Biomedical subjects

S Frydas

Publications and source records attributed to S Frydas.

At least 19 recordsLinked to original sources

PubMed2006

Expression and secretion of RANTES (CCL5) in granulomatous calcified tissue before and after lipopolysaccharide treatment in vivo.

RANTES (regulated on activation, normal T cell-expressed and secreted) is a CC chemokine appearing to be involved in the recruitment of leukocytes at inflammation sites. RANTES is produced by CD8(+) T cells, epithelial cells, fibroblasts, and platelets. It acts in vitro in leukocyte activation and human immunodeficiency virus suppression, but its role in vivo is still uncertain. In our study, we established the involvement of RANTES in an in vivo model of chronic inflammation induced by potassium permanganate, leading to calcified granulomas. In our rat model, RANTES expression (mRNA and protein) was significantly upregulated in granulomatous tissue; RANTES expression was further increased upon i.p. injection of lipopolysaccharide (LPS), while it was kept at basal levels by dexamethasone (Dex) given 18 hours before sacrifice. LPS and Dex increased and decreased, respectively, the recruitment of mononuclear cells in granulomatous tissue compared with control granulomas from phosphate-buffered saline (PBS)-treated animals. In granuloma tissue, levels of RANTES were higher in LPS-treated rats and lower in the Dex group compared to controls. RANTES was also found in the conditioned medium of granuloma tissue from treated (LPS or Dex) and untreated (PBS) rats. When LPS was added in vitro for 18 hours, RANTES was further increased, except in the Dex group (P > 0.05). On serum analysis, RANTES levels were higher in the LPS group and lower in the Dex group compared to controls. This study shows for the first time that RANTES is produced in vivo in chronic, experimental inflammatory states, an effect increased by LPS and inhibited by Dex.

Animals↗

PubMed2006

Immunological activation of human umbilical cord blood mast cells induces tryptase secretion and interleukin-6, and histidine decarboxilase mRNA gene expression.

Allergy is the result of a complex immune cascade leading to the disregulated production of Th2 cytokines, the generation of allergen-specific IgE-producing B cells and the subsequent activation and degranulation of mast cells upon allergen challenge. Mast cell effector function significantly influences the quantity, duration and magnitude of most allergic reactions. Here, using isolated human umbilical cord blood mast cells (HUCBMC) from CD34+ cells, activated with anti-IgE (10 microg/ml) in culture, we found an augmented release of IL-6, tryptase and histamine (p < 0.01 compared with control). In addition, in these cells anti-IgE (10 microg/ml) activated the expression of histidine decarboxylase (HDC) and IL-6. In these studies we describe a new biological activity of anti-IgE in inducing histidine decarboxylase and IL-6, suggesting that this cytokine may have an important effect on allergic and inflammatory diseases mediated by mast cells. Moreover, with these data we confirm the immunoregulatory and inflammatory function of mast cells.

Cells, Cultured↗

PubMed2006

Inhibitory effect of quercetin on tryptase and interleukin-6 release, and histidine decarboxylase mRNA transcription by human mast cell-1 cell line.

Mast cells are involved in inflammatory processes and in allergic reactions where immunologic stimulation leads to degranulation and generation of numerous cytokines and inflammatory mediators. Mast cells have been proposed as an immune gate to the brain, as well as sensors of environmental and emotional stress, and are likely involved in neuropathologic processes such as multiple sclerosis. Among mast cell products, the protease tryptase could be associated with neurodegenerative processes through the activation of specific receptors (PARs) expressed in the brain, while interleukin (IL)-6 likely causes neurodegeneration and exacerbates dysfunction induced by other cytokines; or it could have a protective effect against demyelinisation. In this report we show that quercetin, a natural compound able to act as an inhibitor of mast cell secretion, causes a decrease in the release of tryptase and IL-6 and the down-regulation of histidine decarboxylase (HDC) mRNA from human mast cell (HMC)-1 cells. As quercetin dramatically inhibits mast cell tryptase and IL-6 release and HDC mRNA transcription by HMC-1 cell line, these results nominate quercetin as a therapeutical compound in association with other therapeutical molecules for neurological diseases mediated by mast cell degranulation.

Blotting, Northern↗

PubMed2005

Serum adenosine deaminase and procalcitonin concentrations in neutropenic febrile children with acute lymphoblastic leukaemia.

