chiniofon and Inflammation

Chronic gut inflammation disposes to an increased risk of colitis-associated cancer. Chemoprevention is an attractive complementary strategy. We aimed to evaluate the chemopreventive effects of M10, a novel derivative of Myricetin, in the murine azoxymethane/dextran sodium sulfate model. Oral administration of M10 at 50-100 mg/kg once a day for consecutive 12 weeks significantly prevented ulcerative colitis (UC) and colorectal tumor. Pathological analysis of intestines showed that M10 reduced the degree of chronic inflammation and prevented the progression of colorectal tumorigenesis. Flow cytometry analysis of the immunocytes isolated from intraepithelial and lamina propria showed that M10 prevented the infiltration of myeloid-derived suppressor cells and increased CD8+T and CD4+T cells in colorectal tissues. Enzyme-linked immunosorbent analysis revealed the reduction of pro-inflammatory mediators granulocyte-macrophage colony-stimulating factor/macrophage colony-stimulating factor, IL-6 and TNF-α in colonic mucosa. Western blot assay also showed M10 prevention of the NF-κB/IL-6/STAT3 pathways and the biomarkers of inflammation and colorectal tumorigenesis. Electron microscopy analysis revealed that M10 prevent robust endoplasmic reticulum (ER) stress-induced autophagy in inflamed colonic mucosal cells. In conclusion, oral administration of Myricetin derivative M10 exerts chemoprevention of UC and colorectal tumor in mice. The mechanism of chemoprevention is associated with the reduction of biomarkers of chronic inflammation and proliferation through attenuating robust ER stress in inflamed colonic mucosal cells. M10 exerts chemoprevention activity without evidence of toxicity in mice. These results justify further evaluation of M10 in clinical trials. M10 could develop a promising regimen in the chemoprevention of colitis and colorectal cancer.

Topics: Alanine; Animals; Anticarcinogenic Agents; Colitis, Ulcerative; Colon; Colorectal Neoplasms; Disease Models, Animal; Endoplasmic Reticulum Stress; Flavonoids; Hydroxyquinolines; Inflammation; Inflammation Mediators; Interleukin-6; Intestinal Mucosa; Male; Mice; Mice, Inbred C57BL; NF-kappa B; Signal Transduction; STAT3 Transcription Factor; Tumor Necrosis Factor-alpha

Monoamine oxidases (MAO), downstream targets of glucocorticoid, maintain the turnover and homeostasis of monoamine neurotransmitters; yet, its pathophysiological role in monoamine deficiency, oxidative stress and neuroinflammation remains controversial. Protective effects of M30, a brain selective MAO inhibitor with iron-chelating antioxidant properties, have been shown in models of neurodegenerative diseases. This study aims to examine the neuroprotective mechanism of M30 against depressive-like behavior induced by corticosterone (CORT). Sprague-Dawley rats were given CORT subcutaneous injections with or without concomitant M30 administration for two weeks. CORT-treated rats exhibited depressive-like behavior with significant elevated levels of MAO activities, serotonin turnover, oxidative stress, neuroinflammation and apoptosis in the hippocampus with significant losses of synaptic proteins when compared to the control. The expression and activity of cytokine-responsive indoleamine 2,3-dioxygenase (IDO-1), a catabolic enzyme of serotonin and tryptophan, was significantly increased in the CORT-treated group with lowered levels of serotonin. Besides, CORT markedly reduced dendritic length and spine density. Remarkably, M30 administration neutralized the aberrant changes in the hippocampus and prevented the induction of depressive-like behavior induced by CORT. Our results suggest that M30 is neuroprotective against CORT-induced depression targeting elevated MAO activities that cause oxidative stress and neuroinflammation, resulting in IDO-1 activation, serotonin deficiency and neurodegeneration.

