Background: Associative data and some controlled studies suggest that the inflammatory cytokine tumor necrosis factor（TNF） α can induce fatty liver in dairy cattle. However, research demonstrating that TNFα is a necessary component in the etiology of bovine fatty liver is lacking. The aim of this work was to evaluate whether blocking TNFα signaling with a synthetic cyclic peptide（TNF receptor loop peptide; TRLP） would improve liver metabolic function and reduce triglyceride accumulation during feed restriction.Results: Capability of TRLP to inhibit TNFα signaling was confirmed on primary bovine hepatocytes treated with recombinant bovine TNFα and 4 doses of TRLP（0, 1, 10, 50 μmol/L） over 24 h. Next, 4 lactating Holstein cows（parity 1.4 ± 0.5, 433 ± 131 d in milk） in an incomplete Latin rectangle design（3 × 2） were subcutaneously administered with different TRLP doses（0, 1.5, 3.0 mg/kg BW） every 4 h for 24 h, followed by an intravenous injection of TNFα（5 μg/kg BW）. Before and for 2 h after TNFα injection, TRLP decreased plasma non-esterified fatty acid（NEFA）concentration（P ≤ 0.05）, suggesting an altered metabolic response to inflammation. Finally, 10 non-pregnant, nonlactating Holstein cows（3.9 ± 1.1 yr of age） were randomly assigned to treatments: control（carrier: 57% DMSO in PBS）or TRLP（1.75 mg TRLP/kg BW per day）. Treatments were administrated every 4 h for 7 d by subcutaneous injection to feed-restricted cows fed 30% of maintenance energy requirements. Daily blood samples were analyzed for glucose,insulin, β-hydroxybutyrate, NEFA, and haptoglobin concentrations, with no treatment effects detected. On d 7, cows completed a glucose tolerance test（GTT） by i.v. administration of a dextrose bolus（300 mg glucose/kg BW）. Glucose,insulin, and NEFA responses failed to demonstrate any significant effect of treatment during the GTT. However, plasma and liver analyses were not indicative of dramatic lipolysis or hepatic lipidosis, suggesting that the feed restriction protocol failed to induce the metabolic state of interest. Injection site inflammation, assessed by a scorer blinded to treatment, was enhanced by TRLP compared to control.Conclusions: Although the TRLP inhibited bovine TNFα signaling and altered responses to i.v. administration of TNFα,repeated use over 7 d caused apparent local allergic responses and it failed to alter metabolism during a feed restriction-induced negative energy balance. Although responses to feed restriction seemed atypical in this study, side effects of TRLP argue against its future use as a tool for investigating the role of inflammation in metabolic impacts of negative energy balance.

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.

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.

Dietary omega-3 fatty acids (n-3 PUFA), notably eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), impart health benefits in humans and animals. In horses, dietary n-3 PUFAs elevate EPA and DHA and may promote anti-inflammatory effects. No reports document effects of dietary n-3 PUFA on fatty acyl components of circulating and cellular phospholipids in horses nor whether responses to dietary n-3 PUFA are similar among horse breeds. Ten Quarter Horse and 10 American Miniature Horse mares were assigned to n-3 PUFA (64.4 mg. kg body weight [BW](-1).d(-1)) or control diet for 56 days. Blood was sampled at 0, 28, and 56 days. Apparent phospholipid molecular species from several classes (phosphatidylcholine [PC]; "ether-linked" phosphatidylcholine [i.e., alk(en)yl, acyl glycerophosphocholine] [ePC]; phosphatidylethanolamine [PE]; phosphatidylinositol [PI]; and phosphatidylserine [PS]) were determined in plasma and peripheral blood mononuclear cells (PBMC) by mass spectrometry. Statistical analysis showed that six phospholipid species had diet x day interactions (P < .05) for both plasma and PBMC. Further evaluation of these species demonstrated that the mole percentage of PC(38:6), PC(40:7), PC(42:10), PE(38:5), PE(40:6), and PE(40:7) (where x:y represents total acyl carbon:total carbon-carbon double bonds) in both plasma and PBMC phospholipids was elevated in horses fed n-3 PUFA (P < .001 for all). Analysis of the acyl product ions revealed that these contained an acyl chain of mass consistent with an n-3 PUFA. Thus, supplementation increased n-3 PUFA in selected plasma and PBMC phospholipids. The absence of breed effects suggests that miniature and full-size horses responded similarly to dietary treatment. (C) 2013 Elsevier Inc. All rights reserved.

