potential confounders.

show abstract

“…Development of allergic respiratory diseases requires sensitization, which may be triggered by dermal or respiratory exposure to the sensitizing chemical [4]. Airways are also exposed to irritants which are noncorrosive chemicals that cause a reversible inflammatory change of the bronchial mucosa [5 ].…”

Section: Introductionmentioning

confidence: 99%

Pesticides and asthma

Hernández

Parrón²,

Alarcón³

2011

Current Opinion in Allergy &Amp; Clinical Immunology

138

View full text Add to dashboard Cite

Many pesticides are sensitizers or irritants capable of directly damaging the bronchial mucosa, thus making the airway very sensitive to allergens or other stimuli. However, most pesticides are weakly immunogenic so that their potential to sensitize airways in exposed populations is limited. Pesticides may increase the risk of developing asthma, exacerbate a previous asthmatic condition or even trigger asthma attacks by increasing bronchial hyper-responsiveness.

show abstract

Inhaled chemicals may enhance allergic airway inflammation in ovalbumin-sensitised mice

Cited by 22 publications

References 31 publications

Lung exposure to nanoparticles modulates an asthmatic response in a mouse model

Lung exposure to nanoparticles modulates an asthmatic response in a mouse model

Mechanisms of asthma in Olympic athletes – practical implications

Pesticides and asthma

Contact Info

Product

Resources

About