Change of Vertebral Left Atrial Size in Dogs With Preclinical Myxomatous Mitral Valve Disease Prior to the Onset of Congestive Heart Failure.

INTRODUCTION/OBJECTIVES: It has been proposed that vertebral left atrial size (VLAS) on thoracic radiographs can be used to assess the left atrial enlargement in dogs with myxomatous mitral valve disease (MMVD). However, it remains unclear whether VLAS can be used to distinguish dogs between pre-clinical MMVD that are at a greater risk of developing congestive heart failure (CHF) from those at a lower risk. We investigated this possibility. ANIMALS, MATERIALS AND METHODS: Forty-one dogs with MMVD were retrospectively classified into one of two groups, a group that developed CHF (group CHF, n = 17) or remained CHF-free (group no-CHF, n = 24). The value of vertebral heart scale (VHS) and VLAS at three time-points, change in VHS and VLAS at a specific time interval (ΔVHS, ΔVLAS) and rate of change in the values per month (ΔVHS/month, ΔVLAS/month) were compared. RESULTS: At the first visit, there were no significant differences in VLAS between the groups. At the median of 105 (interquartile ranges 83-155) days prior to the onset of CHF (group CHF) or the last visit (group no-CHF), VLAS was significantly higher in group CHF (mean, 2.9; standard deviation ± 0.4) than in group no-CHF (2.6 ± 0.3) (p = 0.028). ΔVLAS/month (area under the curve, 0.91; p<0.001) showed high diagnostic accuracy in distinguishing which dogs would develop CHF within 180 days and which would not. CONCLUSIONS: VLAS and ΔVLAS/month in dogs with pre-clinical MMVD may be useful to identify dogs at risk of developing CHF within the next 180 days.

Suspected human intravenous immunoglobulin-induced acute haemolytic anaemia in a dog.

A 2-year-old mixed breed dog presented with a 1-year history of crust and erosion on the nasal planum. Because histopathological examination revealed ruptured intraepidermal pustules and superficial dermal inflammation, the dog was diagnosed with pemphigus foliaceus. Human intravenous immunoglobulin was administered in two consecutive doses of 0.5 g/kg/day due to poor therapeutic response to previous immunosuppressive therapy. From Day 3 after the first dose of human intravenous immunoglobulin, tachypnoea, pale mucous membrane, haemoglobinuria and haemoglobinemia were observed, thus confirming haemolytic anaemia. Other drug-induced haemolytic anaemias were excluded because no additional drugs had been administered before the haemolysis occurred. Immune-mediated haemolytic anaemia was also excluded because the direct antiglobulin test was negative. Two transfusions were performed, and haemolysis was not observed from Day 4 of haemolytic anaemia onset. In conclusion, human intravenous immunoglobulin-induced haemolytic anaemia should be considered in dogs that develop haemolysis following the administration of human intravenous immunoglobulin.

A preliminary evaluation of the circulating leptin/adiponectin ratio in dogs with pituitary-dependent hyperadrenocorticism and concurrent diabetes mellitus.

Leptin and adiponectin are thought to modulate insulin sensitivity and pancreatic ß-cell function, but there is limited information regarding the adipokine status of hyperglycemic dogs with hyperadrenocorticism. This study aimed to determine whether alterations in the leptin/adiponectin ratio, insulin sensitivity, and/or pancreatic ß-cell function are associated with diabetes mellitus (DM) in dogs with pituitary-dependent hyperadrenocorticism (PDH). A total of 48 client-owned dogs were included in this prospective observational study: 20 dogs with PDH (10 normoglycemic and 10 with DM), 15 dogs with DM, and 13 healthy dogs. The serum concentrations of leptin, adiponectin, resistin, interleukin (IL)-1ß, IL-6, IL-10, IL-18, and tumor necrosis factor (TNF)-α were measured, and homeostatic model assessment indices (HOMAs) were calculated and compared among the groups. Serum leptin was significantly higher in PDH dogs with and without DM than in healthy and DM dogs, and it was lower in DM dogs than in PDH dogs without DM. Serum adiponectin was significantly lower in PDH dogs with DM than in healthy and PDH dogs, and it was significantly lower in DM dogs than in healthy dogs. Serum IL-10 was significantly higher in PDH dogs with DM than in healthy and PDH dogs without DM. The leptin/adiponectin ratio was significantly higher in PDH dogs with DM than in normoglycemic PDH dogs. Serum IL-6 concentrations were significantly higher in DM dogs than in healthy dogs. Serum IL-1ß concentration was significantly higher in DM dogs than in healthy dogs and PDH dogs with DM and without DM. Serum TNF-α and IL-18 concentrations were not different among groups. The HOMAß-cell function was significantly lower in PDH dogs with DM than in normoglycemic PDH dogs, while HOMAinsulin sensitivity was significantly lower in PDH dogs with DM than in healthy dogs. These results suggest that adipokine dysregulation, a reduction in insulin sensitivity, and a further impairment in pancreatic ß-cell function might predispose PDH dogs to DM. Further longitudinal study will be necessary to confirm this result.

