Leukocyte Telomere Length Reflects Prenatal Stress Exposure, But Does Not Predict Atopic Dermatitis Development at 1 Year
10.4168/aair.2019.11.3.357
- Author:
Dong In SUH
1
;
Mi Jin KANG
;
Yoon Mee PARK
;
Jun Kyu LEE
;
So Yeon LEE
;
Youn Ho SHEEN
;
Kyung Won KIM
;
Kangmo AHN
;
Hye Sung WON
;
Mi Young LEE
;
Suk Joo CHOI
;
Ja Young KWON
;
Hee Jin PARK
;
Jong Kwan JUN
;
Soo Jong HONG
;
Young Yull KOH
Author Information
1. Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea. kohyy@plaza.snu.ac.kr
- Publication Type:Original Article
- Keywords:
Atopic dermatitis;
cohort studies;
child;
cord blood;
telomere shortening;
psychological stress
- MeSH:
Asthma;
Child;
Cohort Studies;
Dermatitis, Atopic;
Fetal Blood;
Humans;
Infant;
Leukocytes;
Oxidative Stress;
Parturition;
Risk Assessment;
Risk Factors;
Stress, Psychological;
Telomere Shortening;
Telomere
- From:Allergy, Asthma & Immunology Research
2019;11(3):357-366
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Prenatal maternal stress affects offspring's atopic dermatitis (AD) development, which is thought to be mediated by the oxidative stress. We aimed to evaluate the difference in leukocyte telomere length (LTL), a marker for exposure to oxidative stress, according to the prenatal stress exposure and the later AD development. METHODS: From a birth cohort (the COhort for Childhood Origin of Asthma and allergic diseases) that had displayed a good epidemiologic association between the exposure to prenatal stress and AD development in the offspring, we selected 68 pairs of samples from 4 subject groups based on the level of prenatal maternal stress and later AD development. The LTL was measured from both cord blood and 1-year peripheral blood, and their LTLs were compared between subject groups. Finally, the proportion of AD development was examined in the subject groups that are reclassified based on subjects' exposure to prenatal stress and there LTL. RESULTS: Cord-blood LTL was shorter in prenatally stressed infants than in unstressed ones (P = 0.026), which difference was still significant when subjects became 1 year old (P = 0.008). LTL of cord blood, as well as one of the 1-year peripheral blood, was not different according to later AD development at 1 year (P = 0.915 and 0.174, respectively). Shorter LTL made no increase in the proportion of later AD development in either prenatally high-stressed or low-stressed groups (P = 1.000 and 0.473, respectively). CONCLUSIONS: Cord-blood LTL may reflect subjects' exposure to maternal prenatal stress. However, the LTL shortening is not a risk factor of increasing AD development until the age of 1, and a longer investigation may be necessary for validation. Currently, the results doubt the role of LTL shortening as a marker for risk assessment tool for the prenatal stress associated with AD development in the offspring.
