Mouse models to unravel the role of inhaled pollutants on allergic sensitization and airway inflammation

Maes, Tania; Provoost, Sharen; Lanckacker, Ellen; Cataldo, Didier; Vanoirbeek, Jeroen; Nemery, Benoît; Tournoy, Kurt G.; Joos, Guy

doi:10.1186/1465-9921-11-7

Cited by 82 publications

(98 citation statements)

References 186 publications

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“…The sequence of cellular events may exacerbate asthma symptoms, as reflected in the allergic reactions. Furthermore, the recruitment of eosinophils in the lungs is primarily controlled by Th lymphocytes and is enhanced by cytokines (eg, IL-13); 38 infiltration is characteristic of airway inflammation during bronchial asthma. Lymphocytes, including T and B cells, are considered cells of the adaptive immune system.…”

Section: Discussionmentioning

confidence: 99%

Allergenicity and toxicology of inhaled silver nanoparticles in allergen-provocation mice models

Chuang¹,

Hsiao²,

Wu³

et al. 2013

IJN

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Silver nanoparticles (AgNP) have been associated with the exacerbation of airway hyperresponsiveness. However, the allergenicity and toxicology of AgNP in healthy and allergic individuals are unclear. We investigated the pathophysiological responses to AgNP inhalation in a murine model of asthma. Continuous and stable levels of 33 nm AgNP were maintained at 3.3 mg/m 3 during the experimental period. AgNP exposure concomitant with ovalbumin challenge increased the enhanced pause (Penh) in the control and allergic groups. AgNP evoked neutrophil, lymphocyte and eosinophil infiltration into the airways and elevated the levels of allergic markers (immunoglobulin E [IgE] and leukotriene E 4 [LTE 4 ]), the type 2 T helper (Th2) cytokine interleukin-13 (IL-13), and oxidative stress (8-hydroxy-2′-deoxyguanosine [8-OHdG]) in healthy and allergic mice. Bronchocentric interstitial inflammation was observed after AgNP inhalation. After inhalation, the AgNP accumulated predominantly in the lungs, and trivial amounts of AgNP were excreted in the urine and feces. Furthermore, the AgNP induced inflammatory responses in the peritoneum. The inhalation of AgNP may present safety concerns in healthy and susceptible individuals.

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Section: Discussionmentioning

confidence: 99%

Allergenicity and toxicology of inhaled silver nanoparticles in allergen-provocation mice models

Chuang¹,

Hsiao²,

Wu³

et al. 2013

IJN

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“…26 Other effects include allergic reaction, nasal cavity inflammation and damage, pharyngeal problems, larynx damage, and influenza-like illness. 27,28 After passing the lung, the particles merge into the blood and cause erythrocyte damage. Most damages were characterized by changes of the geometrical dimension of the erythrocytes.…”

Section: -7mentioning

confidence: 99%

An observation of histological evidence on internal organ damages in mice caused by repeated exposures to motorcycle emissions

Wardoyo

Juswono

Noor

2017

AIP Conference Proceedings

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Abstract. Motor vehicle emissions have been identified as a source of ultrafine particles, which have significant impacts on human health. Repeated and prolonged exposure to ultrafine particles may have a significant association with organ damage. Here, we evaluated the correlation between repeated exposure to ultrafine particles and organ damage in mice. Motorcycle emissions were injected into an exposure chamber with mice for a period of 20 seconds. This treatment was conducted over 10 days. The mice were sacrificed on the 2nd, 4th, 6th, 8th, and 10th days for organ preparations. Based on the results, motorcycle emission exposure caused organ damage in mice, with different severities depending on the organ. The highest damage was found for the lung, followed by the kidney, erythrocytes, and liver.

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“…Exposure to DEP promotes sensitization toward coinhaled allergens and aggravates asthma (2). To investigate the molecular mechanisms, we set up a model wherein we exposed mice to saline, DEP or HDM alone, or combined DEP and HDM (experimental protocol in Fig.…”

Section: Role Of Chemr23 Signaling In a Model Of Dep-induced Lung Infmentioning

confidence: 99%

“…Experimental studies in mice showed that exposure to DEP can enhance allergic airway responses, including eosinophilia, goblet cell metaplasia, and T H 2 production (2). In addition, in controlled human exposure studies, combined exposure to DEP plus allergens increased allergen-specific Ig levels and induced a T H 2 cytokine pattern (2,3). The mechanistic basis of the inflammatory response in the lung to DEP inhalation and the adjuvant response to DEP on allergen-induced airway inflammation remain incompletely known.…”

mentioning

confidence: 99%

Pro- and Anti-Inflammatory Role of ChemR23 Signaling in Pollutant-Induced Inflammatory Lung Responses

Provoost

Grove

Fraser

et al. 2016

The Journal of Immunology

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Inhalation of traffic-related particulate matter (e.g., diesel exhaust particles [DEPs]) is associated with acute inflammatory responses in the lung, and it promotes the development and aggravation of allergic airway diseases. We previously demonstrated that exposure to DEP was associated with increased recruitment and maturation of monocytes and conventional dendritic cells (DCs), resulting in TH2 polarization. Monocytes and immature DCs express the G-protein coupled receptor chemR23, which binds the chemoattractant chemerin. Using chemR23 knockout (KO) and corresponding wild-type (WT) mice, we determined the role of chemR23 signaling in response to acute exposure to DEPs and in response to DEP-enhanced house dust mite (HDM)-induced allergic airway inflammation. Exposure to DEP alone, as well as combined exposure to DEP plus HDM, elevated the levels of chemerin in the bronchoalveolar lavage fluid of WT mice. In response to acute exposure to DEPs, monocytes and monocyte-derived DCs accumulated in the lungs of WT mice, but this response was significantly attenuated in chemR23 KO mice. Concomitant exposure to DEP plus HDM resulted in allergic airway inflammation with increased eosinophilia, goblet cell metaplasia, and TH2 cytokine production in WT mice, which was further enhanced in chemR23 KO mice. In conclusion, we demonstrated an opposing role for chemR23 signaling depending on the context of DEP-induced inflammation. The chemR23 axis showed proinflammatory properties in a model of DEP-induced acute lung inflammation, in contrast to anti-inflammatory effects in a model of DEP-enhanced allergic airway inflammation.

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Mouse models to unravel the role of inhaled pollutants on allergic sensitization and airway inflammation

Cited by 82 publications

References 186 publications

Allergenicity and toxicology of inhaled silver nanoparticles in allergen-provocation mice models

Allergenicity and toxicology of inhaled silver nanoparticles in allergen-provocation mice models

An observation of histological evidence on internal organ damages in mice caused by repeated exposures to motorcycle emissions

Pro- and Anti-Inflammatory Role of ChemR23 Signaling in Pollutant-Induced Inflammatory Lung Responses

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