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Abstract

Objective

To measure and compare values of interleukin 6 (IL-6), tumor necrosis factor (TNF), and nitric oxide (NO) metabolites in synovial fluid from canine joints with osteoarthritis (OA) secondary to naturally acquired cranial cruciate ligament (CCL) rupture and experimental CCL transection.

Animals

57 dogs (clinical group) with OA secondary to CCL rupture; 5 dogs (experimental group) with OA secondary to CCL transection; 19 control dogs with normal joints.

Procedure

Joints were radiographed and graded for severity of OA. Synovial fluid was collected from dogs: at surgery from the clinical group, at 90 days after surgery from the experimental group, and at necropsy from the control group. Activities of IL-6 and TNF, as well as concentration of the NO metabolites (NO2 /NO3 ) were measured, and results were reported as mean ± SEM.

Results

IL-6 activity in dogs of the clinical (290 ± 40 U/ml) and experimental (494 ± 165 U/ml) groups was greater than that in control dogs (6 ± 1.6 U/ml; P < 0.05). The TNF values in dogs of the clinical (3.0 ± 0.5 pg/ml) and experimental (2.0 ± 0.9 pg/ml) groups were lower than those in control dogs (8.6 ± 2.3 pg/ml; P < 0.05). The IL-6 values were negatively associated with radiographic score of OA and were positively associated with age (R 2 = 26.5%, P < 0.05).

Conclusion

Dogs with OA secondary to naturally acquired CCL rupture and experimental CCL transection had significantly different alterations in synovial fluid IL-6 and TNF values. The decrease in IL-6 activity with advancing OA was independent of the increase in IL-6 activity with aging.

Clinical Relevance

IL-6 and TNF may be involved in pathogenesis of OA secondary to naturally acquired and experimentally induced CCL rupture. (Am J Vet Res 1997;58:1027–1032)

Free access
in American Journal of Veterinary Research

Summary

Before dogs with lung tumors were treated by adoptive immunotherapy, the ability of canine blood lymphocytes (pbl) from the peripheral circulation to differentiate in vitro in the presence of human recombinant interleukin-2 (rIL-2) and become tumoricidal was investigated. The pbl from healthy dogs (n = 6) and dogs with lung tumors (n = 5) were grown in culture medium alone, in the presence of rIL-2 to generate lymphokine-activated killer (lak) cells, or with phytohemagglutinin (pha) and rIL-2 to generate autologous-stimulated lymphocytes (asl). After 4 days, cytotoxicity by the asl, lak, and pbl was determined in a 4-hour 51chromium-release assay. Target cells in the assay were short-term cultured enzyme digests of autologous (self), allogeneic (genetically different) primary tumors, and Raji, the xenogeneic human lymphoma cell line. The pbl cultured without rIL-2 were not cytotoxic against any tumor. However, when a dog's pbl were activated in vitro, they killed the dog's own tumor, asl more effectively than lak cells. Pulmonary adenocarcinomas and an osteosarcoma metastasis to lung were among the autologous tumors assayed. Against an allogeneic canine osteosarcoma, asl generated from healthy dogs were significantly more cytolytic than lak from healthy dogs, or than asl generated from tumorbearing dogs. Cytotoxicity was greater against allogeneic tumor than against Raji. Lectin-dependent cellular cytotoxicity, tested by including pha in the assay medium with lymphocytes and Raji cells, by asl and lak was greater than cytotoxicity of Raji without pha. Because asl were more cytolytic than lak against all targets in vitro, they may be more beneficial than lak for immunotherapy of canine tumors.

Free access
in American Journal of Veterinary Research

this to be appreciated and is not effective for Culicoides spp IBH. 6 , 9 , 10 In humans and dogs, the relevance of interleukin 31 (IL-31) in allergic skin disease is now well established, and the treatments of choice for canine allergic skin

Full access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To characterize the mucosal IgE network in dogs affected with inflammatory bowel disease (IBD) and compare it with that for healthy dogs.

Animals—9 healthy dogs and 20 dogs with IBD.

Procedure—In situ hybridization of mRNA specific for IgE and interleukin 4 (IL-4) and immunohistochemical analysis for IgE protein and 2 markers of mast cells (ie, tryptase and chymase) were performed on tissue sections obtained from the gastrointestinal (GI) tract and lymph nodes of dogs.

Results—Dogs with IBD had significantly more cells positive for IgE protein and more mast cells in the GI mucosa than healthy dogs. Despite this significant increase in number of cells positive for IgE, cells positive for IgE mRNA were rarely detected in the GI mucosa; most cells positive for IgE mRNA were found in mesenteric lymph nodes. Signal pattern of IL-4 mRNA was similar to that of IgE mRNA.