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.

The gastrointestinal tract (GIT) constitutes one of the largest immunological organs of the body. The GIT must permit absorption of nutrients while also maintaining the ability to respond appropriately to a diverse milieu of dietary and microbial antigenic components. Because of the diverse population of antigenic components within the GIT, a sophisticated mucosal immune system has evolved that relies on collaboration between the innate and adaptive arms of immunity. The collaborative, mucosal immune effort offers protection from harmful pathogens while also being tolerant of dietary antigens and normal microbial flora. Knowledge with respect to porcine mucosal immunity is important as we strive to understand the interrelationships among GIT physiology, immunology, and the resident microbiota. The aim of this review is to provide a descriptive overview of GIT immunity and components of the mucosal immune system and to highlight differences that exist between the porcine species and other mammals.

Multiple lines of inquiry have suggested that a high degree of inflammation in early lactation cows is associated with low productivity and increased disease incidence. In addition, some small studies have suggested that milk production increases in response to antiinflammatory treatment in the first week of lactation. Our objective was to determine if administration of sodium salicylate (SS), a nonsteroidal antiinflammatory drug (NSAID), in the first week of lactation changes whole-lactation productivity and retention in the herd. At calving, 78 cows [n = 39 primiparous (1P); n = 24 second parity (2P); n = 15 third parity or greater (3P)] were alternately assigned to either control (CON) or SS treatments for 7 d postpartum. Sodium salicylate treatment was administered via individual water bowls at a concentration of 1.95 g/L, delivering a mean of 123.3 ± 5.5 g of salicylate/d during the 7-d treatment. For the first 21 d of lactation, dry matter intake, water intake, milk yield, and health were monitored daily, and milk samples were collected twice weekly for milk component analysis. Monthly milk yield and component testing through the rest of the lactation provided data to assess long-term responses, and the effects of treatment on the risk of leaving the herd and on 305-d milk, fat, and protein yields were assessed. During the first 21 d of lactation, we observed no differences in morbidity, except for increased risk of metritis in 3P SS cows. Treatment interacted with parity to influence both 305-d milk and milk fat yields, and a tendency for an interaction was detected for 305-d milk protein yield. Milk yield was 2,469 ± 646 kg greater over the lactation in 3P SS cows compared with 3P CON cows (21% increase) and tended to decrease by 8% in 1P cows treated with SS; no effects were detected in 2P cows. Furthermore, 3P SS cows produced 130 ± 23 kg more milk fat over the lactation (30% increase), with no effects detected for 1P or 2P. Treatment with SS tended to increase 305-d milk protein yield in 3P cows by 14%, with no effects in 1P or 2P cows. A tendency for a treatment × parity interaction was also observed for the risk of leaving the herd. First-parity cows treated with SS tended to have greater risk of leaving the herd than controls (30 vs. 6% risk); however, treatment did not alter herd retention in 2P or 3P groups, and SS had no effect on the risk of leaving the herd overall. Results indicate that SS has long-term effects on lactation of mature dairy cows, particularly on fat yield, but may have negative effects for primiparous cows.