Long noncoding RNA MIAT promotes the growth and metastasis of non-small cell lung cancer by upregulating TDP43.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA MIAT promotes the growth and metastasis of non-small cell lung cancer by upregulating TDP43, by H.-L. Zhao, S.-Q. Xu, Q. Li, Y.-B. Zhao, X. Li, M.-P. Yang, published in Eur Rev Med Pharmacol Sci 2019; 23 (8): 3383-3389-DOI: 10.26355/eurrev_201904_17702-PMID: 31081093" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17702.

Long noncoding RNA MIAT promotes the growth and metastasis of non-small cell lung cancer by upregulating TDP43.

OBJECTIVE: Recent researches have proved that long noncoding RNAs (lncRNAs) act and have an important role in many diseases. In this research, lncRNA MIAT was explored to identify how it functions in the development of non-small cell lung cancer (NSCLC). PATIENTS AND METHODS: Real-time quantitative polymerase chain reaction (RT-qPCR) was utilized to detect MIAT expression in NSCLC patients. Next, we conducted cell counting kit-8 (CCK-8) assay, colony formation assay, ethynyl deoxyuridine (EdU) incorporation assay, wound healing assay and transwell assay to identify its biological function. Further experiments were performed to explore the potential mechanism. RESULTS: By comparing with MIAT expression in adjacent tissues, MIAT expression level was significantly higher in NSCLC samples. Moreover, functional assays showed that cell growth ability of NSCLC cells was inhibited after MIAT was knocked down. In addition, the migrated and invaded ability of NSCLC cells was inhibited after MIAT was knocked down. Furthermore, the expression of TDP43 was downregulated by knockdown of MIAT. Meanwhile, it was found that TDP43 expression positively correlated to MIAT expression in NSCLC tissues. CONCLUSIONS: Results above suggest that MIAT could enhance cell proliferation and metastasis of NSCLC by upregulating TDP43, which suggests that MIAT may be a potential therapeutic target in NSCLC.

Serum Concentrations of Leptin and Adiponectin in Dogs with Myxomatous Mitral Valve Disease.

BACKGROUND: The concentrations of circulating adipokines in dogs with myxomatous mitral valve disease (MMVD) have not been investigated in detail. OBJECTIVES: To determine whether serum concentrations of adipokines differ between healthy dogs and dogs with MMVD and whether circulating concentrations depend on the severity of heart failure resulting from MMVD. ANIMALS: In the preliminary study, 30 healthy dogs and 17 client-owned dogs with MMVD, and in the subsequent study, 30 healthy dogs and 46 client-owned dogs with MMVD. METHODS: Prospective case-controlled observational study. In the preliminary study, serum concentrations of leptin, adiponectin, resistin, visfatin, interleukin (IL)-1ß, IL-6, IL-10, IL-18, and tumor necrosis factor-α were measured. In the subsequent study, MMVD dogs were divided into three groups according to the International Small Animal Cardiac Health Council (ISACHC) classification, and serum concentrations of leptin and adiponectin were measured. RESULTS: In the preliminary study, serum leptin and adiponectin concentrations differed significantly between dogs with MMVD and healthy dogs. Serum leptin (P = .0013) concentrations were significantly higher in dogs with MMVD than in healthy dogs, whereas adiponectin (P = .0009) concentrations were significantly lower in dogs with MMVD. However, we observed no significant differences in the other variables. In the subsequent study, dogs classified as ISACHC class 3 had higher serum concentrations of leptin (P = .0022) than healthy dogs but ISACHC class 1 or 2 dogs did not. Serum adiponectin concentrations were significantly lower in ISACHC class 1 (P < .0001) dogs than in healthy dogs, whereas adiponectin concentrations in ISACHC class 3 dogs were significantly higher than in ISACHC class 1 dogs (P = .0081). CONCLUSIONS AND CLINICAL IMPORTANCE: Circulating concentrations of leptin and adiponectin might be altered in dogs with MMVD.