Conclusions and Clinical Relevance—The increased numbers of cells positive for IgE and mast cells in dogs with IBD suggest hypersensitivity such as hypersensitivity to bacterial or dietary-derived antigens in the intestinal lumen. Future studies need to elucidate whether this represents a cause of inflammation or is a result of the inflammatory process of IBD. (Am J Vet Res 2001;62:211–216)

Full access
in American Journal of Veterinary Research

SUMMARY

Twenty-four horses were randomly allocated to 3 groups. Horses were anesthetized, subjected to a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls. Group-2 horses were subjected to 6 hours of low-flow colonic arterial ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline (bl) samples were collected, then low-flow ischemia was induced by reducing ventral colonic arterial blood flow to 20% of bl. All horses were monitored for 6 hours after bl data were collected. blood samples were collected from the colonic vein and main pulmonary artery (systemic venous [sv]) for measurement of plasma endotoxin, 6-keto prostaglandin F (6-kPG), thromboxane B2 (txb 2), and prostaglandin E2 (pge 2) concentrations. Tumor necrosis factor and interleukin-6 activities were measured in colonic venous (cv) serum samples. Data were analyzed, using two-way anova, and post-hoc comparisons were made, using Dunnett's and Tu- key's tests. Statistical significance was set at P < 0.05. Endotoxin was not detected in CV or sv plasma at any time. There was no detectable tumor necrosis factor or interleukin-6 activity in CV samples at any time. There were no differences at bl among groups for CV or sv 6-kPG, pge 2, or txb 2 concentrations, nor were there any changes across time in group-1 horses. Colonic venous 6-kPG concentration increased during ischemia in horses of groups 2 and 3; CV 6-kPG concentration peaked at 3 hours in group-3 horses, then decreased during reperfusion, but remained increased through 6 hours in group-2 horses. Systemic venous 6-kPG concentration increased during reperfusion in group-3 horses, but there were no changes in group- 2 horses. Colonic venous pge 2 concentration increased during ischemia in horses of groups 2 and 3, and remained increased for the first hour of reperfusion in group-3 horses and for the 6-hour duration of ischemia in group-2 horses. There were no temporal alterations in sv pge 2 concentration. There was no difference in CV or sv ixb2 concentration among or within groups across time; however, there was a trend (P = 0.075) toward greater CV txb 2 concentration at 3.25 hours, compared with bl, in group-3 horses. Eicosanoid concentrations were significantly lower in sv, compared with CV plasma. Prostaglandin E2 and 6-kPG concentrations were approximately 3 to 8 and 5 to 10 times greater, respectively, in CV than in sv plasma. The increased concentrations of 6-kPG and pge 2 in CV plasma were likely attributable to their accumulation secondary to colonic ischemia. The increased values of these vasodilator eicosanoids may have a role in the reactive hyperemia observed during reperfusion. The increased 6-kPG concentration in sv plasma may represent spillover from the colonic vasculature, but more likely reflects systemic production.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To determine the effects of prostaglandin E2 (PGE2) on recombinant equine interleukin (IL)-1β-stimulated expression of matrix metalloproteinases (MMP 1, MMP 3, MMP 13) and tissue inhibitor of matrix metalloproteinase 1 (TIMP 1) in vitro.

Sample Population—Cultured equine chondrocytes.

Procedure—Stationary monolayers of first-passage chondrocytes were exposed to graduated concentrations of PGE2 with or without a subsaturating dose (50 pg/ml) of recombinant equine IL-1β (reIL-1β) to induce expression of MMP 1, MMP 3, MMP 13, and TIMP 1, followed by RNA isolation and northern blotting. In subsequent experiments, gene expression was similarly quantified from mRNA isolated from cultures pretreated with phenylbutazone to quench endogenous PGE2 synthesis, followed by exposure to reIL-1β and exogenous PGE2 (5 mg/ml) with appropriate controls.

Results—Exogenous PGE2 (10 mg/ml) significantly reduced reIL-1β-induced expression of MMP 1, MMP 3, MMP 13, and TIMP 1. Abrogation of cytokine induction with this dose of PGE2 was comparable to that for dexamethasone (10–5 M) control. Similarly, pretreatment with phenylbutazone, followed by exposure to reIL-1β and PGE2 (5 mg/ml), was associated with a reduced expression of the genes of interest, an effect that was significant for MMP 1, MMP 13, and TIMP 1.

Conclusions and Clinical Relevance—The MMP and TIMP 1 are important mediators in the pathophysiologic events in osteoarthritis. The potential for physiologically relevant regulation of expression of these genes by PGE2 is a consideration in the use of drugs that inhibit prostanoid synthesis in the treatment of equine arthropathies. (Am J Vet Res 2002;63:987–993)

Full access
in American Journal of Veterinary Research

commercially available kit d used in accordance with the manufacturer's instructions. A DNase treatment was performed before RNA was eluted from the filter, and samples were stored at −80°C until analyzed. Interleukin-1, IL-6, and TNFα mRNA expression in blood

Full access
in American Journal of Veterinary Research

associated with systemic inflammatory responses was targeted for quantification as previously described. 31 These 14 genes encoded an adenosine A 2A receptor, cyclooxygenase-2, interleukin-1B, interleukin-1 receptor antagonist, interleukin-6, interleukin-8

Full access
in American Journal of Veterinary Research

concentrations of supernatant from the cell culture for both the medium (control) and cells exposed to the fecal extract following a 24-hour incubation were determined by ELISA using commercial kits (Associates of Cape Cod Inc) for interleukin-1β (IL-1β

Full access
in American Journal of Veterinary Research