Inflammation has been proposed as a contributor to metabolic disorders in transition dairy cows. The purpose of this experiment was to determine if a non-steroidal anti-inflammatory drug, sodium salicylate (SS), benefits transition cows. At calving, 78 cows [primiparous (1P) n = 39; 2nd lactation (2P) n = 24; ≥3 lactations (3P) n = 15] were assigned alternately to either a control or SS treatment for 7 days and production responses were evaluated through the entire lactation. Treatment was administered via individual water bowls, delivering a mean of 123 ± 5.5 (mean ± standard deviation) grams salicylate per day during the 7 days of treatment. Cows were followed throughout the lactation by monthly milk yield and component testing, and the effects of treatment on the risk of leaving the herd and on normalized 305-day milk, fat, and protein yields were determined by Fisher’s exact test and mixed model analysis, respectively. Treatment influenced both 305-day milk and fat yields differently across parities. Milk yield was increased by 17% in 3P SS cows (4,374 ± 1,549 lb greater for 3P SS cows). Primiparous SS cows tended to produce 2,155 ± 824 lb less 305-day milk than control cows; no differences were detected for 2P cows. Furthermore, 3P SS cows produced 285 ± 50 lb more 305-day milk fat and tended to produce 108 ± 40 lb more 305-day milk protein. No effects were detected in 1P or 2P cows. A treatment by parity interaction was observed for the risk of leaving the herd where 1P cows treated with SS tended to have a greater risk of leaving the herd than controls (30% vs. 6% risk). Treatment did not alter herd retention in 2P or 3P groups, and SS had no effect on the risk of leaving the herd overall. Results indicate that SS has long-term effects on lactation characteristics of aged cows, particularly on fat metabolism, but has potential negative effects for primiparous cows.

Steroidal implants are used extensively in beef cattle management to take advantage of welldocumented improvements in growth performance and efficiency. In addition to muscle growth, steroids bring about changes in bone and cartilage formation, hastening bone ageing. The current study was designed to test the hypothesis that recently identified indicators of bone and cartilage turnover could be detected in the peripheral circulation, and that these markers might reflect accelerated ageing effects of the widely used steroidal implants, trenbolone acetate (TBA) and estradiol-17β (E2). Thirty-two crossbred yearling steers were given one of four treatments to determine whether these markers of bone turnover could be detected and reflect steroid-induced bone maturity in the periphery: non-implanted controls; 25.7 mg estradiol-17β (E2); 120 mg trenbolone acetate (TBA); or 120 mg TBA and 24 mg E2 (T+E). Blood was collected on days 0, 7, 14 and 28 and serum analysed by ELISA for concentrations of IGF-I, osteocalcin, C-terminal telopeptides of Type I collagen (CTX-I) and C-terminal telopeptides of Type II collagen (CTX-II), as markers of the somatotropic-endocrine axis, bone formation, bone resorption and cartilage resorption, respectively. Circulating IGF-I was greater in E2 or T+E treated steers than controls on days 7 and 14. Osteocalcin was unaffected by treatment, but increased from day 0 on days 7, 14 and 28. Treatment did not affect CTX-I. However, CTX-II was elevated in the treated animals as opposed to the controls. Although these markers of bone and cartilage turnover are detectable, results suggest that implant-induced changes are not evident in the circulatory system. Keywords: Bone, cartilage, cattle, oestradiol 17-β, growth, trenbolone acetate

Inflammation has been proposed as a contributor to metabolic disorders in transition dairy cows. The purpose of this experiment was to determine whether a non-steroidal anti-inflammatory drug, sodium salicylate (SS), benefits transition cows. At calving, 78 cows (primiparous, n = 39; second lactation, n = 28; ≥3 lactations, n = 11) were assigned alternately to either a control (CON) or SS treatment for 7 days and remained on study until 21 days postpartum. Treatment was administered via individual water bowls at a concentration of 2.5 g/L, delivering a mean of 183 ± 8.5 g/day SS during the 7 days of treatment. Milk yields were collected daily and milk samples were collected twice weekly. Data were analyzed using mixed models with repeated measures over time. No treatment effects were detected for daily feed or water intake. Milk yield for third or greater lactation cows tended to increase (P < 0.10) with SS at the end of the trial (days 19 to 20). Milk protein content increased (P < 0.05) with SS in firstand second-lactation cows during week 1 and milk urea nitrogen (MUN) decreased (P < 0.01) with SS. Milk fat content increased (P < 0.05) with SS in weeks 2 and 3 postpartum. A 10% increase (P < 0.05) in energy-corrected milk (ECM) was observed for SS cows during week 3. Metritis incidence increased (P < 0.01) with SS in third or greater lactation cows, but no other effects on disease incidence were detected. In contrast to our hypothesis that SS treatment would decrease transition disorder incidences, SS treatment seemed to promote increased milk fat content and milk energy output during early lactation with no effect on total disorder incidence.