Topics: Animals; Corticosterone; Dendritic Spines; Depression; Enzyme Activation; Hippocampus; Hydroxyquinolines; Indoleamine-Pyrrole 2,3,-Dioxygenase; Inflammation; Male; Neurodegenerative Diseases; Oxidative Stress; Rats; Rats, Sprague-Dawley; Serotonin

In this study, we investigated the effect of 3,4,5-trihydroxy-N-(8-hydroxyquinolin-2-yl)benzamide) (SG-HQ2), a synthetic analogue of gallic acid (3,4,5-trihydroxybenzoic acid), on the mast cell-mediated allergic inflammation and the possible mechanism of action. Mast cells play major roles in immunoglobulin E-mediated allergic responses by the release of histamine, lipid-derived mediators, and pro-inflammatory cytokines. We previously reported the potential effects of gallic acid using allergic inflammation models. For incremental research, we synthesized the SG-HQ2 by the modification of functional groups from gallic acid. SG-HQ2 attenuated histamine release by the reduction of intracellular calcium in human mast cells and primary peritoneal mast cells. The inhibitory efficacy of SG-HQ2 was similar with gallic acid. Enhanced expression of pro-inflammatory cytokines such as tumor necrosis factor-α, interleukin-1β, interleukin-4, and interleukin-6 in activated mast cells was significantly diminished by SG-HQ2 100 times lower concentration of gallic acid. This inhibitory effect was mediated by the reduction of nuclear factor-κB. In animal models, SG-HQ2 inhibited compound 48/80-induced serum histamine release and immunoglobulin E-mediated local allergic reaction, passive cutaneous anaphylaxis. Our results indicate that SG-HQ2, an analogue of gallic acid, might be a possible therapeutic candidate for mast cell-mediated allergic inflammatory diseases through suppression of histamine release and pro-inflammatory cytokines.

Topics: Animals; Calcium; Cytokines; Gallic Acid; Histamine Release; Hydroxyquinolines; Hypersensitivity; Immunoglobulin E; Inflammation; Inflammation Mediators; Male; Mast Cells; Mice; NF-kappa B; Passive Cutaneous Anaphylaxis; Rats; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction

P-selectin inhibition has been evaluated as a therapeutic for prevention and treatment of venous thrombosis. In this study, a novel oral small-molecule inhibitor of P-selectin, PSI-421, was evaluated in a baboon model of stasis induced deep vein thrombosis (DVT). Experimental groups included i) primates receiving a single oral dose of 1 mg/kg PSI-421 two days prior and continued six days after thrombosis (n = 3); ii) primates receiving a single daily subcutaneous dose of 0.57 mg/kg enoxaparin sodium two days prior and continued six days post thrombosis (n = 3); and iii) primates receiving no treatment (n = 3). PSI-421 treated primates had greater percent vein reopening and less vein wall inflammation than the enoxaparin and controls at day 6. Microparticle tissue factor activity (MPTFA) was significantly lower in the animals receiving PSI-421 immediately after thrombosis (T+6 hours day 0) suggesting lower potential for thrombogenesis in these animals. PSI-421 also reduced soluble P-selectin levels versus controls at T+6 hours day 0, day 2 and 6. Experimental animals in any group showed no adverse effects on coagulation. This study is the first to demonstrate a reduction in MPTFA associated with vein reopening and reduced vein inflammation due to oral P-selectin inhibition in a baboon model of DVT.

Topics: Administration, Oral; Animals; Anticoagulants; Blood Coagulation; Blood Platelets; Disease Models, Animal; Enoxaparin; Factor Xa Inhibitors; Fibrinolytic Agents; Hydroxyquinolines; Iliac Vein; Inflammation; Injections, Subcutaneous; Male; P-Selectin; Papio anubis; Phlebography; Thromboplastin; Time Factors; Ultrasonography, Doppler, Color; Vascular Patency; Venous Thrombosis

Linomide prevents the development of autoimmune insulitis and insulin-deficient diabetes mellitus in female NOD mice. Linomide prevents development of autoimmune manifestations in other experimentally induced and spontaneous autoimmune diseases as well, but the mechanism of action is unknown. The present report summarizes our investigations on the effect of Linomide on different functional T cell subsets in NOD mice analyzed according to their cytokine profile. Supernatants from cultured splenocytes and peritoneal cells taken from Linomide-treated mice contained lower levels of TNFalpha, IL-1 beta, IFN gamma and IL-12 versus higher levels of IL-4, IL-6 and IL-10 in comparison with supernatants from cultures of untreated mice. Our results suggest that regulation of autoimmunity following oral Linomide administration in NOD mice induces a shift from Th(1) to Th(2) phenotype response, thereby preventing the development of diabetes by active cytokine-induced immunoregulation of T cell subsets, including downregulation of Th(1) and upregulation of Th(2).

