Reduced allergic lung inflammation in rats following formaldehyde exposure: Long-term effects on multiple effector systems

Author(s)

dos Santos Franco, Adriana Lino ; Dorningos, Helori Vanni ; Damazo, Amilcar Sabino ^[1] ; Breithaupt-Faloppa, Ana Cristina ; Ligeiro de Oliveira, Ana Paula ; Pereira Costa, Soraia Katia ; Oliani, Sonia Maria ^[1] ; Oliveira-Filho, Ricardo Martins ; Vargaftig, B. Boris ; Tavares-de-Lima, Wothan ^[2]

Affiliation

^[1] Sao Paulo State Univ, UNESP, IBILCE, Dept Biol, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Inst Ciencias Biomed, Lab Fisiopatol Inflamacao Expt, Dept Pharmacol, BR-05508900 Sao Paulo - Brazil

• Document type: Journal article
• Source: Toxicology; v. 256, n. 3, p. 157-163, 2009.
• Web of Science Citations: 21

Abstract

Clinical and experimental evidences show that formaldehyde (FA) exposure has an irritant effect on the upper airways. As being an indoor and outdoor pollutant, FA is known to be a causal factor of occupational asthma. This study aimed to investigate the repercussion of FA exposure on the course of a lung allergic process triggered by an antigen unrelated to FA. For this purpose, male Wistar rats were subjected to FA inhalation for 3 consecutive days (1%, 90-min daily), subsequently sensitized with ovalbumin (OVA)-alum via the intraperitoneal route, and 2 weeks later challenged with aerosolized OVA. The OVA challenge in rats after FA inhalation (FA/OVA group) evoked a low-intensity lung inflammation as indicated by the reduced enumerated number of inflammatory cells in bronchoalveolar lavage as compared to FA-untreated allergic rats (OVA/OVA group). Treatment with FA also reduced the number of bone marrow cells and blood leukocytes in sensitized animals challenged with OVA, which suggests that the effects of FA had not been only localized to the airways. As indicated by passive cutaneous anaphylactic reaction, FA treatment did not impair the anti-OVA IgE synthesis, but reduced the magnitude of OVA challenge-induced mast cell degranulation. Moreover, FA treatment was associated to a diminished lung expression of PECAM-1 (platelet-endothelial cell adhesion molecule 1) in lung endothelial cells after OVA challenge and an exacerbated release of nitrites by BAL-cultured cells. Keeping in mind that rats subjected solely to either FA or OVA challenge were able to significantly increase the cell influx into lung, our study shows that FA inhalation triggers long-lasting effects that affect multiple mediator systems associated to OVA-induced allergic lung such as the reduction of mast cells activation, PECAM-1 expression and exacerbation of NO generation, thereby contributing to the decrease of cell recruitment after the OVA challenge. In conclusion, repeated expositions to air-borne FA may impair the lung cell recruitment after an allergic stimulus, thereby leading to a non-responsive condition against inflammatory stimuli likely those where mast cells are involved. (C) 2008 Elsevier Ireland Ltd. All rights reserved. (AU)