Enteric disease and immune challenge are processes that have detrimental effects on the growth performance of young swine. The current study tested the hypothesis that salmonella-induced enteric disease would perturb the endocrine growth axis in a serovar-dependent fashion. Specifically, we evaluated the effects of Salmonella enterica serovar Typhimurium (Typhimurium) and serovar Choleraesuis (Choleraesuis) on critical regulatory components of growth in young swine. Weaned pigs were housed 2 per pen with ad libitum access to feed and water in a 14-d experiment. Pigs were then repeatedly fed 10(8) cfu of either Choleraesuis or Typhimurium in dough balls, with control pigs receiving dough without bacteria. Bacteria were refed twice weekly. Rectal temperatures were monitored daily from d 0 to 7 and ADFI was measured through d 14. Pigs were weighed and samples of serum were obtained for circulating IGF-I on d 0, 7, and 14. At the conclusion of the study, samples of semitendinosus muscle and liver were obtained and subsequently assayed for IGF-I, IGFBP-3, and IGFBP-5 mRNA. Rectal temperatures were elevated in pigs given Choleraesuis from d 2 through 7 (P < 0.05) when compared with control pigs and pigs fed Typhimurium. Pigs receiving Choleraesuis had a substantially decreased feed intake on d 2, 3, 4, 7, 8, 9, and 10 (P < 0.01), with a trend for a reduction on d 5 (P = 0.08), and they experienced an approximately 25% reduction in BW compared with control pigs and pigs given Typhimurium by the conclusion of the study. Pigs given Choleraesuis also experienced marked reductions in circulating IGF-I on d 7 (P < 0.01 vs. control and Typhimurium), with reductions of lesser magnitude on d 14 (P = 0.07 vs. control and P < 0.05 vs. Typhimurium). Inoculation tended to affect liver IGFBP-3 mRNA (P = 0.08), for which expression tended to be elevated in pigs given Typhimurium and Choleraesuis. In contrast, IGFBP-3 mRNA relative abundance was increased (P < 0.03) in pigs given Typhimurium compared with control pigs. Muscle IGF-I mRNA was reduced in pigs given Choleraesuis compared with control pigs and pigs given Typhimurium (P < 0.05). Treatment tended to affect muscle IGFBP-3 mRNA (P = 0.10). Oral inoculation of growing pigs with Choleraesuis disrupted feed intake and BW gain, and this was accompanied by decreases in circulating IGF-I and reduced muscle expression of mRNA for IGF-I and IGFBP-3.

Previous research evaluated a laboratory strain of Bacillus licheniformis (BL) in a model swine epithelium and found it exerted antiinflammatory effects on Salmonella enterica serovar Typhimurium (Sal)-induced secretion of IL-8. The current investigation evaluated the antiinflammatory actions of Bacillus bacteria available commercially as feed additives for the swine industry. Three isolates were obtained from the product, 2 Bacillus subtilis (BS1 and BS3) and 1 BL (BL2). Swine jejunal epithelial IPEC-J2 cells were seeded into wells on permeable membrane supports and allowed to form confluent monolayers. Treatments included apical pretreatment with BL, BS1, BL2, or BS3 for 17 h without Sal, and the same Bacillus treatments but with 10(8) cfu of Sal added in the final hour of Bacillus incubation. Two additional treatments included negative control wells receiving no bacteria (control) and positive control wells receiving only Sal (10 total treatments). After bacterial incubation, wells were washed and fresh medium containing gentamicin was added. Cells were incubated for an additional 5 h, after which apical and basolateral media were recovered for determination of IL-8 and bacitracin. In addition, inserts with epithelial cells that had received Sal were lysed and lysates were cultured to determine treatment effects on Sal invasion. Exposure to Sal alone provoked an increase in IL-8 secretion from IPEC-J2 cells compared with control wells (P < 0.001 for both the apical and basolateral directions). Pretreatment with each Bacillus isolate followed by challenge with Sal reduced Sal-induced IL-8 secretion in both the apical and basolateral compartments compared with wells receiving only Sal (P < 0.001; except for BS3 apical, P < 0.01). The residual presence of bacitracin could be detected only in BL2 and BL2+Sal. Fewer Sal colonies could be cultured from lysates of BL2+Sal than from the Sal, BS1+Sal, and BS3+Sal treatments (P < 0.001). Results indicate that B. subtilis and BL have the ability to intervene in secretion of the neutrophil chemoattractant IL-8 from swine intestinal epithelial cells. This effect on chemokine secretion by gastrointestinal epithelial cells in vitro could not be explained solely by reduced invasion of epithelial cells by Sal.

