Abstract Title:

Prenatal Oexposure increases the severity of OVA-induced asthma in offspring.

Abstract Source:

Ecotoxicol Environ Saf. 2020 Jan 30 ;188:109867. Epub 2019 Nov 2. PMID: 31689658

Abstract Author(s):

Lingling Fu, Xiwei Yang, Xinai Liu, Gongchang Yu, Zhiping Wang

Article Affiliation:

Lingling Fu


BACKGROUND: Accumulating epidemiological studies showed that prenatal and early life exposure to ambient air pollution was important contributor to the development of childhood asthma. However, the effects and mechanisms of prenatal exposure to ozone (O), a type of ambient air pollution, on the progression of asthma in offspring remain unclear.

OBJECTIVE: This study aimed to determine the effects and mechanism of asthma in offspring after prenatal Oexposure.

METHODS: Pregnant BALB/c mice were exposed to Oor air on gestational days (GDs) 13-18. Their offspring were sensitized and challenged to ovalbumin (OVA) to establish asthma model, and the asthma features were evaluated. The splenic natural killer (NK) cells in the offspring were measured to explore the mechanism on the effects of asthma in the offspring. The responses of the pregnant mice and dams after Oexposure were evaluated.

RESULTS: Airway inflammation, mucus secretion, OVA-specific immunoglobulin (Ig) E, T helper (Th) 2-skewed response, the frequency of CD3εCD49bsplenic NK cells, the expression of tumor necrosis factor (TNF)-α, and IL (interleukin)-17 were significantly exacerbated in the OVA-induced asthma offspring after prenatal Oexposure. In addition, airway inflammation, a lower number of CD3εCD49bsplenic NK cells, and systemic oxidative stress were caused at the end of pregnancy after Oexposure, which did not recover at the end of lactation for the first two responses.

CONCLUSIONS: Prenatal Oexposure increased the severity of OVA-induced asthma in the offspring, which might be directly induced by CD3εCD49bsplenic NK cells in the offspring and indirectly related to the damaged maternal immune system.

Study Type : Animal Study

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