Topics: Adjuvants, Immunologic; Animals; Autoimmunity; Concanavalin A; Cytokines; Diabetes Mellitus, Type 1; Female; Hydroxyquinolines; Inflammation; Mice; Mice, Inbred NOD; Spleen; Th1 Cells; Th2 Cells

Multiple sclerosis (MS) is characterized by high levels of circulating mononuclear cells (MNC) that respond to myelin proteins like myelin basic protein (MBP) in vitro by expressing mRNA of both pro-inflammatory cytokines, e.g. interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha) and lymphotoxin (LT) that may make MS worse, and anti-inflammatory cytokines like IL-4, IL-10 and transforming growth factor-beta (TGF-beta) that may act beneficially. Substances that down-regulate cytokines such as TNF-alpha or promote IL-10 or TGF-beta can be anticipated to affect MS beneficially.. In situ hybridization to detect and enumerate IFN-gamma, TNF-alpha, LT, IL-4, IL-10 and TGF-beta mRNA expressing blood MNC after stimulation with myelin basic protein (MBP), control antigens and without antigen in presence and absence of Linomide (roquinimex, LS-2616) was employed. In parallel, ELISPOT assay to detect MBP- and PHA-reactive IFN-gamma secreting blood MNC+/-Linomide was used.. Here we report that Linomide, a synthetic immunomodulator, at concentrations effective in vivo reduces the number of MBP-reactive TNF-alpha and increases MBP-reactive IL-10 and TGF-beta mRNA expressing MNC from MS patients' blood when analysed in vitro. Compared to dexamethasone, Linomide up-regulated levels of blood MNC expressing mRNA of TGF-beta after culture in presence of MBP.. Changes of cytokine balance towards a production of anti-inflammatory cytokines could be a desirable effect to be evaluated in future drug studies of Linomide-like substances. At present, Linomide is not evaluable in MS clinical trials due to side-effects.

Topics: Adjuvants, Immunologic; Adult; Aged; Cytokines; Female; Humans; Hydroxyquinolines; Inflammation; Male; Middle Aged; Multiple Sclerosis; RNA, Messenger

Two series of compounds, N-[(arylmethoxy)phenyl] sulfonamides and N-[(arylmethoxy)naphthyl] sulfonamides, were prepared as leukotriene D4 (LTD4) antagonists. In the phenyl series, N-[3-(2-quinolinylmethoxy)phenyl]-trifluoromethanesulfonamide (Wy-48,252, 16) was the most potent inhibitor of LTD4-induced bronchoconstriction in the guinea pig. With an intragastric ID50 of 0.1 mg/kg (2-h pretreatment), 16 was 300 times more potent than LY-171,883. Compound 16 also intragastrically inhibited ovalbumin-induced bronchoconstriction in the guinea pig with an ID50 of 0.6 mg/kg. In vitro against LTD4-induced contraction of isolated guinea pig trachea pretreated with indomethacin and L-cysteine, 16 produced a pKB value of 7.7. In the rat PMN assay 16 inhibited both 5-lipoxygenase and cyclooxygenase (IC50's = 4.6 and 3.3 microM). In the naphthyl series, N-[7-(2-quinolinylmethoxy)-2-naphthyl]trifluoromethanesulfonamide (Wy-48,090, 47) in addition to potent LTD4 antagonist activity (on isolated guinea pig trachea 47 had a pKB value of 7.04) also had antiinflammatory activity (63% inhibition at 50 mg/kg in the rat carrageenan paw edema assay and 34% inhibition of TPA-induced inflammation at 1 mg/ear in the mouse ear edema model). Perhaps the antiinflammatory activity of 47 was due to its additional activity of inhibiting both 5-lipoxygenase and cyclooxygenase enzymes (IC50's = 0.23 and 11.9 microM, respectively, in rat PMN).

Topics: Acetophenones; Animals; Bronchi; Chemical Phenomena; Chemistry; Constriction, Pathologic; Cyclooxygenase Inhibitors; Cysteine; Edema; Guinea Pigs; Hydroxyquinolines; Indomethacin; Inflammation; Lipoxygenase Inhibitors; Molecular Structure; Muscle Contraction; Naphthalenes; SRS-A; Structure-Activity Relationship; Sulfonamides; Tetrazoles; Trachea