Serum adipokine concentrations in dogs with acute pancreatitis.

BACKGROUND: Limited information is available about the role of adipokines in the development and progression of acute pancreatitis (AP) in dogs. OBJECTIVES: To determine whether the circulating concentrations of adipokines differed between healthy dogs and dogs with AP, and whether the circulating concentrations differed between AP survivors and AP nonsurvivors. ANIMALS: Twenty-eight healthy dogs and 25 client-owned dogs with AP. METHODS: Prospective observational cohort study of 25 client-owned dogs with newly diagnosed AP and 28 otherwise healthy dogs with similar body condition scores. The serum concentrations of leptin, adiponectin, resistin, visfatin, interleukin (IL)-1ß, IL-6, IL-10, IL-18, and tumor necrosis factor (TNF)-α were measured. RESULTS: The serum concentrations of leptin (P = .0021), resistin (P = .0010), visfatin (P < .0001), IL-1ß (P < .0001), IL-6 (P = .0002), IL-10 (P < .0001), and IL-18 (P < .0001) were significantly higher in dogs with AP than healthy dogs, whereas the adiponectin concentration (P = .0011) was significantly lower. There were significant differences in the serum concentrations of leptin (P = .028) and adiponectin (P = .046) in survivors and nonsurvivors. After the disappearance of clinical signs, the concentrations of resistin (P = .037) and IL-1ß (P = .027) decreased significantly, whereas the serum concentrations of leptin (P > .999), adiponectin (P = .11), visfatin (P = .83), IL-6 (P = .82), IL-10 (P = .82), IL-18 (P = .56), and TNF-α (P = .94) did not differ significantly. CONCLUSION AND CLINICAL IMPORTANCE: This study showed that dysregulation of adipokines might be involved in the pathogenesis of AP. In addition, leptin and adiponectin are likely to be associated with mortality rate in AP.

Serum adipokine concentrations in dogs with naturally occurring pituitary-dependent hyperadrenocorticism.

BACKGROUND: An excess of intra-abdominal fat is observed frequently in dogs with hyperadrenocorticism (HAC). Adipokine dysregulation is a possible cause of complications related to visceral obesity, but little information is available on adipokine in dogs with naturally occurring HAC. OBJECTIVES: To examine the differences in the circulating adipokines concentrations in overweight dogs with and without pituitary-dependent HAC (PDH). ANIMALS: Thirty healthy dogs and 15 client-owned dogs with PDH. METHODS: Case-controlled observational study, which enrolled 15 overweight dogs diagnosed with PDH and 30 otherwise healthy dogs of similar body condition score. Nine of 15 dogs with PDH were treated with low-dose trilostane twice daily and reassessed after treatment. RESULTS: The serum leptin (P < .0001) and insulin (P < .0001) concentrations were significantly higher in the PDH group (leptin, 22.8 ± 8.8 [mean ± SD]; insulin, 9.1 ± 6.1) than the healthy group (leptin, 4.9 ± 3.7; insulin, 1.9 ± 0.9). However, there were no significant differences in the adiponectin, resistin, tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, IL-10, and IL-18 levels between the 2 groups. In the PDH group, the serum cortisol concentrations had a linear association with the leptin concentrations, and there were significant decreases in the leptin (P = .0039) and insulin (P = .0039) levels after trilostane treatment. However, the leptin and insulin levels remained higher after trilostane treatment than in healthy control dogs with similar body condition score. CONCLUSIONS AND CLINICAL IMPORTANCE: Hypercortisolemia in dogs with PDH might upregulate the circulating leptin levels. However, a large population-based study will be necessary to determine whether the upregulation of leptin is involved directly with the complications caused by HAC.

Efficacy of low- and high-dose trilostane treatment in dogs (< 5 kg) with pituitary-dependent hyperadrenocorticism.

