Activation of Pulmonary Dendritic Cells and Th2-Type Inflammatory Responses on Instillation of Engineered, Environmental Diesel Emission Source or Ambient Air Pollutant Particles in vivo

Bezemer, Gillina; Bauer, Stephen M.; Oberdörster, Günter; Breysse, Patrick N.; Pieters, Raymond; Georas, Steve N.; Williams, Marc A.

doi:10.1159/000321725

Cited by 65 publications

(56 citation statements)

References 116 publications

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“…The activated dendritic cells selectively provoked a Th2-biased immune activation of allogeneic CD4 + T cells. 136 Although engineered nanoparticles (carbon black and silver nanoparticles) were not shown to cause similar responses in the same investigation, the involvement of nanoparticles in the observed immunological effects cannot be excluded. Oral or peritoneal exposure of mice to polyethylene glycol-coated poly-DL-lactic-co-glycolic acid (PLGA) nanoparticles induced immune reactions.…”

Section: Immunotoxicitymentioning

confidence: 89%

Perturbation of physiological systems by nanoparticles

et al. 2014

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Nanotechnology is having a tremendous impact on our society. However, societal concerns about human safety under nanoparticle exposure may derail the broad application of this promising technology. Nanoparticles may enter the human body via various routes, including respiratory pathways, the digestive tract, skin contact, intravenous injection, and implantation. After absorption, nanoparticles are carried to distal organs by the bloodstream and the lymphatic system. During this process, they interact with biological molecules and perturb physiological systems. Although some ingested or absorbed nanoparticles are eliminated, others remain in the body for a long time. The human body is composed of multiple systems that work together to maintain physiological homeostasis. The unexpected invasion of these systems by nanoparticles disturbs normal cell signaling, impairs cell and organ functions, and may even cause pathological disorders. This review examines the comprehensive health risks of exposure to nanoparticles by discussing how nanoparticles perturb various physiological systems as revealed by animal studies. The potential toxicity of nanoparticles to each physiological system and the implications of disrupting the balance among systems are emphasized.

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Section: Immunotoxicitymentioning

confidence: 89%

Perturbation of physiological systems by nanoparticles

et al. 2014

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“…The effect was not observed in the AgNP-treated and OVA-sensitized mice. Previous studies have established that AgNP are causative agents of asthma development, 33,34 and the disease could be attributed to inflammatory responses. Indeed, our findings also suggested that the exposure of healthy mice to AgNP resulted in an increase in inflammatory reactions (ie, interstitial lymphocytic and neutrophilic inflammatory infiltration in the lungs).…”

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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“…Oxidant stress seems to be involved in diesel-associated increases in allergic inflammation and airway hyperresponsiveness as evidenced by experiments in Nrf2 knockout mice (19) and exposure of dendritic cells (DC) to diesel exhaust particle extracts (20,21). Ambient and diesel particulates instilled into the oropharynx have been shown to activate pulmonary DC and promote eosinophilia and Th2-type responses in mice (22). In a study comparing responses to several chemically distinct preparations of diesel exhaust particles, potentiation of murine allergic immune responses seemed to correlate with diesel exhaust content of polycyclic aromatic hydrocarbons (23).…”

Section: Discussionmentioning

confidence: 99%

Diesel Exhaust Exposure and Nasal Response to Attenuated Influenza in Normal and Allergic Volunteers

Noah

Zhou

Zhang³

et al. 2012

Am J Respir Crit Care Med

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Rationale: Diesel exhaust enhances allergic inflammation, and pollutants are associated with heightened susceptibility to viral respiratory infections. The effects of combined diesel and virus exposure in humans are unknown. Objectives: Test whether acute exposure to diesel modifies inflammatory responses to influenza virus in normal humans and those with allergies. Methods: We conducted a double-blind, randomized, placebocontrolled study of nasal responses to live attenuated influenza virus in normal volunteers and those with allergic rhinitis exposed to diesel (100 mg/m 3 ) or clean air for 2 hours, followed by standard dose of virus and serial nasal lavages. Endpoints were inflammatory mediators (ELISA) and virus quantity (quantitative reverse-transcriptase polymerase chain reaction). To test for exposure effect, we used multiple regression with exposure group (diesel vs. air) as the main explanatory variable and allergic status as an additional factor. Measurements and Main Results: Baseline levels of mediators did not differ among groups. For most postvirus nasal cytokine responses, there was no significant diesel effect, and no significant interaction with allergy. However, diesel was associated with significantly increased IFN-g responses (P ¼ 0.02), with no interaction with allergy in the regression model. Eotaxin-1 (P ¼ 0.01), eosinophil cationic protein (P , 0.01), and influenza RNA sequences in nasal cells (P ¼ 0.03) were significantly increased with diesel exposure, linked to allergy. Conclusions: Short-term exposure to diesel exhaust leads to increased eosinophil activation and increased virus quantity after virus inoculation in those with allergic rhinitis. This is consistent with previous literature suggesting a diesel "adjuvant" effect promoting allergic inflammation, and our data further suggest this change may be associated with reduced virus clearance. Clinical trial registered with www.clinicaltrials.gov (NCT00617110).

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Activation of Pulmonary Dendritic Cells and Th2-Type Inflammatory Responses on Instillation of Engineered, Environmental Diesel Emission Source or Ambient Air Pollutant Particles in vivo

Cited by 65 publications

References 116 publications

Perturbation of physiological systems by nanoparticles

Perturbation of physiological systems by nanoparticles

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

Diesel Exhaust Exposure and Nasal Response to Attenuated Influenza in Normal and Allergic Volunteers

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