Abstract
BackgroundAll cows experience bacterial contamination and tissue injury in the uterus postpartum, instigating a local inflammatory immune response. However mechanisms that control inflammation and achieve a physiologically functioning endometrium, while avoiding disease in the postpartum cow are not succinctly defined. This study aimed to identify novel candidate genes indicative of inflammation resolution during involution in healthy beef cows. Previous histological analysis of the endometrium revealed elevated inflammation 15 days postpartum (DPP) which was significantly decreased by 30 DPP. The current study generated a genome-wide transcriptomic profile of endometrial biopsies from these cows at both time points using mRNA-Seq. The pathway analysis tool GoSeq identified KEGG pathways enriched by significantly differentially expressed genes at both time points. Novel candidate genes associated with inflammatory resolution were subsequently validated in additional postpartum animals using quantitative real-time PCR (qRT-PCR).ResultsmRNA-Seq revealed 1,107 significantly differentially expressed genes, 73 of which were increased 15 DPP and 1,034 were increased 30 DPP. Early postpartum, enriched immune pathways (adjusted P < 0.1) included the T cell receptor signalling pathway, graft-versus-host disease and cytokine-cytokine receptor interaction pathways. However 30 DPP, where the majority of genes were differentially expressed, the enrichment (adjusted P < 0.1) of tissue repair and proliferative activity pathways was observed. Nineteen candidate genes selected from mRNA-Seq results, were independently assessed by qRT-PCR in additional postpartum cows (5 animals) at both time points. SAA1/2, GATA2, IGF1, SHC2, and SERPINA14 genes were significantly elevated 30 DPP and are functionally associated with tissue repair and the restoration of uterine homeostasis postpartum.ConclusionsThe results of this study reveal an early activation of the immune response which undergoes a temporal functional change toward tissue proliferation and regeneration during endometrial involution in healthy postpartum cows. These molecular changes mirror the activation and resolution of endometrial inflammation during involution previously classified by the degree of neutrophil infiltration. SAA1/2, GATA2, IGF1, SHC2, and SERPINA14 genes may become potential markers for resolution of endometrial inflammation in the postpartum cow.
Highlights
All cows experience bacterial contamination and tissue injury in the uterus postpartum, instigating a local inflammatory immune response
It is established that the postpartum endometrial inflammatory response and its allied immune gene activation is a transient feature of the normal physiological events associated with uterine involution [6]
It is evident that a pro-inflammatory immune response is instigated early postpartum by the influx of leukocytes into the endometrium, at a cellular level, and by the significant expression of immune genes and pathways 15 days postpartum (DPP), at a molecular level
Summary
All cows experience bacterial contamination and tissue injury in the uterus postpartum, instigating a local inflammatory immune response. This study aimed to identify novel candidate genes indicative of inflammation resolution during involution in healthy beef cows. The postpartum bovine uterus undergoes involution - a process involving uterine size reduction, contraction, caruncle shedding, necrosis and rejuvenation of endometrial tissue. The involvement of inflammatory processes and the immune response during involution in the cow has been the subject of numerous recent studies. Resolution of endometrial inflammation is identifiable in healthy animals by the reduction of the number of neutrophils as involution progresses [5,6,9]. It is established that the postpartum endometrial inflammatory response and its allied immune gene activation is a transient feature of the normal physiological events associated with uterine involution [6]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
