PMID- 29737898
OWN - NLM
STAT- MEDLINE
DCOM- 20181003
LR  - 20200225
IS  - 2058-7384 (Electronic)
IS  - 0394-6320 (Print)
IS  - 0394-6320 (Linking)
VI  - 32
DP  - 2018 Jan-Dec
TI  - Exposure to low-dose bisphenol A during the juvenile period of development 
      disrupts the immune system and aggravates allergic airway inflammation in mice.
PG  - 2058738418774897
LID - 10.1177/2058738418774897 [doi]
LID - 2058738418774897
AB  - Bisphenol A (BPA) is used in the production of polycarbonate plastics and epoxy 
      resins and found in many consumer products. Previous studies have reported that 
      perinatal exposure to BPA through the oral route promotes the development of 
      allergic airway inflammation. We investigated the effects of exposure to low-dose 
      BPA during the juvenile period of development on allergic airway inflammation. 
      Six-week-old male C3H/HeJ mice were intratracheally administered ovalbumin (OVA, 
      1 mug) every 2 weeks and/or BPA (0, 0.0625, 1.25, and 25 pmol/animal/week) once 
      per week for 6 weeks. Following the final intratracheal instillation, we examined 
      the cellular profile of the bronchoalveolar lavage fluid, histological changes 
      and expression of inflammatory/anti-inflammatory mediators in the lungs, 
      OVA-specific immunoglobulin (Ig) production, serum corticosterone levels, and 
      changes in the lymphoid tissues (mediastinal lymph node (MLN) and spleen). 
      Exposure to OVA + BPA enhanced inflammatory cell infiltration and protein 
      expression of Th2 cytokines/chemokines (e.g. interleukin (IL)-13 and IL-33) in 
      the lungs, OVA-specific immunoglobulin E (IgE) production, the numbers of total 
      cells and activated antigen-presenting cells (MHC class II(+) CD86(+), CD11c(+)), 
      as well as the production of Th2 cytokines (i.e. IL-4 and IL-5) and stromal 
      cell-derived factor-1alpha in MLN cells compared to OVA exposure alone. These effects 
      were more prominent with 0.0625 or 1.25 pmol/animal/week of BPA. Furthermore, 
      exposure to OVA + BPA altered serum levels of anti-inflammatory corticosterone, 
      estrogen receptor 2 messenger RNA (mRNA) expression in the lungs and spleen 
      functionality. These findings suggest that low-dose BPA exposure may aggravate 
      allergic airway inflammation by enhancing Th2 responses via disruption of the 
      immune system.
FAU - Koike, Eiko
AU  - Koike E
AD  - 1 Center for Health and Environmental Risk Research, National Institute for 
      Environmental Studies, Tsukuba, Japan.
FAU - Yanagisawa, Rie
AU  - Yanagisawa R
AD  - 1 Center for Health and Environmental Risk Research, National Institute for 
      Environmental Studies, Tsukuba, Japan.
FAU - Win-Shwe, Tin-Tin
AU  - Win-Shwe TT
AD  - 1 Center for Health and Environmental Risk Research, National Institute for 
      Environmental Studies, Tsukuba, Japan.
FAU - Takano, Hirohisa
AU  - Takano H
AD  - 2 Graduate School of Engineering, Kyoto University, Kyoto, Japan.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Int J Immunopathol Pharmacol
JT  - International journal of immunopathology and pharmacology
JID - 8911335
RN  - 0 (Benzhydryl Compounds)
RN  - 0 (Cytokines)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Estrogen Receptor beta)
RN  - 0 (Immunoglobulins)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Phenols)
RN  - 0 (RNA, Messenger)
RN  - 9006-59-1 (Ovalbumin)
RN  - MLT3645I99 (bisphenol A)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Age Factors
MH  - Animals
MH  - Benzhydryl Compounds/*toxicity
MH  - Cells, Cultured
MH  - Corticosterone/blood
MH  - Cytokines/metabolism
MH  - Disease Models, Animal
MH  - Environmental Pollutants/*toxicity
MH  - Estrogen Receptor beta/genetics/metabolism
MH  - Immunoglobulins/blood
MH  - Inflammation Mediators/metabolism
MH  - Lung/*drug effects/immunology/metabolism/pathology
MH  - Lymph Nodes/drug effects/immunology/metabolism
MH  - Male
MH  - Mice, Inbred C3H
MH  - Ovalbumin
MH  - Phenols/*toxicity
MH  - RNA, Messenger/genetics/metabolism
MH  - Respiratory Hypersensitivity/*chemically induced/immunology/metabolism/pathology
MH  - Spleen/drug effects/immunology/metabolism
MH  - Th2 Cells/*drug effects/immunology/metabolism
PMC - PMC5946358
OTO - NOTNLM
OT  - allergic airway inflammation
OT  - bisphenol A
OT  - endocrine-disrupting chemicals
OT  - immune system disruption
OT  - inflammatory/anti-inflammatory mediators
COIS- Declaration of conflicting interests: The author(s) declared no potential 
      conflicts of interest with respect to the research, authorship, and/or 
      publication of this article.
EDAT- 2018/05/09 06:00
MHDA- 2018/10/04 06:00
PMCR- 2018/05/08
CRDT- 2018/05/09 06:00
PHST- 2018/05/09 06:00 [entrez]
PHST- 2018/05/09 06:00 [pubmed]
PHST- 2018/10/04 06:00 [medline]
PHST- 2018/05/08 00:00 [pmc-release]
AID - 10.1177_2058738418774897 [pii]
AID - 10.1177/2058738418774897 [doi]
PST - ppublish
SO  - Int J Immunopathol Pharmacol. 2018 Jan-Dec;32:2058738418774897. doi: 
      10.1177/2058738418774897.