Inflammation and oxidative stress impair preimplantation embryonic morphogenesis in allergic asthma model

The incidence of allergic asthma has been increasing worldwide in recent decades. Also, an increasing number of women are suffering from poor pregnancy outcome. However, the causal relationship between allergic asthma and embryonic growth in terms of cell morphogenesis has not been well elucidated. Here, we investigated the impact of allergic asthma on the morphogenesis of preimplantation embryos. Twenty-four female BALB/c were randomly divided into control (PBS), 50-μg (OVA1), 100-μg (OVA2) and 150-μg (OVA3). On Days-0 and -14, mice were induced intraperitoneally (i.p) with ovalbumin (OVA). On Days-21 until −23, mice were challenged with OVA via intranasal instillation (i.n). Control animals were sensitized and challenged with PBS. At the end of treatment (Day-25), 2-cell embryos were retrieved and cultured in vitro until the blastocysts hatched. Results showed reduced number of preimplantation embryos at all developing stages in all treated groups (p ≤ 0.0001). Uneven blastomere size, partial compaction- and cavitation-activity, low formation of trophectoderm (TE), as well as cell fragmentation were noted in all the treated groups. Maternal serum interleukin (IL)-4, immunoglobulin (Ig)-E and 8-hydroxydeoxyguanosine (8-OHdG) were notably high (p ≤ 0.0001, p ≤ 0.01) in contrast with low total antioxidant capacity (TAOC) (p ≤ 0.0001). Our findings indicated that OVA-induced allergic asthma had compromised cell morphogenesis through reduced blastomere cleavage division, partial compaction and cavitation-activity, impairment of TE production, and cell fragmentation leading to embryonic cell death via OS mechanism.