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.

Recent data have shown that bovine fatty liver is associated with inflammation, but a causative role of inflammatory mediators has not been demonstrated. To determine whether inflammation can induce fatty liver, recombinant bovine tumor necrosis factor alpha (TNF) was administered to late-lactation Holstein cows in a randomized complete block design. Cows (n = 5 per treatment) were blocked by feed intake and milk production and randomly assigned within block to control (saline), TNF at 2 μg/kg per d, or pair-fed control (saline, intake matched) treatments. Treatments were delivered once daily by subcutaneous injection for 7 d. Plasma samples were collected daily for analysis of glucose and non-esterified fatty acids (NEFA) and a liver biopsy was collected on d 7 for triglyceride (TG) and quantitative real-time PCR analyses. Data were analyzed with mixed models using treatment contrasts to assess effects of TNF administration and decreased feed intake. By d 7, feed intake and milk production decreased by 15% and 12%, respectively, for both TNF and pair-fed cows compared to controls. TNF administration significantly increased hepatic TNF mRNA and protein abundance and increased liver TG content by 103% (P < 0.05) without affecting plasma NEFA concentration. TNF tended to decrease hepatic carnitine palmitoyltransferase 1 and increase fatty acid translocase (CD36) and 1-acyl-glycerol-3-phosphate acyltransferase transcript abundance (all P < 0.10), effects which are consistent with increased NEFA uptake and storage as TG. TNF also decreased transcript abundance for glucose6-phosphatase (P = 0.02) and phosphoenolpyruvate carboxykinase 1 (P = 0.09), genes important for gluconeogenesis. Plasma glucose concentration was not affected by treatment. These findings indicate that TNF promotes liver TG accumulation and suggest that inflammatory pathways may also be responsible for decreased glucose production in cows with fatty liver.

Salmonella enterica serovar Typhimurium (ST) and Choleraesuis (SC) are among the most frequently isolated salmonellae serovars causing enteric disease in swine. Enteric disease in young pigs is of major concern in modern production systems due to the negative implications on animal health, food safety and economic return. Epithelial cells express Toll-like receptors (TLR) that recognize conserved microbial structures and act as mediators of innate and adaptive immune responses. However, little is known about the expression of TLR gene transcripts in swine. The objective of the current study was to characterize the relative abundance of porcine TLR2, 4 and 9 gene transcripts in vitro in a porcine jejunal epithelial cell line (IPEC-J2) and in porcine mononuclear phagocytes (pMP) in the presence of ST or SC, as well as in vivo in the distal ileum of pigs orally challenged with ST. Our results indicate that TLR2, 4 and 9 are constitutively expressed in vitro in IPEC-J2 cells and pMP and in vivo in the distal ileum. Additionally, transient modulation of porcine TLR was observed in vitro and in vivo in the presence of ST and SC. Further investigation is warranted to determine the effects of ST and SC on functional TLR.

The gastrointestinal tract (GIT) constitutes one of the largest immunological organs of the body. The GIT must permit absorption of nutrients while also maintaining the ability to respond appropriately to a diverse milieu of dietary and microbial antigenic components. Because of the diverse population of antigenic components within the GIT, a sophisticated mucosal immune system has evolved that relies on collaboration between the innate and adaptive arms of immunity. The collaborative, mucosal immune effort offers protection from harmful pathogens while also being tolerant of dietary antigens and normal microbial flora. Knowledge with respect to porcine mucosal immunity is important as we strive to understand the interrelationships among GIT physiology, immunology, and the resident microbiota. The aim of this review is to provide a descriptive overview of GIT immunity and components of the mucosal immune system and to highlight differences that exist between the porcine species and other mammals.

