Transcriptomic analysis of equine chorioallantois reveals immune networks and molecular mechanisms involved in nocardioform placentitis

Veterinary Research

Alejandro Esteller-Vico¹  Shavahn C. Loux²  Theodore S. Kalbfleisch²  Pouya Dini²  Kirsten E. Scoggin²  Carleigh E. Fedorka²  David W. Horohov²  Hossam El-Sheikh Ali²  Barry A. Ball²  Erdal Erol³  Craig N. Carter³  Jackie L. Smith³  Laura Kennedy³ 

[1] Department of Biomedical and Diagnostic Sciences, University of Tennessee;Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky;UK Veterinary Diagnostic Laboratory, University of Kentucky;

关键词: Equine;    Nocardioform placentitis;    Chorioallantois;    Transcriptome;    Amycolatopsis spp.;   

DOI  :  10.1186/s13567-021-00972-4

来源: DOAJ

【 摘 要 】

Abstract Nocardioform placentitis (NP) continues to result in episodic outbreaks of abortion and preterm birth in mares and remains a poorly understood disease. The objective of this study was to characterize the transcriptome of the chorioallantois (CA) of mares with NP. The CA were collected from mares with confirmed NP based upon histopathology, microbiological culture and PCR for Amycolatopsis spp. Samples were collected from the margin of the NP lesion (NPL, n = 4) and grossly normal region (NPN, n = 4). Additionally, CA samples were collected from normal postpartum mares (Control; CRL, n = 4). Transcriptome analysis identified 2892 differentially expressed genes (DEGs) in NPL vs. CRL and 2450 DEGs in NPL vs. NPN. Functional genomics analysis elucidated that inflammatory signaling, toll-like receptor signaling, inflammasome activation, chemotaxis, and apoptosis pathways are involved in NP. The increased leukocytic infiltration in NPL was associated with the upregulation of matrix metalloproteinase (MMP1, MMP3, and MMP8) and apoptosis-related genes, such as caspases (CASP3 and CASP7), which could explain placental separation associated with NP. Also, NP was associated with downregulation of several placenta-regulatory genes (ABCG2, GCM1, EPAS1, and NR3C1), angiogenesis-related genes (VEGFA, FLT1, KDR, and ANGPT2), and glucose transporter coding genes (GLUT1, GLUT10, and GLUT12), as well as upregulation of hypoxia-related genes (HIF1A and EGLN3), which could elucidate placental insufficiency accompanying NP. In conclusion, our findings revealed for the first time, the key regulators and mechanisms underlying placental inflammation, separation, and insufficiency during NP, which might lead to the development of efficacious therapies or diagnostic aids by targeting the key molecular pathways.

【 授权许可】

Unknown