RESUMEN
BACKGROUND: Failure to expel fetal membranes within 24 h of calving is a pathological condition defined as retained placenta (RP). The objective of this investigation was to evaluate whether there are alterations in several selected serum variables related to innate immunity and carbohydrate and lipid metabolism that precede occurrence of RP in transition Holstein dairy cows. METHODS: One hundred multiparous Holstein dairy cows were involved in the study. Blood samples were collected from the coccygeal vein during the -8 to +4 wks around parturition, once per week before the morning feeding. Six healthy control cows (CON) and 6 cows with RP were selected and serum samples at -8, -4, time of diagnosis of disease, and +4 wks relative to parturition were used for analyses. All samples were analyzed for lactate, non-esterified fatty acids (NEFA), ß-hydroxybutyrate (BHBA), interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor (TNF), haptoglobin (Hp), and serum amyloid A (SAA). RESULTS: Cows with RP had greater concentrations of serum lactate, IL-1, IL-6, TNF, and SAA in comparison with CON cows. Intriguingly, elevated concentrations of all five variables were observed at -8 and -4 wks before the occurrence of RP compared to healthy cows. Cows with RP also had lower DMI and milk production vs CON animals; however milk composition was not affected by RP. CONCLUSIONS: Cows with RP showed an activated innate immunity 8 wks prior to diagnosis of disease. Overall results suggest that serum IL-1, IL- 6, and TNF, and lactate can be used as screening biomarkers to indicate cows that might have health issues during the transition period.
RESUMEN
BACKGROUND: This study examined whether activation of innate immunity and alterations of carbohydrate and lipid metabolism precede development of subclinical mastitis (SCM). METHODS: Blood samples were collected from the coccygeal vein from 100 Holstein dairy cows at -8, -4, disease diagnosis week, and +4 weeks postpartum. Six healthy cows (controls - CON) and six cows that showed clinical signs of SCM were selected for serum analyses. All serum samples were analyzed for acute phase proteins (APP) haptoglobin (Hp) and serum amyloid A (SAA); proinflammatory cytokines including interleukin 1 (IL-1), IL-6, and tumor necrosis factor (TNF) and serum lactate, BHBA, and NEFA concentration. Data of DMI, milk production, and milk composition were recorded and analyzed. RESULTS: The results showed that cows with SCM had greater concentrations of SAA, TNF (P < 0.01), and lactate before expected day of parturition (P < 0.05) compared to CON cows. Cows with SCM showed greater concentrations of lactate starting at -8 weeks (P < 0.05) and TNF starting at -4 weeks prior to the expected day of parturition (P < 0.01). Interestingly, at -4 weeks, concentrations of IL-1 and Hp were lower in cows with SCM compared to healthy cows (P < 0.01) followed by an increase during the week of disease diagnosis (P < 0.05). Subclinical mastitis was associated with lower DMI, at -4 weeks before calving, milk production (P < 0.05) and increased somatic cell counts (SCC) (P < 0.01). CONCLUSIONS: Results of this study suggest that SCM is preceded by activated innate immunity and altered carbohydrate metabolism in transition dairy cows. Moreover the results support the idea that Hp, lactate, and SAA, at -8 weeks, and TNF and IL-1 at -4 weeks can be used as early indicators to screen cows during dry off for disease state.
RESUMEN
The objectives of this study were to test whether recombinant mouse (mo)PrP alone or in combination with LPS or under simulated endotoxemia would affect expression of genes related to host inflammatory and antimicrobial responses. To test our hypotheses colon tissues were collected from 16 male mice (FVB/N strain) and mounted in an Ussing chamber. Application of moPrP to the mucosal side of the colon affected genes related to TLR- and NLR- signaling and antimicrobial responses. When LPS was added on the mucosal side of the colon, genes related to TLR, Nlrp3 inflammasome, and iron transport proteins were over-expressed. Addition of LPS to the serosal side of the colon up-regulated genes related to TLR- and NLR-signaling, Nlrp3 inflammasome, and a chemokine. Treatment with both moPrP and LPS to the mucosal side of the colon upregulated genes associated with TLR, downstream signal transduction (DST), inflammatory response, attraction of dendritic cells to the site of inflammation, and the JNK-apoptosis pathway. Administration of moPrP to the mucosal side and LPS to the serosal side of the colon affected genes related to TLR- and NLR-signaling, DST, apoptosis, inflammatory response, cytokines, chemokines, and antimicrobial peptides. Overall this study suggests a potential role for moPrP as an endogenous 'danger signal' associated with activation of colon genes related to innate immunity and antibacterial responses.