PMID- 24554396
OWN - NLM
STAT- MEDLINE
DCOM- 20150330
LR  - 20140725
IS  - 1432-0738 (Electronic)
IS  - 0340-5761 (Linking)
VI  - 88
IP  - 8
DP  - 2014 Aug
TI  - Early postnatal, but not late, exposure to chemical ambient pollutant 
      1,2-naphthoquinone increases susceptibility to pulmonary allergic inflammation at 
      adulthood.
PG  - 1589-605
LID - 10.1007/s00204-014-1212-z [doi]
AB  - High diesel exhaust particle levels are associated with increased health effects; 
      however, knowledge on the impact of its chemical contaminant 1,2-naphthoquinone 
      (1,2-NQ) is limited. We investigated whether postnatal and adult exposures to 
      1,2-NQ influence allergic reaction and the roles of innate and adaptive immunity. 
      Male neonate (6 days) and adult (56 days) C57Bl/6 mice were exposed to 1,2-NQ 
      (100 nM; 15 min) for 3 days, and on day 59, they were sensitized and later 
      challenged with ovalbumin (OVA). Airway hyper-responsiveness (AHR) and production 
      of cytokines, immunoglobulin E (IgE) and leukotriene B4 (LTB4) were measured in 
      the airways. Postnatal exposure to 1,2-NQ activated dendritic cells in 
      splenocytes by increasing expressing cell surface molecules (e.g., CD11c). 
      Co-exposure to OVA effectively polarized T helper (Th) type 2 (Th2) by secreting 
      Th2-mediated cytokines. Re-stimulation with unspecific stimuli (PMA and 
      ionomycin) generated a mixed Th1 (CD4(+)/IFN-gamma(+)) and Th17 (CD4(+)/IL-17(+)) 
      phenotype in comparison with the vehicle-matched group. Postnatal exposure to 
      1,2-NQ did not induce eosinophilia in the airways at adulthood, although it 
      evoked neutrophilia and exacerbated OVA-induced eosinophilia, Th2 cytokines, IgE 
      and LTB4 production without affecting AHR and mast cell degranulation. At 
      adulthood, 1,2-NQ exposure evoked neutrophilia and increased Th1/Th2 cytokine 
      levels, but failed to affect OVA-induced eosinophilia. In conclusion, postnatal 
      exposure to 1,2-NQ increases the susceptibility to antigen-induced asthma. The 
      mechanism appears to be dependent on increased expression of co-stimulatory 
      molecules, which leads to cell presentation amplification, Th2 polarization and 
      enhanced LTB4, humoral response and Th1/Th2 cytokines. These findings may be 
      useful for future investigations on treatments focused on pulmonary illnesses 
      observed in children living in heavy polluted areas.
FAU - Santos, Karen T
AU  - Santos KT
AD  - Department of Pharmacology, Institute of Biomedical Sciences, University of Sao 
      Paulo, Av Prof Lineu Prestes, 1524, Sao Paulo, SP, 05508-900, Brazil.
FAU - Florenzano, Juliana
AU  - Florenzano J
FAU - Rodrigues, Leandro
AU  - Rodrigues L
FAU - Favaro, Rodolfo R
AU  - Favaro RR
FAU - Ventura, Fernanda F
AU  - Ventura FF
FAU - Ribeiro, Marcela G
AU  - Ribeiro MG
FAU - Teixeira, Simone A
AU  - Teixeira SA
FAU - Ferreira, Heloisa H A
AU  - Ferreira HH
FAU - Brain, Susan D
AU  - Brain SD
FAU - Damazo, Amilcar S
AU  - Damazo AS
FAU - Zorn, Telma M
AU  - Zorn TM
FAU - Camara, Niels O
AU  - Camara NO
FAU - Muscara, Marcelo N
AU  - Muscara MN
FAU - Peron, Jean Pierre
AU  - Peron JP
FAU - Costa, Soraia K
AU  - Costa SK
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140220
PL  - Germany
TA  - Arch Toxicol
JT  - Archives of toxicology
JID - 0417615
RN  - 0 (Air Pollutants)
RN  - 0 (Cytokines)
RN  - 0 (Naphthoquinones)
RN  - 0 (Vehicle Emissions)
RN  - 1HGW4DR56D (Leukotriene B4)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 804K62F61Q (1,2-naphthoquinone)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Adaptive Immunity/drug effects
MH  - Aging/drug effects/*immunology
MH  - Air Pollutants/*toxicity
MH  - Animals
MH  - Animals, Newborn
MH  - Cytokines/immunology
MH  - Disease Susceptibility/chemically induced
MH  - Immunity, Innate/drug effects
MH  - Immunoglobulin E/immunology
MH  - Inhalation Exposure/*adverse effects/analysis
MH  - Leukotriene B4/immunology
MH  - Male
MH  - Naphthoquinones/*toxicity
MH  - Ovalbumin/immunology
MH  - Pneumonia/*chemically induced/immunology
MH  - Respiratory Hypersensitivity/*chemically induced/immunology
MH  - Vehicle Emissions/analysis/*toxicity
EDAT- 2014/02/21 06:00
MHDA- 2015/03/31 06:00
CRDT- 2014/02/21 06:00
PHST- 2013/11/22 00:00 [received]
PHST- 2014/02/03 00:00 [accepted]
PHST- 2014/02/21 06:00 [entrez]
PHST- 2014/02/21 06:00 [pubmed]
PHST- 2015/03/31 06:00 [medline]
AID - 10.1007/s00204-014-1212-z [doi]
PST - ppublish
SO  - Arch Toxicol. 2014 Aug;88(8):1589-605. doi: 10.1007/s00204-014-1212-z. Epub 2014 
      Feb 20.