By the use of fluorophotometry, ocular inflammation induced by lens proteins can be objectively quantified. This method of measuring inflammation was applied to studying the effectiveness of a cyclooxygenase inhibitor, indomethacin, and a lipoxygenase inhibitor, REV 5901, in reducing ocular inflammation induced by lens proteins. Pretreatment with indomethacin prevented the leakage of fluorescein into the anterior chamber up to 2 hrs after intracameral injection of lens proteins. After the first 2 hrs, fluorescein concentration in the pretreated eye rapidly increased to equal the control eye by 4 hrs. When REV 5901 was used to pretreat the eye, there was an increase in fluorescein leakage up to 3 hrs after lens protein injection. However, when a combination of indomethacin and REV 5901 was used to pretreat the eye, there was a significant reduction in fluorescein leakage up to 5 hrs after the injection of lens proteins. The reduction of fluorescein leakage with a combination of indomethacin and REV 5901 was greater than that obtained with prednisolone alone. These results indicate that prostaglandins are the primary mediators of inflammation in the early phase (less than 3 hr) of lens protein induced ocular inflammation and leukotrienes are the primary mediators in the late phase (greater than 3 hr) of lens protein induced ocular inflammation. Also the use of a nonsteroidal antiinflammatory drug which blocks only one arm of the arachidonic acid cascade may potentiate the production of metabolites in the other arm of the cascade. By using a combination of a cyclooxygenase inhibitor and a lipoxygenase inhibitor, metabolites from both arms of arachidonic acid cascade are reduced, hence reducing inflammation in both the early phase and late phase of lens protein induced ocular inflammation.

Topics: Animals; Crystallins; Cyclooxygenase Inhibitors; Drug Therapy, Combination; Eye Diseases; Female; Fluoresceins; Fluorophotometry; Hydroxyquinolines; Indomethacin; Inflammation; Lipoxygenase Inhibitors; Male; Prednisolone; Quinolines; Rabbits

The LTD4 antagonist, Wy-48,252 (1,1,1-trifluoro-N-[3-(2-quinolinylmethoxy)phenyl]methanesulfonamide), was assessed for its ability to modulate arachidonic acid metabolism in several inflammatory cells. In A23187-stimulated rat neutrophils, Wy-48,252 effectively inhibited the conversion of exogenous [14C]arachidonic acid to radiolabeled 5-hydroxyeicosatetraenoic acid (5-HETE) and thromboxane B2 (TxB2) (IC50 = 2 and 9.1 microM, respectively). Synthesis of immunoreactive leukotriene B4 (LTB4) (IC50 = 4.6 microM) and TxB2 (IC50 = 3.3 microM) from endogenous substrate by these cells in the absence of [14C]arachidonic acid was similarly reduced. Wy-48,252 also reduced leukotriene C4 (LTC4) and PGE2 synthesis by zymosan-activated mouse peritoneal macrophages (IC50 = 4.4 and 4.3 microM, respectively). 5-Lipoxygenase (5-LO) catalyzed reactions in human neutrophils, lung mast cells and basophils activated by various stimuli were dose dependently inhibited by Wy-48,252 while PGD2 synthesis by lung mast cells was inhibited at 100 microM. By contrast, 12-LO, 15-LO, phosphodiesterase activity and histamine release from mast cells and basophils were unaffected by Wy-48,252. These data suggested that the LTD4 antagonist, Wy-48,252, also inhibited the synthesis of eicosanoids, a feature that may contribute to its pharmacological actions in vivo.

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Cattle; Eicosanoic Acids; Female; Histamine Release; Humans; Hydroxyeicosatetraenoic Acids; Hydroxyquinolines; Inflammation; Lung; Macrophages; Mice; Rats; Rats, Inbred Strains; SRS-A

The in vitro and in vivo behaviour of 99Tcm-HMPAO (hexamethylpropyleneamineoxime) (n = 12) and 111In-oxine (n = 11) labelled granulocytes, isolated by density-gradient centrifugation (Metrizamide/plasma gradients), was compared in patients with suspected inflammatory diseases. The in vitro elution of both labels and the viability of the labelled cells (99Tcm, 98.5%; 111In, 96.5%) was comparable but the labelling efficiency was different (99Tcm, 44 +/- 13%; 111In, 72.5 +/- 5.5%). In vivo, the lung (t1/2 max: 7.7 min), liver and spleen perfusion patterns were nearly identical; the image quality for detail in 99Tcm scans was superior to 111In images. The blood disappearance curves of 99Tcm and 111In were comparable. In the small number of patients examined all infections could be diagnosed correctly, without false-positive or false-negative results. Disadvantageous is the renal excretion of 99Tcm complexes (3+% over 20 h) with kidney and bladder activity from the beginning of the study. The biliary excretion in half of the patients (n = 6) with unspecific positive small and large bowel visualization and the late intestinal excretion also render the diagnosis more difficult. The recommended best imaging times for abdominal and retroperitoneal inflammations are 30 min to 2 h after injection. Late scans in septic prosthetic joints have disproportionate long acquisition times. As a potential cell labelling compound, 99Tcm-HMPAO has a promising future in comparison to 111In scans because of the good availability of 99Tcm, the image quality and the lower radiation exposure to the patient when lower activities for the early diagnosis of abdominal inflammatory diseases are reinjected.

