Impact of uterine macrophage phenotype on placental retention in dairy cows
THERIOGENOLOGY
Authors: Nelli, Rahul K.; De Koster, Jenne; Roberts, Jennifer N.; de Souza, Jonas; Lock, Adam L.; Raphael, William; Agnew, Dalen; Contreras, G. Andres
Abstract
Reproductive diseases affect 25% of dairy cows in the US and often develop from retention of the placenta. It is well established that expulsion of the placenta is a highly regulated inflammatory process, but the mechanisms by which dysregulation of uterine immune responses impair this process are poorly understood. In healthy non-ruminants, pro-inflammatory M1 macrophages are predominant in uterine tissue after parturition. However, macrophage phenotype in the postpartum bovine uterus is unknown. Our study compared macrophage phenotypes in the uterine caruncles of multiparous dairy cows that during the first day postpartum either retained (RET, n = 5) or had normal expulsion (NOR, n = 5) of placenta. Immune cells were sorted magnetically from the caruncular endometrial cell fraction using the CD172a marker and monocyte/macrophage population was characterized using flow cytometry. Transcriptional and protein expression studies were performed on uterine caruncles. Compared to NOR, RET samples showed a lower CD14(+)/CD16(+) expression (P < 0.05) in caruncle monocyte/macrophage population. As opposed to NOR, RET further demonstrated greater expression of anti-inflammatory M2 macrophage associated genes CD206, C-type lectin domain family 7 member A (CLEC7A), and RNASE6. In addition, caruncles from RET showed decreased signal transducer and activator of transcription 3 (STAT3) activation, an important promoter of proteolytic activity, compared to NOR. Our studies demonstrate that there is an overall lower number of macrophage populations in the caruncle of cows with RET placenta and these are polarized towards M2 phenotype. Excessive accumulation of M2 macrophages may lead to reduced trafficking of immune cells into the caruncle thus impairing the inflammatory, phagocytic and proteolytic processes that lead to placental expulsion. (C) 2019 Elsevier Inc. All rights reserved.
Variation in the Yak Dectin-1 Gene (CLEC7A)
DNA AND CELL BIOLOGY
Authors: Yang, Guo; Zhou, Huitong; Hu, Jiang; Luo, Yuzhu; Hickford, Jon G. H.
Abstract
C-type lectin domain family 7, member A (CLEC7A, dectin-1) plays an important role in antifungal immunity and belongs to the family of C-type lectin receptors. Variation in the extended exon 4-6 region of the yak dectin-1 gene (CLEC7A), which encodes the beta-glucan recognition domain, was investigated using polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP). Three and two variant sequences were identified in exons 4 and 5, respectively, and no variation was found in exon 6. The variation included two single-nucleotide substitutions in exon 4 and one single-nucleotide polymorphism in exon 5, and two of these substitutions would nominally cause amino acid substitutions (p. I158T and p. S197G) in yak dectin-1. This is the first report identifying the yak dectin-1 gene, revealing that it is polymorphic and this polymorphism might affect the structure and function of this gene in yak.