Worker Injuries Involving the Interaction of Cattle, Cattle Handlers, and Farm Structures or Equipment.

Cattle have been identified as leading sources of injuries to agricultural workers. The present study focused on worker injuries that involved the interaction of cattle, cattle handlers, and farm structures or equipment. The goal of the study was to identify opportunities for injury prevention. We examined 221 reports of injury to cattle handlers from the Consumer Product Safety Commission's National Electronic Injury Surveillance System (NEISS). Expected interactions led to many of the cattle-handling injuries reported in the NEISS database. In almost 30% of cases, cattle pushed workers into structures such as fences, gates, posts, and walls. In another 16% to 19% of injuries, cattle struck gates and other objects, propelling them at the victims. The present research makes several important contributions to the study of cattle-handling injuries. First, the research supports an increased emphasis on the development of safer gate designs (e.g., gates that are remotely operated or that absorb energy to limit the speed at which they may be propelled by animals). Second, the research suggests a need for additional study of energy-absorbing fence and wall structures. We view these two points to be of significance because gates and associated structures (e.g., posts, fences, and walls) accounted for 45% of the injuries in the dataset, based on the associated injury narrative. Finally, the research identifies a previously unexplored source of agricultural injury data, namely the NEISS database.

Continuous low-dose infusion of tumor necrosis factor alpha in adipose tissue elevates adipose tissue interleukin 10 abundance and fails to alter metabolism in lactating dairy cows.

Repeated bolus doses of tumor necrosis factor-α (TNFα) alters systemic metabolism in lactating cows, but whether chronic release of inflammatory cytokines from adipose tissue has similar effects is unclear. Late-lactation Holstein cows (n=9-10/treatment) were used to evaluate the effects of continuous adipose tissue TNFα administration on glucose and fatty acid (FA) metabolism. Cows were blocked by feed intake and milk yield and randomly assigned within block to control or TNFα treatments. Treatments (4mL of saline or 14µg/kg of TNFα in 4mL of saline) were infused continuously over 7d via 2 osmotic pumps implanted in a subcutaneous adipose depot. Plasma, milk samples, milk yield, and feed intake data were collected daily, and plasma glucose turnover rate was measured on d 7. At the end of d 7, pumps were removed and liver and contralateral tail-head adipose biopsies were collected. Results were modeled with the fixed effect of treatment and the random effect of block. Treatment with TNFα increased plasma concentrations of the acute phase protein haptoglobin, but did not alter plasma TNFα, IL-4, IL-6, or IFN-γ concentrations, feed intake, or rectal temperature. Milk yield and composition were unchanged, and treatments did not alter the proportion of short- versus long-chain FA in milk on d 7. Treatments did not alter plasma free FA concentration, liver triglyceride content, or plasma glucose turnover rate. Surprisingly, TNFα infusion tended to decrease liver TNFα and IL-1 receptor 1 mRNA abundance and significantly increased adipose tissue IL-10 protein concentration. Continuous infusion of TNFα did not induce the metabolic responses previously observed following bolus doses delivered at the same rate per day. Metabolic homeostasis may have been protected by an adaptive anti-inflammatory response to control systemic inflammation.

Anti-inflammatory salicylate treatment alters the metabolic adaptations to lactation in dairy cattle.

Adapting to the lactating state requires metabolic adjustments in multiple tissues, especially in the dairy cow, which must meet glucose demands that can exceed 5 kg/day in the face of negligible gastrointestinal glucose absorption. These challenges are met through the process of homeorhesis, the alteration of metabolic setpoints to adapt to a shift in physiological state. To investigate the role of inflammation-associated pathways in these homeorhetic adaptations, we treated cows with the nonsteroidal anti-inflammatory drug sodium salicylate (SS) for the first 7 days of lactation. Administration of SS decreased liver TNF-α mRNA and marginally decreased plasma TNF-α concentration, but plasma eicosanoids and liver NF-κB activity were unaltered during treatment. Despite the mild impact on these inflammatory markers, SS clearly altered metabolic function. Plasma glucose concentration was decreased by SS, but this was not explained by a shift in hepatic gluconeogenic gene expression or by altered milk lactose secretion. Insulin concentrations decreased in SS-treated cows on day 7 compared with controls, which was consistent with the decline in plasma glucose concentration. The revised quantitative insulin sensitivity check index (RQUICKI) was then used to assess whether altered insulin sensitivity may have influenced glucose utilization rate with SS. The RQUICKI estimate of insulin sensitivity was significantly elevated by SS on day 7, coincident with the decline in plasma glucose concentration. Salicylate prevented postpartum insulin resistance, likely causing excessive glucose utilization in peripheral tissues and hypoglycemia. These results represent the first evidence that inflammation-associated pathways are involved in homeorhetic adaptations to lactation.

Daily injection of tumor necrosis factor-{alpha} increases hepatic triglycerides and alters transcript abundance of metabolic genes in lactating dairy cattle.

