Provision of a probiotic-postbiotic blend to lactating dairy cows and the effect on circulating neutrophils following an intramammary lipopolysaccharide challenge.

This study evaluated the effects of feeding a probiotic-postbiotic blend on transcript abundance in circulating neutrophils following an intramammary (IMM) LPS challenge in lactating dairy cattle. Lactating Holstein cows (n = 16 at 57 ± 4 DIM) with SCC <250,000 cells/mL received either 28 g/d of probiotic-postbiotic (PB; n = 8, Dairyman's Edge Pro, Papillon Agricultural Company) or no PB (NP; n = 8) for 27 d before IMM infusion of 200 µg of Escherichia coli O111:B4 LPS into both rear quarters. Blood PMN were isolated at 0 (30 min before the IMM LPS challenge), 24, and 72 h following IMM LPS infusion for transcript abundance analysis using real-time reverse-transcription quantitative PCR. The PB group had 32% less PMN in blood compared with NP, and IMM LPS resulted in 59% and 63% reductions in blood PMN across both NP and PB at 24 and 72 h, respectively, relative to 0 h. Transcript abundances for SOD2, S100A8, and S100A9 increased 3.0-, 7.0-, and 5.3-fold, respectively, at 24 h relative to 0 h, but no longer differed at 72 h. TLR4, STAT3, IL1B, and CXCR1 transcript abundances were downregulated at 24 h and 72 h compared with 0 h. CXCL8 expression was reduced at 24 h relative to 0 h, but not at 72 h relative to 0 or 24 h. There was no effect of diet, time, or their interaction on the expression of transcripts for TLR2, IL6, IL10, TNF, or MPO. A diet × time interaction was detected for NFKB1 such that NP at 0 h tended to be greater than PB at 0 h (P = 0.061) and was greater than all other treatments at 24 and 72 h, and PB at 0 h did not differ from PB or NP at 24 or 72 h. In conclusion, IMM inflammation coincided with decreased PMN count in blood and was associated with a downregulated proinflammatory transcript abundance profile in circulating PMN based on the genes analyzed. This attenuated molecular phenotype may reflect accelerated PMN turnover and an increased proportion of immature PMN in circulation or, alternatively, a regulatory mechanism aimed at minimizing systemic inflammation and preserving peripheral tissue homeostasis during localized immune activation. Although PB reduced PMN abundance in blood, no measurable effect on PMN transcript abundance was detected for the genes measured.