Differential effects of formaldehyde exposure on the cell influx and vascular permeability in a rat model of allergic lung inflammation


Autoria(s): LINO-DOS-SANTOS-FRANCO, Adriana; DOMINGOS, Helori Vanni; OLIVEIRA, Ana Paula Ligeiro de; BREITHAUPT-FALOPPA, Ana Cristina; PERON, Jean Pierre Schatzmann; BOLONHEIS, Simone; MUSCARA, Marcelo Nicolas; 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

2010

Resumo

Exposure to air pollutants such as formaldehyde (FA) leads to inflammation, oxidative stress and immune-modulation in the airways and is associated with airway inflammatory disorders such as asthma. The purpose of our study was to investigate the effects of exposure to FA on the allergic lung inflammation. The hypothesized link between reactive oxygen species and the effects of FA was also studied. To do so, male Wistar rats were exposed to FA inhalation (1%, 90 min daily) for 3 days. and subsequently sensitized with ovalbumin (OVA)-alum by subcutaneous route One week later the rats received another OVA-alum injection by the same route (booster). Two weeks later the rats were challenged with aerosolized OVA. The OVA challenge of rats upon FA exposure induced an elevated release of LTB(4). TXB(2), IL-1 beta, IL-6 and VEGF in lung cells, increased phagocytosis and lung vascular permeability, whereas the cell recruitment into lung was reduced. FA inhalation induced the oxidative burst and the nitration of proteins in the lung Vitamins C, E and apocynin reduced the levels of LTB(4) in BAL-cultured cells of the FA and FA/OVA groups, but Increased the cell influx into the lung of the FA/OVA rats. In OVA-challenged rats, the exposure to FA was associated to a reduced lung endothelial cells expression of intercellular cell adhesion molecule 1 (ICAM-1) In conclusion, our findings suggest that FA down regulate the cellular migration into the lungs after an allergic challenge and increase the ability of resident lung cells likely macrophages to generate inflammatory mediators, explaining the increased lung vascular permeability Our data are indicative that the actions of FA involve mechanisms related to endothelium-leukocyte interactions and oxidative stress, as far as the deleterious effects of this air pollutant on airways are concerned. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

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

Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)[07/55631-4]

Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)[09/51886-3]

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

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

Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)[08/50766-1]

Conselho Nacional de Pesquisa (CNPq)

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Identificador

TOXICOLOGY LETTERS, v.197, n.3, p.211-218, 2010

0378-4274

http://producao.usp.br/handle/BDPI/28163

10.1016/j.toxlet.2010.05.022

http://dx.doi.org/10.1016/j.toxlet.2010.05.022

Idioma(s)

eng

Publicador

ELSEVIER IRELAND LTD

Relação

Toxicology Letters

Direitos

restrictedAccess

Copyright ELSEVIER IRELAND LTD

Palavras-Chave #Formaldehyde #Vascular permeability #Allergic lung inflammation #Inflammatory mediators #Reactive oxygen species #Rat #EPIDEMIOLOGIC EVIDENCE #OXIDATIVE STRESS #AIR #PARTICLES #INDOOR #ASTHMA #DAMAGE #Toxicology
Tipo

article

original article

publishedVersion