BACKGROUND: Trilostane is commonly used to treat pituitary-dependent hyperadrenocorticism (PDH) in dogs. There are differing opinions regarding the dose and frequency of trilostane administration in dogs with PDH. OBJECTIVES: To compare the efficacy of 2 trilostane protocols in the treatment of dogs with PDH. ANIMALS: Sixteen client-owned dogs with PDH and a body weight <5 kg. METHODS: Prospective observational study. Group A (n=9; low-dose treatment group) received 0.78 ± 0.26 mg of trilostane/kg PO every 12 h and group B (n = 7; high-dose treatment group) 30 mg of trilostane/dog PO every 24 h. All of the dogs were reassessed at 2, 4, 8, 12, 16, and 24 weeks after the initiation of treatment. RESULTS: An improvement in both ACTH-stimulated serum cortisol concentrations and clinical signs occurred more slowly in group A than in group B; however, after 20 weeks of treatment, 2/7 dog in group B had clinical signs and abnormal laboratory findings consistent with hypoadrenocorticism. At 24 weeks, an improvement in the clinical findings of all of the dogs in both groups was detected. CONCLUSIONS AND CLINICAL IMPORTANCE: In dogs with PDH, twice-daily administration of low-dose trilostane is an effective approach to the management of PDH. In addition, our results suggest fewer potential adverse effects if trilostane is administered twice daily in the lower dose.

Effect of a short-term infusion with soybean oil-based lipid emulsion on phagocytic responses of canine peripheral blood polymorphonuclear neutrophilic leukocytes.

BACKGROUND: The use of soybean oil-based lipid emulsion (SO-based LE) in parenteral nutrition has been reported to impair neutrophil functions in humans and rodents. As yet, little is understood about the effects of SO-based LE on canine immune responses. HYPOTHESIS: A short-term infusion with SO-based LE affects the phagocytic responses of canine peripheral blood polymorphonuclear neutrophilic leukocytes (PMNs). ANIMALS: Twenty-four healthy Beagle dogs. METHODS: Experimental study. Dogs were randomly assigned into groups of six and administered a 2-hour IV infusion with 0.9% NaCl solution or sufficient SO-based LE (INTRALIPOS 20%) to supply 40, 100, and 200% of the basal energy requirement (BER). PMN functions were determined after collecting blood samples before, immediately after, and 24 hours after the infusion. RESULTS: None of the treatments significantly affected the phagocytic capacity of PMNs or circulating leukocyte numbers. The infusion providing 200% of BERs significantly reduced PMN oxidative burst activity, filamentous actin polymerization, and Cdc42 Rho guanosine triphosphatase activity immediately after its delivery. However, these functions were restored to pre-infusion values 24 hours after the infusion. The lower calorie infusions did not have these effects. CONCLUSIONS AND CLINICAL IMPORTANCE: These results suggest that short-term infusions with a supraphysiological dose of SO-based LE may decrease the immune functions of canine PMNs. However, more long-term studies will be needed to extrapolate the effect of SO-based LE with clinically relevant doses in a practical situation.

Ginseng total saponin enhances the phagocytic capacity of canine peripheral blood phagocytes in vitro.

The clinical and pharmacological activities of ginseng are known to modulate immune function, metabolic processes and neuro-endocrine system activities. Ginseng saponins are the principle active ingredients in the formation of immune stimulating complexes. The objective of this study was to evaluate the in vitro effect of ginseng total saponin (GTS) on the phagocytic capacity of canine peripheral blood phagocytes. GTS itself did not cause any direct effect on the phagocytic capacity of peripheral blood mononuclear cells (PBMC) and polymorphonuclear cells (PMN) but not peripheral blood monocytes. However, the phagocytic capacity of PMN and monocytes, but not PBMC, was enhanced by the culture supernatant from PBMC treated with GTS. The phagocytic capacity of PMN and monocytes was also increased by treatment with recombinant canine (rc) tumor necrosis factor (TNF)-alpha. The ability of the culture supernatant from GTS-treated PBMC to stimulate the phagocytic capacity of phagocytes was inhibited by addition of anti-rc TNF-alpha polyclonal antibody (pAb) prior to the culture. The amount of TNF-alpha in the culture supernatant from PBMC was shown to increase upon treatment of GTS as compared with that of vehicle-treated PBMC culture supernatant. These results suggest that GTS has an immunoenhancing effect on the phagocytic capacity of canine peripheral blood phagocytes, which is mainly mediated by TNF-alpha released from GTS-stimulated PBMC.

Secondary malignant lymphoedema after mastectomy in two dogs.