Topics: Colitis, Ulcerative; Crohn Disease; Female; Granulocytes; Humans; Hydroxyquinolines; Indium Radioisotopes; Inflammation; Isotope Labeling; Joint Diseases; Lung Diseases; Male; Organometallic Compounds; Oximes; Oxyquinoline; Polycystic Kidney Diseases; Radionuclide Imaging; Technetium; Technetium Tc 99m Exametazime

The uptake of indium-111 labelled neutrophils was examined in 30 patients with acute myocardial infarction by planar imaging and single photon emission computed tomography. The time from venepuncture to reinjection of the autologous labelled neutrophils was less than 2.5 hours and imaging was carried out 24 hours later. Twenty three patients had a positive uptake of neutrophils in the myocardium and imaging was improved by single photon emission computed tomography. There was a significant difference between the intervals from the onset of chest pain to injection of labelled neutrophils between patients with positive and negative images; early reinjection was more likely to produce a positive image. Indeed, all nine patients reinjected within 18 hours of the onset of symptoms had positive images. The results suggest that the stimulus for activation and migration of neutrophils is transient; this is an important factor if neutrophil release products play a role in cell damage after coronary occlusion.

Topics: Acute Disease; Acute-Phase Reaction; Female; Heart; Humans; Hydroxyquinolines; Indium; Inflammation; Liver; Male; Middle Aged; Myocardial Infarction; Neutrophils; Organometallic Compounds; Oxyquinoline; Radioisotopes; Spleen; Tomography, Emission-Computed

Topics: Humans; Hydroxyquinolines; Indium; Inflammation; Leukocytes; Oxyquinoline; Radioisotopes; Radionuclide Imaging; United States; United States Food and Drug Administration

using a single step separation procedure, we have developed a method for labelling human neutrophils with 111In-oxine. This method allows a rapid separation of neutrophils from whole blood, with negligible mononuclear or red cell contamination. Preliminary studies using 111In-labelled neutrophils show minimal lung retention and early accumulation in the spleen consistent with viable cells. In addition, focal accumulation of 111In has been imaged in patients with localized inflammation or sepsis.

Topics: Cell Separation; Humans; Hydroxyquinolines; Indium; Inflammation; Isotope Labeling; Neutrophils; Oxyquinoline; Radioisotopes

Autologous lymphocytes were labeled with In-111 oxine in 26 patients with chronic inflammatory disease. Whole body gamma camera scans were performed at 24 and 48 hours post injection. Activity was normally seen in spleen, liver, bone marrow, and cervical and inguinal lymph nodes; any activity outside there areas was considered abnormal. Five out of 11 patients with proven or suspected chronic osteomyelitis had positive scans. Four out of five patients with chronic arthritic diseases had positive scans. Also, three patients had bladder uptake suggesting bladder inflammation on a chronic basis.

Topics: Adult; Aged; Chronic Disease; Humans; Hydroxyquinolines; Indium; Inflammation; Lymphocytes; Male; Middle Aged; Organometallic Compounds; Oxyquinoline; Radionuclide Imaging; Time Factors; Whole-Body Counting

A method for the concentration of leucocytes from blood and labelling of the separated cells with 111-Indium oxine is described. This method guaranteed a good preparation. On average there were 64.8% of leucocytes from the blood in the concentrate. The yield of the labelling averaged 93%. Seventy-two patients from various departments were examined to test the clinical application of the labelled leucocytes in the diagnosis of inflammatory diseases. The results obtained led to the formulation of six indications for the appropriate application of leucocyte scanning in everyday clinical routine.

