4.3 Article

Differential expression of endometrial toll-like receptors (TLRs) and antimicrobial peptides (AMPs) in the buffalo (Bubalus bubalis) with endometritis

Journal

VETERINARY RESEARCH COMMUNICATIONS
Volume 43, Issue 4, Pages 261-269

Publisher

SPRINGER
DOI: 10.1007/s11259-019-09761-z

Keywords

Buffalo; Toll like receptors (TLRs); beta-Defensins; Uterine infection; mRNA expression

Funding

  1. ICAR-Indian Veterinary Research Institute [OXX03079] Funding Source: Medline
  2. Indian Council of Agricultural Research [OXX03803] Funding Source: Medline

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Toll like receptors (TLRs) and beta-defensins expressed in the endometrium are part of the innate uterine defense mechanism (UDM). In the present study, transcriptional profile of TLRs (1-3, 6-8, 10, and) and beta-defensins such as lingual antimicrobial peptide (LAP), tracheal antimicrobial peptide (TAP) and bovine neutrophil beta-defensin 4 (BNBD4) were studied. Bubaline genitalia were collected from abattoir and the endometrium was categorized into one of the following seven groups (n = 7/group) based on cyclicity and endometritis: follicular non-endometritis (FNE), luteal non-endometritis (LNE), follicular cytological endometritis (FCE), luteal cytological endometritis (LCE), follicular purulent endometritis (FPE), luteal purulent endometritis (LPE) and acyclic non-endometritis (ANE). Cytological endometritis (CE) was diagnosed by uterine cytology while purulent endometritis (PE) was diagnosed by the presence of purulent or mucopurulent exudate in the uterine lumen. Real time PCR was performed and the relative fold change was analysed. TLR1 and BNBD4 transcripts were not found in the buffalo endometrium. Of all the innate immune genes studied, upregulation of TLR and beta-defensins was mostly contributed by the inflammatory status of endometrium. Further, there was a prominent upregulation of TAP in buffaloes with endometritis. However, no association could be found between the inflammatory status of the endometrium and phase of estrous cycle with respect to the expression of TLRs and beta-defensins.

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