This case report describes the diagnosis of secondary malignant lymphoedema in two dogs that had undergone a mastectomy. A remarkable severe oedematous lesion associated with lameness in the right hindlimb was observed in both cases. Diagnostic imaging examinations, including direct pedal lymphangiography (case 1) and lymphoscintigraphy (case 2), showed obstruction of lymph flow in the lymphatics of the right hindlimbs. Although the recommended medical management and physiotherapy had been applied to resolve the problems, oedema did not improve in the damaged region in both cases. Results of histopathological examinations suggested that the cause of the obstructed lymph flow was neoplastic cells in the lymphatics of the right hindlimb in both dogs.

Enhanced phagocytic activity of neutrophils caused by administration of egg white derivatives (EWD) in cats injected with cyclophosphamide (CPA).

To examine in vivo effects of egg white derivatives (EWD), the numbers of peripheral blood cells and neutrophil phagocytosis were evaluated in cats injected intramuscularly with cyclophosphamide (CPA). There were no changes in the number of red blood cells (RBC) or packed cell volume (PCV) values regardless of oral administration of EWD or injection of CPA, but the numbers of platelets, white blood cells (WBC) and neutrophils in cats administered EWD significantly increased (p<0.05 to 0.01) when compared with those in control cats which received saline solution. In addition, the administration of EWD resulted in a significant enhancement in the phagocytic activity of neutrophils (p<0.01) when compared to control cats, suggesting that EWD has a stimulating effect on leukocyte progenitors. The numbers of platelets, WBC and neutrophils, and the phagocytic activity of neutrophils in cats injected with CPA alone were significantly lower (p<0.05 to 0.01) than those in control cats. However, co-administration of EWD to cats injected with CPA resulted in a significant increase in the numbers of platelets, WBC and neutrophils (p<0.05 to 0.01), and in the phagocytic response of neutrophils (p<0.01) when compared to cats injected with CPA alone. Therefore, these results suggest that co-administration of EWD may be effective in reducing some possible side effects in animals treated with immunosuppressive or antitumor agents.

Acetaldehyde inhibits chymotrypsin and serum anti-chymotrypsin activity.

BACKGROUND: Chymotrypsin (CT) and CT-like enzymes contribute to the dynamics of metabolism by their participation in digestion, peptide hormone generation and catabolism, fertilization of ova and inhibition of thrombin-induced platelet aggregation, among other processes. The frequency of pancreatitis is observably higher in alcoholics, and pancreatic enzymes have been associated with localized vascular damage, thrombosis and pancreatic necrosis. METHODS: Since CT is a major pancreatic enzyme and may serve as a link between pancreatitis, coagulopathy, and alcoholism, the affect of acetaldehyde (AcH) the primary metabolite of ethanol, upon the enzyme and upon the influence of human serum thereon was studied. RESULTS: It was observed that CT activity upon glutaryl-L-phenylalanine-b-naphthylamide was inhibited to the extent of 23.7%, 52.5%, and 96.7% by 44.7, 89.4, and 447 mmol/L AcH in a fluorometric assay whereby the enzyme was dialyzed to remove excess AcH prior to assay. The p values were < 0.04. Aliquots of human serum (10 microL, 20 microL, 30 microL, 40 microL, 50 microL, and 100 microL) inhibited 40 micrograms of CT by 13%, 37.7%, 65.3%, 89.8%, and 92.8%, respectively (n = 6; p = < 0.05). The serum did not hydrolyze the fluorogenic substrate. On the other hand, AcH added to serum at 447, 224, 112, or 56 mmol/L resulted in 42.6%, 42.6%, 52.9%, and 60.3% inhibition of CT relative to a 69.1% inhibition of the enzyme by serum alone (n = 6; = p < 0.01). CONCLUSIONS: These data show that AcH clearly decreases the antichymotryptic activity of serum (consisting of alpha 1-proteinase inhibitor, alpha 1-antichymotrypsin, and alpha 2-macroglobulin). The incomplete inactivation of chymotrypsin by serum and partial inactivation of CT inhibitor(s) by AcH suggest the possibility that CT leaked into the circulation, (in alcoholic pancreatitis) may be available in blood to lower the clotting potential induced by thrombin-activated platelets, and that a greater amount of CT might be available in the blood of alcoholics, thereby contributing, in part, to the prolongation of clotting times.

Enhancing effects of chicken egg white derivatives on the phagocytic response in the dog.

