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However, the mechanism involved in LPS\u2010induced cardiac malformation in prenatal fetus is still unknown. In this study, we demonstrated that LPS was induced in gut microbiota imbalance mice, and next, LPS exposure during gastrulation in the chick embryo increased the incidence of cardia bifida. Gene transfection and tissue transplantation trajectory indicated that LPS exposure restricted the cell migration of cardiac progenitors to primary heart field in gastrula chick embryos. In vitro explant allograft of GFP\u2010labeled anterior primitive streak demonstrated that LPS treatments could inhibit cell migration. A similar observation was also obtained from the cell migration assay of scratch wounds using primary culture of cardiomyocytes or H9c2 cells. In the embryos exposed to LPS, expressions of Nkx2.5 and GATA5 were disturbed. These genes are associated with cardiomyocyte differentiation when heart tube fusion occurs. Furthermore, pHIS3, C\u2010caspase3 immunohistological staining indicated that cell proliferation decreased, cell apoptosis increased in the heart tube of chick embryo. Meanwhile, in vivo, pHIS3 immunohistological staining and Hochest\/PI staining also draw the similar conclusions. The LPS exposure also caused the production of excess ROS, which might damage the cardiac precursor cells of developing embryos. At last, we showed that LPS\u2010induced cardia bifida could be partially rescued through the addition of antioxidants. Together, these results reveal that excess ROS generation is involved in the LPS\u2010induced defects in heart tube during chick embryo development.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcp.26175","type":"journal-article","created":{"date-parts":[[2017,9,8]],"date-time":"2017-09-08T12:48:38Z","timestamp":1504874918000},"page":"9271-9283","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Gut microbiota\u2010derived endotoxin enhanced the incidence of cardia bifida during cardiogenesis"],"prefix":"10.1002","volume":"233","author":[{"given":"Jing","family":"Zhang","sequence":"first","affiliation":[{"name":"Division of Histology and Embryology, Key Laboratory for Regenerative Medicine of the Ministry of Education, Medical College Jinan University Guangzhou China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Guang","family":"Wang","sequence":"additional","affiliation":[{"name":"Division of Histology 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