Neutropenia as a state of immunosuppression is probably the major problem in patients suffering from acute lymphoblastic leukaemia undergoing intensive chemotherapy. Fever is frequent in neutropenic patients and often related to infection. Clinically, the presence of infection in patients with neutropenia may be difficult to establish, because there are usually few signs of infection. The aim of this work was to study sensitive markers for early diagnosis of microbial infection in neutropenic children undergoing intensive chemotherapy as a treatment for acute lymphoblastic leukaemia. The study included three groups (A, B and C) of children with acute lymphoblastic leukaemia and neutropenia. Group A consisted of 29 children with febrile neutropenia and microbial infection, aged 1-14 years (5.8+/-2.9), 11 boys and 18 girls; Group B of 38 children with febrile neutropenia without microbial infection, aged 2-14 years (6.8+/-3.1), 14 boys and 24 girls; and Group C of 53 children with neutropenia without fever and without infection, aged 1-14 years (5.9+/-2.1), 21 boys and 32 girls. Blood samples were collected upon admission and before the start of any antimicrobial treatment. The samples were used for blood culture, serological tests, leukocyte count and analysis of levels of C-reactive protein, procalcitonin, total adenosine deaminase (ADA) activity and its isoenzymes, ADA-1 and ADA-2. According to our results the procalcitonin levels and total ADA activity discriminated best between neutropenic febrile (Groups A and B) and neutropenic afebrile episodes (Group C). In conclusion, this study suggests procalcitonin and total ADA activity as two easily measurable and cost effective markers for the assessment of immune response in febrile neutropenic patients with acute lymphoblastic leukaemia.

Adenosine Deaminase↗

PubMed2003

IL-10 subfamily members: IL-19, IL-20, IL-22, IL-24 and IL-26.

It has been reported that the CD4+ T cell is a very important source of interleukin 10 (IL-10), while CD8+ cells produce low amounts. IL-10 exerts several immune stimulating, as well as inhibitory effects. There are at least five novel human IL-10 family-related molecules: IL-19, IL-20, IL-22, IL-24, and IL-26. Activated T cells produce IL-19, IL-22 and IL-26, while IL-24 is produced by activated monocytes and T-cells. IL-20 induces cheratin proliferation and Stat-3 signal transduction pathway, while IL-22 induces acute-phase production by hepatocytes and neonatal lethality with skin abnormalities reminiscent of psoriasic lesions in humans. In addition, IL-22 mediates inflammation and binds class II cytokine receptor heterodimers IL-22 RA1/CRF2-4. This cytokine is also involved in immuno-regulatory responses. IL-26 (AK155) is a novel cytokine generated by memory cells and is involved in the transformed phenotype of human T cells after infection by herpes virus. All these new IL-10 subfamily member cytokines are strongly involved in immune regulation and inflammatory responses.

Animals↗

PubMed2001

Effect of selenium and vitamin E on antibody production by dairy cows vaccinated against Escherichia coli.

Sixty clinically healthy Holstein cows were randomly assigned to one of four groups according to their age and parity and vaccinated in late pregnancy (day 190) with a multivalent vaccine against Escherichia coli. The 15 cows in the first group (SeE) were injected intramuscularly with a solution of sodium selenite (0.1 mg Se/kg bodyweight) and vitamin E (alpha-tocopherol acetate, 8 U/kg bodyweight), the cows in the second group (Se) received only selenium and the cows in the third group (E) received only vitamin E at the same doses and by the same route of administration; the cows in the fourth group were used as controls. The vaccination and the injections of selenium and vitamin E were repeated 42 days later. The concentration of selenium in whole blood and of vitamin E in serum was determined by fluorometric methods. Specific antibody titres against E coli were determined in serum samples by ELISA. The results showed that the injection of selenium either alone or in combination with vitamin E significantly improved the production of specific antibodies against E coli, and that the production of specific antibodies was greater after the administration of selenium alone.

Animals↗

PubMed2001

MCP-1 and MIP-2 levels during Echinococcus granulosus infections in mice.

Ten BALB/c mice were infected with the cestode Echinococcus granulosus. After the infection, serum was collected at different periods of time and monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein-2 (MIP-2) were determined. The level of MCP-1 increased from at day 20 post infection (p.i.), to a maximum of on day 60 p.i., then decreased to on day 130 p.i. A second peak was observed at day 150 p.i. In addition, MIP-2 was detectable in serum as late as day 100 p.i. The highest level was observed on day 130 p.i., and decreased thereafter. Serum from noninfected animals (controls) contained no detectable levels of either MCP-1 or MIP-2. However, MCP-1 and MIP-2 appear to be implicated in E. granulosus infections, but their exact role during the disease is under determination.

Animals↗

PubMed1999

Monocyte chemotactic protein-1 gene expression and translation in formed granulomatous calcified tissue in vivo.

Monocyte chemotactic protein-1 (MCP-1) and related molecules constitute the C-C class of the beta chemokine supergene family with inflammatory properties. However, the exact role, function, and implication in inflammatory diseases remain to be determined. Here we report that subcutaneous injections (0.2 ml) of a saturated water solution (1:40) of potassium permanganate crystals induces the generation of granuloma tissue at the site of injection in the rat, and reaches its peak of formation after 1 week. The size and weight of the granulomas were increased by i.p. lipopolysaccharide (LPS) (6 microgram/200 microliter) and inhibited by intraperitoneal (i.p.) dexamethasone (Dxs) 300 microgram/200 microliter) treatments in rats, injected 18 hours before sacrifice. Moreover, steady-state levels of MCP-1 mRNA in the granuloma tissue (control), were strongly generated. Rats treated i.p. with LPS produced an increase of MCP-1 mRNA in the granuloma tissue compared with controls (i.p. PBS-treated) whereas in animals treated with Dxs, there was a decrease in (P < 0.05) in formation of mRNA protein. When the granuloma tissues were homogenized the generation of MCP-1 was found in the supernatants. The level of MCP-1 was higher (P < 0.05) in the LPS-treated animals and lower (P < 0.05) in the Dxs group compared with the controls (treated with PBS). Similar results were obtained in the serum and in minced granuloma tissue where samples were further incubated in vitro with LPS (100 ng/ml) overnight. A Strong increase (P < 0.01) in MCP-1 in all samples was detected, but not in the minced granuloma tissue from Dxs-treated animals. Our data demonstrate that calcified tissue from chronic inflammation induced by KMnO4 generates MCP-1 gene expression and translation, an effect increased by LPS and decreased by Dxs.