Topics: Adolescent; Adult; Aged; Bone Diseases; Brain Diseases; Child; Humans; Hydroxyquinolines; Indium; Inflammation; Isotope Labeling; Leukocytes; Middle Aged; Neuromuscular Diseases; Organometallic Compounds; Oxyquinoline; Radiation Dosage; Radioisotopes; Radionuclide Imaging; Urologic Diseases

Topics: Abscess; Diagnostic Errors; Humans; Hydroxyquinolines; Indium; Inflammation; Leukocytes; Organometallic Compounds; Oxyquinoline; Radionuclide Imaging

We report here the successful labeling of rabbit peripheral blood neutrophils with [111In]oxine. We found that standard techniques for preparation of rabbit neutrophils, while acceptable for maintenance of in vitro function, rendered the neutrophils ineffective for in vivo use after labeling with 111In. Specifically, rabbit neutrophils were sensitive to the use of hypotonic shock for red cell elimination, centrifugation into a button during preparation, and the presence of oxine during chemotaxis in vitro. Using a carefully modified method of neutrophil preparation and labeling, we found that 111In-labeled rabbit neutrophils retained normal in vitro function, including chemotaxis. In addition, using our method, 34% +/- 5% of labeled neutrophils were recoverable in peripheral blood 5 min after intravenous injection. The half-life of circulating radio-labeled neutrophils was 5.6 +/- 2 h. Continuous external imaging of radio-labeled neutrophils after intravenous injection showed initial lung uptake, followed by rapid clearance of radioactivity in the lungs (50% clearance in 10.5 +/- 3.3 min.) Hepatic radioactivity was maximal by 30 min after injection and thereafter slowly declined. Finally, we found that 111In-labeled rabbit neutrophils migrated to sites of artificially induced inflammation. Our findings indicate that 111In-labeled rabbit neutrophils, if prepared under optimal conditions, should provide a useful tool for investigating the fate of neutrophils in experimental inflammatory conditions in this animal.

Topics: Animals; Cell Survival; Chemotaxis, Leukocyte; Female; Hydroxyquinolines; Indium; Inflammation; Male; N-Formylmethionine; N-Formylmethionine Leucyl-Phenylalanine; Neutrophils; Oligopeptides; Oxyquinoline; Rabbits; Radioisotopes; Skin; Sodium Chloride; Time Factors; Zymosan

Topics: Aged; Diagnosis, Differential; Humans; Hydroxyquinolines; Indium; Inflammation; Ketones; Leukocytes; Organometallic Compounds; Oxyquinoline; Pentanones; Radioisotopes; Radionuclide Imaging

Topics: Female; Humans; Hydroxyquinolines; Inflammation; Isotope Labeling; Male; Middle Aged; Neutrophils; Oxyquinoline; Radionuclide Imaging

The biodistributions of In-111 oxine (with and without leukocyte labeling) of Ga-67 citrate and of In-111 chloride were compared in 30 dogs with chemical and bacterial abscesses and acute joint inflammation. Serial blood samples were taken and tissues radioassayed at 24 hr. The concentration of In-111-oxine leukocytes in all three types of inflammatory lesion was invariably much higher than that of Ga-67 injected simultaneously. For bacterial abscesses, the mean abscess-to-muscle concentration ratio was 3,000 for labeled leukocytes and 72 for Ga-67. Aqueous buffered In-111 oxine sulfate solution appeared better for labeling leukocytes than In-111 oxine in ethanol. When In-111 oxine was not incubated with leukocytes before injection, or if the cells were poorly labeled or damaged, the abscess localization was often inferior to that of gallium. Localization of In-111 chloride also appeared inferior to that of gallium. No significant difference in distribution in the major organs or inflammatory lesions was demonstrable between labeled suspensions of "pure"neutrophils harvested by elutriation and "mixed"cell suspensions of leukocytes after erythrocyte sedimentation with hydroxyethyl starch. For both types of leukocyte suspension labeled with In-111 oxine, the average recovery of cell-bound activity in the circulating blood at 4 hr was 32% of the administered activity, inferior to that of DFP-32. It is concluded, therefore, that In-111 oxine is a more effective agent than Ga-67 for the detection of acute focal inflammatory lesions if leukocytes are properly labeled, but current techniques are unsatisfactory for the study of neutrophil kinetics.

Topics: Abscess; Animals; Arthritis; Dogs; Female; Gallium Radioisotopes; Hydroxyquinolines; Indium; Inflammation; Isotope Labeling; Leukocytes; Male; Oxyquinoline; Radioisotopes; Radionuclide Imaging; Tissue Distribution