Immunostimulative effects of chicken egg white derivatives (EWD) on phagocytic responses of peripheral blood mononuclear cells (MNC) and polymorphonuclear cells (PMN) in dogs were evaluated by flow cytometric analysis. Peripheral blood leukocytes (PBL) cultured with EWD showed the enhanced phagocytic response. The response was maximal when PBL were cultured with 100 - 400 micrograms/ml of EWD for 3 - 12 hr. Furthermore, significantly increased phagocytic responses were also induced even when PBL were cultured with protein components (200 micrograms/ml) of EWD such as conalbumin, flavoprotein and ficin-papain inhibitor for 3 hr. In addition, the enhancing effect of EWD on the phagocytic responses was also observed in MNC cultured with EWD (200 micrograms/ml) for 4 hr but not in PMN cultured with EWD in the same procedures. The supplement of the supernatant (20%) of MNC cultured with EWD (200 micrograms/ml) for 24 hr at 37 degrees C to PBL and MNC resulted in the enhancement of their phagocytic responses. In contrast, the supernatant of PMN cultured with EWD for 24 hr at 37 degrees C did not show any significant enhancing effect on the phagocytic responses of PBL, MNC and PMN. These results suggest that EWD has an enhancing effect on phagocytosis of MNC and PMN, which may be mediated through active humoral substances produced by EWD-stimulated MNC.

Association of tumor-associated antigen on the proliferation of bovine leukemia virus-infected lymphoblastoid B-cell lines.

The association of tumor-associated antigen (TAA) on the proliferation of BLV-infected lymphoblastoid B-cell lines (BL2M3 and BL312) was investigated. Flow cytometric analysis of the expression of TAA with monoclonal antibody (mAb) c143 showed high expression of TAA on the surfaces of BL2M3 and BL312 cells. A large amount of TAA was found in the culture supernatant of BL2M3 and BL312 cells as well as in the lysates of BL2M3 and BL312 cells. Culture supernatant but not lysates of BL2M3 and BL312 cells promoted the growth of either BL2M3 cells or BL312 cells. Furthermore, this growth promoting activity in culture supernatants of BL2M3 and BL312 cells was inhibited in a dose-dependent manner when cultured with mAb c143. These results suggested that TAA may be involved in the growth factor-mediated cell growth of bovine B-lymphoblastoid cell lines expressing TAA on their cell surface.

Proliferative responses of a bovine leukemia virus-infected lymphoblastoid B-cell line by its culture supernatant and cytokines.

The growth-promoting activity in the culture supernatant of bovine lymphoblastoid B-cell lines (BL2M3 and BL312) were examined. BL2M3 cells proliferated well in response to conditioned medium (CM) obtained from BL2M3 and BL312 cell cultures. These BL2M3 and BL312 CM were used as sources of BL2M3 cell growth-promoting factor (BL2M3-GPF). BL2M3-GPF was sensitive to acid (pH 2) and alkali (pH 10) and was heat-labile. Proliferative responses of BL2M3 cells were not induced by human recombinant (r)IL 1, rIL 2, rIL 6, granulocyte-colony stimulating factor (rG-CSF) or tumor necrosis factor (rTNF)-alpha. Human low molecular weight B cell-growth factor (LMW-BCGF) was, however, capable of augmenting the proliferation of BL2M3 cells. BL2M3 cells formed clusters in response to LMW-BCGF, whereas they showed single and discete appearance in the presence of BL2M3-GPF. These results suggested that bovine lymphoblastoid B-cell lines might release and respond to the growth-promoting factor for in vitro proliferation of its own cell line, BL2M3.

Effect of Toxoplasma lysate antigen (TLA) on feline cytotoxicity against FeLV positive lymphoma cells.

The cytotoxic activities of feline spleen cells treated with Toxoplasma lysate antigen (TLA) were assayed against feline leukemia virus (FeLV)-producing lymphoma. FL74 cells, and xenogeneic target lymphoma, mouse YAC-1 cells. The TLA treatments were performed in vivo alone, in vitro alone, and in vivo plus in vitro, respectively. In vivo plus in vitro treatments with TLA induced a marked augmentation in cytotoxic activity of spleen cells to FL74 cells. The treatment with TLA in vivo alone showed an enhancement of cytotoxic activity but in vitro alone did not. The cytotoxic effects of TLA-treated spleen cells obtained from the cats which had been previously immunized with live FL74 cells were similar to those of spleen cells from non-immunized cats treated with TLA. However, no increase of cytotoxicity was shown in the response to mouse YAC-1 cells regardless of TLA treatments. These results indicated that the in vivo TLA treatment augmented the cytotoxicity of feline spleen cells against FeLV-producing lymphoma cell.