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

AI Article Synopsis

  • - The study investigated Nocardioform placentitis (NP) in mares, a disease linked to abortion and preterm births, by analyzing the transcriptome of the chorioallantois (CA) tissue from mares affected by NP and comparing it to normal mares.
  • - Researchers found 2,892 differentially expressed genes (DEGs) in the NP lesion area compared to normal postpartum tissue, revealing significant involvement of inflammatory and apoptosis signaling pathways in NP's pathology.
  • - Key findings show that NP is associated with increased inflammation and placental separation, along with downregulation of crucial genes for placental function and nutrient transport, providing insights that could aid in developing targeted therapies for NP.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8268225PMC
http://dx.doi.org/10.1186/s13567-021-00972-4DOI Listing

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