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


Autoria(s): FRANCO, Adriana Lino dos Santos; DORNINGOS, Helori Vanni; DAMAZO, Amilcar Sabino; BREITHAUPT-FALOPPA, Ana Cristina; OLIVEIRA, Ana Paula Ligeiro de; COSTA, Soraia Katia Pereira; OLIANI, Sonia Maria; OLIVEIRA-FILHO, Ricardo Martins; VARGAFTIG, B. Boris; TAVARES-DE-LIMA, Wothan
Contribuinte(s)

UNIVERSIDADE DE SÃO PAULO

Data(s)

20/10/2012

20/10/2012

2009

Resumo

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.

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

FAPESP Fundacao de Amparo A Pesquisa do Estado cle Sao Paulo[02/6606-3]

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

FAPESP Fundacao de Amparo A Pesquisa do Estado cle Sao Paulo[01/11417-2]

Conselho Nacional de Pesquisa (CNPq)

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Identificador

TOXICOLOGY, v.256, n.3, p.157-163, 2009

0300-483X

http://producao.usp.br/handle/BDPI/28579

10.1016/j.tox.2008.11.011

http://dx.doi.org/10.1016/j.tox.2008.11.011

Idioma(s)

eng

Publicador

ELSEVIER IRELAND LTD

Relação

Toxicology

Direitos

restrictedAccess

Copyright ELSEVIER IRELAND LTD

Palavras-Chave #Allergic lung inflammation #Formaldehyde #Nitric oxide #Mast cells #PECAM-1 #Rats #NITRIC-OXIDE #MAST-CELLS #IN-VIVO #SENSITIZATION #RESPONSES #DISEASE #MODEL #Pharmacology & Pharmacy #Toxicology
Tipo

article

original article

publishedVersion