The gastrointestinal tract (GIT) constitutes one of the largest immunological organs of the body. The GIT must permit absorption of nutrients while also maintaining the ability to respond appropriately to a diverse milieu of dietary and microbial antigenic components. Because of the diverse population of antigenic components within the GIT, a sophisticated mucosal immune system has evolved that relies on collaboration between the innate and adaptive arms of immunity. The collaborative, mucosal immune effort offers protection from harmful pathogens while also being tolerant of dietary antigens and normal microbial flora. Knowledge with respect to porcine mucosal immunity is important as we strive to understand the interrelationships among GIT physiology, immunology, and the resident microbiota. The aim of this review is to provide a descriptive overview of GIT immunity and components of the mucosal immune system and to highlight differences that exist between the porcine species and other mammals.

Long distance transportation may affect the health of pigs; thus, adding a rest stop (lairage) during long journeys may improve their well-being. The objective of this study was to determine whether a mid-journey lairage influenced swine innate immunity and intestinal microbial populations after a 16-h transport. Four replications were conducted, 1 in each of 4 seasons. Eighteen-kilogram pigs were housed in 16 pens (13 to 16 pigs/pen) with 8 pens/treatment. Lairage pigs were transported for 8 h, given a rest with food and water for 8 h, then transported for an additional 8 h. Continuous pigs were continuously transported for 16 h. Jugular blood samples and intestinal tissue and contents were collected from 16 pigs (8/treatment) on d 1, 3, 7, and 14 posttransport. Hematocrit and white blood cell counts were determined and neutrophil cell functions, including phagocytosis/oxidative burst and phagocytosis of latex beads and leukocyte phenotypic cell markers (CD14 and CD18), were analyzed using flow cytometry. Expression of toll-like receptors 2, 4, and 5; IL-8 (a cytokine that is a chemoattractant for neutrophils); CCL20 (a chemokine that is a chemoattractant for dendritic cells); and the antimicrobial peptide PR39 were determined from ileal and jejunal total RNA. Denaturing gradient gel electrophoresis was used to determine shifts in intestinal microbial populations. Total white blood cell and granulocyte counts in continuous pigs were greater (P < 0.01) on d 1 than in lairage pigs. Phagocytosis of microbeads was greater in continuous (P < 0.05) than in lairage pigs on d 7. Expression of IL-8 in jejunum was greater (P < 0.05) for continuous than for lairage pigs on d 1. Expression of CCL20 in the ileum was greater (P < 0.05) on d 14 for the continuous pigs. Expression of PR39 was greatest (P < 0.05) in the jejunum of lairage pigs on d 3. Lairage pigs had a greater (P < 0.05) variation in microbial populations (lower similarity coefficient) in the jejunum contents on d 1 and 7, in the cecum contents and tissue on d 3, and in the jejunum contents and tissue on d 14. However, continuous pigs had greater (P < 0.05) variation in the ileal tissues on d 14. This study indicates that adding a lairage to an extended transport alters immune functions, receptor, cytokine and chemokine expression, and gut microbiota compared with pigs transported for 16 h without lairage.

We investigated the influence of supplemental l-carnitine on foetal blood metabolites, litter characteristics, l-carnitine concentration in skeletal muscle and insulin-like growth factor (IGF) axis components in foetal hepatic and skeletal muscle tissues at day 40, 55 and 70 of gestating gilts. A total of 59 gilts (body weight = 137.7 kg) received a constant feed allowance of 1.75 kg/day and a top-dress containing either 0 or 50 ppm of l-carnitine starting on the first day of breeding through the allotted gestation length. Foetuses from the gilts fed diets with l-carnitine tended to be heavier (p = 0.06) and the circulating IGF-II tended to be lower (p = 0.09) at day 70, compared with the foetuses from the control gilts. Insulin-like growth factor-I messenger RNA (mRNA) was lower (p = 0.05) in hepatic tissue in the foetuses collected from gilts fed l-carnitine. Free and total carnitine concentration increased (p < 0.05) in the skeletal muscle from the foetuses collected from gilts fed supplemental l-carnitine. This study showed that l-carnitine had beneficial effects on the average foetal weight at day 70 of gestation, associated with changes in the foetal IGF system.