In pigs, luteolytic sensitivity to PGF-2α (=LS) is delayed until d 13 of the estrous cycle. While the control of LS is unknown, it is temporally associated with macrophage (MAC; which secretes tumor necrosis factor [TNF]-α) infiltration into the corpora lutea (CL), and previous studies have shown that TNF-α induces LS in porcine luteal cells (LCs) in culture. This study was designed to explore the control of LS by CL macrophage (CL MAC)/TNF-α by progesterone (P4), and to examine the hypothesis that P4 acting via the genomic P4 receptor (PGR) inhibits CL MAC TNF-α and thus plays a key role in regulating LS during the pig estrous cycle. In experiment 1, the effects of LCs on CL MAC cytokine/TNF-α mRNA expression in co-culture were examined (MID cycle; ~d 7–12; no LS); results showed that LC was inhibitory to cytokine/TNF-α. In experiment 2, the effects of P4 or R5020 (PGR-agonist) on CL MAC cytokine/TNF-α mRNA expression were examined (MID cycle; ~d 7–12; no LS); results showed that both P4 and R5020 dose-dependently inhibited TNF-α. In experiment 3, CL MACs were isolated from CL at MID (~d 7–12; no LS) and LATE (~d 13–18; + LS) cycle, and TNF-α/PGR mRNA measured. Results indicated that while TNF-α mRNA was 4.2-fold greater in CL MACs from LATE vs MID cycle, PGR mRNA was 4.5-fold greater in CL MACs from MID vs LATE cycle. These data support our hypothesis and suggest that progesterone, acting via PGR, plays a critical physiological role in the control of TNF-α production by CL MACs and LS during the pig estrous cycle.

在猪中，对PGF-2α（= LS）的溶血敏感性被推迟到发情周期的d 13为止。虽然LS的控制尚不清楚，但它在时间上与巨噬细胞（MAC；分泌肿瘤坏死因子[TNF]-α）渗入黄体（CL）有关，先前的研究表明TNF-α诱导猪中的LS培养中的黄体细胞（LCs）。本研究旨在探讨通过孕酮（P4）控制CL巨噬细胞（CL MAC）/TNF-α对LS的控制，并检验P4的假设通过基因组P4受体（PGR）发挥作用可抑制CL MACTNF-α，因此在猪发情周期中对LS的调节起关键作用。在实验1中，研究了LC对共培养中CL MAC细胞因子/TNF-αmRNA表达的影响（MID周期；〜d 7-12；无LS）；结果表明，LC对细胞因子/TNF-α具有抑制作用。在实验2中，检查了P4或R5020（PGR激动剂）对CL MAC细胞因子/TNF-αmRNA表达的影响（MID周期；〜d 7-12；无LS）；结果表明，P4和R5020均剂量依赖性地抑制TNF-α。在实验3中，在MID（〜d 7-12；无LS）和LATE（〜d 13-18； + LS）周期从CL中分离出CL MACs，并测量了TNF-α/ PGR mRNA。结果表明，虽然从LATE到MID周期，CL MACs中的TNF-αmRNA比在MID周期大4.2倍，但从MID到LATE周期，CL MACs中的PGR mRNA是4.5倍。