Exposure to Diesel Exhaust Aggravates Nasal Allergic Reaction in Guinea Pigs

Abstract

Diesel exhaust particulates (DEP) () and exposure to diesel exhaust (DE) induce nasal mucosal hyperresponsiveness to histamine. Therefore, in the present study, we investigated whether or not exposing guinea pigs to DE aggravates the nasal allergic reaction induced by repeated nasal administration of ovalbumin (OVA). Guinea pigs were exposed to filtered air or to DE (DE containing 0.3 or 1.0 mg/m(3) of DEP) for 5 wk. During exposure to filtered air or to DE, guinea pigs were administered 1% of OVA in saline into the nasal cavities once a week. Sneezes were counted and nasal secretions were measured as indices of sneezing responses and rhinorrhea for 20 min after OVA administration. Titers of specific anti-OVA-IgG and anti-OVA-IgE and the number of eosinophils infiltrated into both nasal epithelium and subepithelium were measured at the end of the exposure to DE. Exposure to DE enhanced the number of sneezes and the amount of nasal secretions induced by OVA. Titers of specific anti-OVA-IgG and anti-OVA-IgE also significantly increased in DE-exposed animals. Exposure to DE also augmented the number of eosinophils that infiltrated both the nasal epithelium and the subepithelium induced by OVA. These results suggest that exposure to DE enhances the nasal allergic reaction induced by repeated antigen administration in guinea pigs.

Metal composition of ambient PM2.5 influences severity of allergic airways disease in mice.

“…Pulmonary administration of ROFA in rats before sensitization with house dust mite antigen increases subsequent allergic responses to antigen challenge, including specific IgE, immediate bronchoconstrictive responses, and BAL eosinophils and proteins (Lambert et al 1999). Similar results have been seen in rats coadministered grass pollen and diesel exhaust particles (Steerenberg et al 1999) and guinea pigs exposed to diesel exhaust and ovalbumin (Kobayashi 2000). Volunteer subjects exposed to diesel particles and a novel antigen (keyhole limpet hemocyanin) developed higher levels of antigen-specific IgE and the Th2 pro-allergic cytokine IL-4 than subjects exposed to diesel particles or antigen alone (Diaz-Sanchez et al 1999).…”

“…These results suggest that repeated exposures are necessary to produce persistent pulmonary effects. Unlike other types of PM 2.5 such as ROFA (Lambert et al 1999;2000) and diesel exhaust particles (Diaz-Sanchez et al 1999;Kobayashi 2000), neither Hettstedt nor Zerbst PM 2.5 administered before sensitization enhanced allergic responses, with the exception that Hettstedt PM 2.5 significantly increased serum Article | Gavett et al . Levels of (A) BAL supernatant protein, (B) LDH, and (C) NAG recovered 2 days after OVA challenge in nonallergic mice exposed at challenge phase, allergic mice exposed at challenge phase, and allergic mice exposed at sensitization phase.…”

The Effects of Air Pollution on Cellular Material Release, Allergenicity and Allergens Proteins of Three Ornamental Plants

“…Although a majority of studies of allergic airway disease are now carried out in the mouse, the guinea pig initially was utilized as an animal model of pulmonary hypersensitivity and AHR for many decades ( Shin et al, 2009as cited in Noelpp &Noelpp-Eschenhagen, 1952. Guinea pigs were used as a histamine-induced rhinitis model, since histamine induces nasal congestion, sneezing, and rhinorrhea well in guinea pigs among small experimental animals (Kobayashi, 2000). The guinea pigs demonstrated airway constrictive responses and production of hypersensitivity antibodies including IgG1 and IgE (Ricciardolo et al, 2008).…”

Pollution atmosphérique et maladies respiratoires allergiques

“…< [2,7] et en majorant l'hyperréactivité bronchique [8]. Chez le cobaye exposé aux particules diesel, l'administration nasale répétée d'allergènes augmente les éternuements, les sécrétions nasales et l'infiltration muqueuse par les polynucléaires éosinophiles [9]. Les études in vitro montrent que les particules diesel peuvent agir sur de nombreux types cellulaires [2,10] (Figure 1 • ➚ de l'inflammation à éosinophiles et de l'hyperplasie des cellules à mucus de l'épithélium respiratoire…”