To determine whether inflammation can induce bovine fatty liver, we administered recombinant bovine tumor necrosis factor-alpha (rbTNF) to late-lactation Holstein cows. Cows (n = 5/treatment) were blocked by feed intake and parity and randomly assigned within block to control (CON; saline), rbTNF at 2 microg/(kg.d), or pair-fed control (saline, intake matched) treatments. Treatments were administered once daily by subcutaneous injection for 7 d. Plasma samples were collected daily for analysis of glucose and FFA and a liver biopsy was collected on d 7 for triglyceride (TG) and quantitative RT-PCR analyses. Data were analyzed using treatment contrasts to assess effects of tumor necrosis factor-alpha (TNFalpha) and decreased feed intake. By d 7, feed intake of both rbTNF and pair-fed cows was approximately 15% less than CON (P < 0.01). Administration of rbTNF resulted in greater hepatic TNFalpha mRNA and protein abundance and 103% higher liver TG content (P < 0.05) without affecting the plasma FFA concentration. Hepatic carnitine palmitoyltransferase 1 transcript abundance tended to be lower (P = 0.09) and transcript abundance of fatty acid translocase and 1-acyl-glycerol-3-phosphate acyltransferase was higher (both P < 0.05) after rbTNF treatment, consistent with increased FFA uptake and storage as TG. Transcript abundance of glucose-6-phosphatase (P < 0.05) and phosphoenolpyruvate carboxykinase 1 (P = 0.09), genes important for gluconeogenesis, was lower for rbTNF-treated cows. These findings indicate that TNFalpha promotes liver TG accumulation and suggest that inflammatory pathways may also be responsible for decreased glucose production in cows with fatty liver.

Porcine liver-expressed antimicrobial peptides, hepcidin and LEAP-2: cloning and induction by bacterial infection.

Hepcidin is a liver-expressed iron-regulating hormone that also is an antimicrobial peptide. Here we report the full-length cDNA sequences of porcine hepcidin and liver-expressed antimicrobial peptide-2 (LEAP-2). Porcine hepcidin and LEAP-2 cDNA sequences contain 411 and 525 bp, and encode predicted peptides of 82 and 77 amino acid residues, respectively. Both porcine hepcidin and LEAP-2 are highly expressed in liver and LEAP-2 also is expressed in intestinal tissues and kidney. Pigs infected with Salmonella enterica serovar Typhimurium showed inducible but differential expression of hepcidin and LEAP-2 in bone marrow and intestinal tissues. Conversely, although highly expressed in liver, expression of hepcidin mRNA in liver was not influenced by Salmonella infection. These findings provide fundamental comparative data showing the relationship of porcine hepcidin and LEAP-2 to other mammalian orthologs and indicate that bacterial infections influence their expression.

PU.1-mediated transcriptional regulation of prophenin-2 in primary bone marrow cells.

Prophenin-2 (PF-2) is a cathelicidin, 97-amino-acid antimicrobial protein stored in neutrophil secondary granules. PF-2 is expressed specifically in porcine immature myeloid cells; however, little is known about its regulation. In this study, we characterized the 5' regulatory regions of the PF-2 gene to understand the molecular mechanisms regulating its expression. Using bioinformatic approaches, site-directed mutagenesis, and transactivation experiments, we found that the PF-2 gene was regulated by transcription factor PU.1. In addition, PF-2 expression also is regulated by the cytokines GM-CSF and IL-3. Taken together, these results identify cis- and trans-acting factors involved in the regulation of PF-2 and clarify mechanisms of cathelidicin gene regulation.

Cloning of porcine triggering receptor expressed on myeloid cells-1 (TREM-1) and its induction by lipopolysaccharide, peptidoglycan, and Salmonella enterica serovar Typhimurium infection.

Triggering receptors expressed on myeloid cells (TREM) are a family of activating receptors expressed on neutrophils and monocytes. These receptors are involved in regulation of immunity by inducing the expression of inflammatory cytokines and adhesion molecules, augmenting dendritic cell maturation, and are implicated in septic shock. Here we report the cloning of full-length TREM cDNA from porcine bone marrow cells, which predicts a 238 amino-acid peptide. Treating porcine bone marrow cells with lipopolysaccharide or peptidoglycan caused an increase in TREM-1 expression. Moreover, bone marrow cells derived from pigs that were orally challenged with Salmonella enterica serovar Typhimurium showed increases in TREM-1 at 8 and 24 h post-infection, respectively. Complete down-regulation of TREM-1 expression was observed at 48 h post-infection. These findings provide fundamental comparative data indicating that bacterial infection induces TREM-1 expression.

Characterization of bovine cDNA encoding triggering receptor expressed on myeloid cells 1 (TREM-1).

Triggering receptor expressed on myeloid cells 1 (TREM-1) is a type I transmembrane receptor of the immunoglobulin superfamily expressed predominantly on neutrophils and monocytes. TREM-1 induces the expression of inflammatory cytokines and adhesion molecules, and augments osteoclast, microglia, oligodendrocyte, and dendritic cell differentiation. Here, we report the cloning of TREM-1 from bovine bone marrow cells. Full-length bovine TREM-1 cDNA is 1202 base pairs in length and encodes a predicted 232 amino acid peptide. Comparative analyses showed that bovine TREM-1 has 48 to 61% amino acid identity with other TREM-1 proteins, sharing the greatest identity with porcine TREM-1. Cysteine residues characteristic of the immunoglobulin superfamily were conserved in bovine TREM-1 and RT-PCR analysis revealed diverse mRNA tissue expression for bovine TREM-1. Molecular cloning of bovine TREM-1 extends the repertoire of bovine pattern recognition receptors and provides information important for investigating their role in bovine innate immunity.