Subchronic effects of nasally instilled diesel exhaust particulates on the nasal and airway epithelia in mice

Abstract

Diesel exhaust is the major source of ultrafine particles released during traffic-related pollution. Subjects with chronic respiratory diseases are at greater risk for exacerbations during exposure to air pollution. This study evaluated the effects of subchronic exposure to a low-dose of diesel exhaust particles (DEP). Sixty male BALB/c mice were divided into two groups: (a) Saline: nasal instillation of saline (n = 30); and (b) DEP: nasal instillation of 30 microg of DEP/10 microl of saline (n = 30). Nasal instillations were performed 5 days a week, over 30 and 60 days. Animals were anesthetized with pentobarbital sodium (50 mg/kg intraperitoneal [i.p.]) and sacrificed by exsanguination. Bronchoalveolar lavage (BAL) fluid was performed to evaluate the inflammatory cell count and the concentrations of the interleukin (IL)-4, IL-10, and IL-13 by enzyme-linked immunosorbent assay (ELISA). The gene expression of oligomeric mucus/gel-forming (Muc5ac) was evaluated by real-time polymerase chain reaction (PCR). Histological analysis in the nasal septum and bronchioles was used to evaluate the bronchial and nasal epithelium thickness as well as the acidic and neutral nasal mucus content. The saline group (30 and 60 days) did not show any changes in any of the parameters. However, the instillation of DEP over 60 days increased the expression of Muc5ac in the lungs and the acid mucus content in the nose compared with the 30-day treatment, and it increased the total leukocytes in the BAL and the nasal epithelium thickness compared with saline for 60 days. Cytokines concentrations in the BAL were detectable, with no differences among the groups. Our data suggest that a low-dose of DEP over 60 days induces respiratory tract inflammation.

Repeated intranasal exposure to microcystin-LR affects lungs but not nasal epithelium in mice

“…Likewise, Yoshizaki et al (2010) found no significant changes in the nasal epithelium thickness and mucus content of mice intranasally instilled with saline or diesel exhaust particles released from automotive engines in the traffic during 30 days. Thereby, assuming that the nasal cavity is prepared to take challenges from potentially harmful airborne substances, we hypothesize that all mice in our study produced enough mucus to protect their epithelia from the daily intranasal instillations of MC-LR.…”

Contribution of Lung Macrophages to the Inflammatory Responses Induced by Exposure to Air Pollutants

“…Although PM shares many of the same ingredients and characteristics as cigarette smoke, the M1 cytokines (IL-12 and IFN- γ ) are increased consistently in bronchoalveolar lavage fluid (BALF) from PM-exposed animals [63, 64] while the M2 cytokines (IL-4, IL-10, and IL-13) remain at lower levels [65]. Our group previously showed that primary cultured human AM, stimulated in vitro with urban PM 10 , produced an array of cytokines without significantly increased levels of IL-10 compared to nonstimulated AM [13].…”

Nasal response after exercise in swimmers, runners and handball players

“…In addition, thanks to the nose's barrier feature, particles of specific sizes cannot pass through it and are cleared with mucociliary clearance. [10] To meet the air requirement which increases during exercise, nasal resistance decreases and the amount and speed of the air that passes through the nose increases. [1,2] Drying in the mucosa and thickened secretions cause changes in mucociliary transport mechanisms.…”