PMID- 27976742
OWN - NLM
STAT- MEDLINE
DCOM- 20180615
LR  - 20220321
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 6
DP  - 2016 Dec 15
TI  - Increased Fetal Thymocytes Apoptosis Contributes to Prenatal Nicotine 
      Exposure-induced Th1/Th2 Imbalance in Male Offspring Mice.
PG  - 39013
LID - 10.1038/srep39013 [doi]
LID - 39013
AB  - Nicotine, a definite risk factor during pregnancy, is an immunomodulator. This 
      study was designed to investigate the effects of prenatal nicotine exposure (PNE) 
      on the balance of Th1/Th2 in offspring, and further explore the developmental 
      origin mechanisms from the perspective of fetal thymocytes apoptosis. Pregnant 
      Balb/c mice were administered 1.5 mg/kg nicotine subcutaneously twice per day 
      from gestational day (GD) 9 to GD18. Results showed that PNE could cause a Th2 
      shift in male offspring, manifested as increased ratio of IgG1/IgG2a, IL-4 
      production in serum, and IL-4/IFN-gamma expression ratio in spleen. Increased 
      apoptosis of total thymocytes and CD4SP and reduced cell proportion of CD4SP were 
      found in PNE male offspring on postnatal day (PND) 14 and PND 49. In the fetuses, 
      decreased body weight and organ index of fetal thymus, histological changes in 
      fetal thymus, reduced CD4SP proportion and increased fetal thymocyte apoptosis 
      were observed in nicotine group. The increased mRNA expression of genes involved 
      in Fas-mediated apoptotic pathway and protein expression of Fas were also 
      detected. In conclusion, PNE could cause a Th2 shift in male offspring mediated 
      by reduced CD4(+) T cells output, which may result from the increasing apoptosis 
      of total thymocytes and CD4SP.
FAU - Chen, Ting
AU  - Chen T
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan 430071, China.
FAU - Yan, You-E
AU  - Yan YE
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan 430071, China.
FAU - Liu, Sha
AU  - Liu S
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan 430071, China.
FAU - Liu, Han-Xiao
AU  - Liu HX
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan 430071, China.
FAU - Yan, Hui-Yi
AU  - Yan HY
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan 430071, China.
FAU - Hou, Li-Fang
AU  - Hou LF
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan 430071, China.
FAU - Qu, Wen
AU  - Qu W
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan 430071, China.
FAU - Ping, Jie
AU  - Ping J
AD  - Department of Pharmacology, Wuhan University School of Basic Medical Sciences, 
      Wuhan 430071, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20161215
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 6M3C89ZY6R (Nicotine)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects/immunology
MH  - Female
MH  - Fetus/*immunology/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Nicotine/*toxicity
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/*immunology/pathology
MH  - Th1 Cells/*immunology/pathology
MH  - Th2 Cells/*immunology/pathology
MH  - Thymocytes/*immunology/pathology
PMC - PMC5157046
EDAT- 2016/12/16 06:00
MHDA- 2018/06/16 06:00
PMCR- 2016/12/15
CRDT- 2016/12/16 06:00
PHST- 2016/08/19 00:00 [received]
PHST- 2016/11/16 00:00 [accepted]
PHST- 2016/12/16 06:00 [entrez]
PHST- 2016/12/16 06:00 [pubmed]
PHST- 2018/06/16 06:00 [medline]
PHST- 2016/12/15 00:00 [pmc-release]
AID - srep39013 [pii]
AID - 10.1038/srep39013 [doi]
PST - epublish
SO  - Sci Rep. 2016 Dec 15;6:39013. doi: 10.1038/srep39013.