Animals↗

PubMed1999

Vitamin B6-deficient diet plus 4-deoxypyridoxine (4-DPD) reduces the inflammatory response induced by T. spiralis in diaphragm, masseter and heart muscle tissue of mice.

Animals fed diets deficient in vitamin B6 develop microcytic anemia, alterations of growth, and other pathologies. 4-deoxypirydoxine is a potent antagonist of vitamin B6 coenzyme which depresses IL-1, TNF and IL-6 and has anti-inflammatory properties. The aim of this study was to show the anti-inflammatory effects of 4-DPD on chronic inflammation caused by the nematode parasite T. spiralis, specifically on the recruitment and the activation of inflammatory cells. Two groups of mice, 6 weeks of age, were used: one was maintained on a vitamin B6-deficient synthetic pellet diet for 15 days before injection of the nematode, and administered an intraperitoneal injection (i.p.) of 4-DPD (250 microg/mouse) for 15 days (the first, 5 days before infection), and the second group was maintained on a normal diet for the total duration of the experiment. These two groups were then injected with 150 larvae (L1-T7 spiralis) per os. Chronic inflammation was caused by infection of treated or untreated mice with T7 spiralis parasite. After 14 days post-infection all mice developed a chronic inflammatory response. Mice fed with a B6-deficient diet showed a significant decrease in the number of cysts found in the diaphragm when compared to mice treated with normal diet. In addition, in all mice treated with vitamin B6-deficient diet plus 4-DPD the average body weight was significantly lower, compared to the mice on normal diet in all weeks examined. Moreover, in sections of the diaphragm, masseter and myocardium muscles, the infiltration of inflammatory cells, such as macrophages, lymphocytes, and eosinophils were more intense in untreated mice compared to those fed a vitamin B6-deficient diet. These results show that BALB/c mice infected with T. spiralis and fed a vitamin B6-deficient diet plus the vitamin B6 antagonist, 4-DPD, prolong the time of invasion of the larvae in the muscle cells, influence the recruitment of inflammatory cells and the intensity of the inflammatory reaction compared to infected untreated mice (control).

Animals↗

PubMed1999

IgG, IgG1 and IgM response in Trichinella spiralis-infected mice treated with 4-deoxypirydoxine or fed a Vitamin B6-deficient diet.

The aim of this study was to investigate the effect of pyridoxine (Vitamin B6) deficiency on the immunological response of BALB/c mice infected with the parasite T. spiralis. Specific anti-parasite IgM and IgG immunoglobulins were detected by ELISA method in the serum of treated animals at different periods for 60 days post infection. Vitamin B6-deficiency was induced in two separate groups of mice by either (1) maintaining the mice on a Vitamin B6-deficient synthetic pellet diet for 40 days before infection, or (2) by daily intraperitoneal injection of 8 x 10(5) M/100 microl of 4-Deoxypyridoxine (4-DPD), a potent antagonist of Vitamin B6 for 20 days prior to infection. These two groups of mice were then injected with 100 larvae (L1-T. spiralis) per os. Parasite burdens in the mice were observed by light microscopy. Cysts were present in the diaphragms of the mice after 60 days post-infection. Parasite specific IgG, as well as IgG1 levels were determined in the sera of infected mice fed a normal diet. These levels were found to be lower in the 4-DPD-treated mice compared to the untreated mice. The inhibition started from the 10th day and continued to the 60th day, and in the 4-DPD-treated group the inhibition initiated after 24 h to 60 days. IgM level also was depressed by 4-DPD, starting from 24 h after injection of the compound. In mice fed Vitamin B6-deficient diets the levels of IgG were lower than in mice fed normal diets. These results show that BALB/c mice infected with T. spiralis and fed either a Vitamin B6-deficient diet or a diet which included the Vitamin B6-antagonist, 4-DPD, both influence the course of IgG, IgG1 and IgM production.

Animals↗

PubMed1998

Induction of monocyte chemotactic protein-1 (MCP-1) and TNF alpha by Trichinella spiralis in serum of mice in vivo.

MCP-1 is a small (8-10 KDa) protein and a prototype member of the CC chemokine beta subfamily, which plays a critical role in acute and chronic inflammation. Recent evidence suggests an important role for MCP- 1, MCP-2 and MCP-3 in a number of pathological states, including delayed type hypersensitivity conditions, parasitic infections and rheumatoid arthritis. Forty BALB-c mice were treated with the parasite Trichinella spiralis. After the infection the animals were sacrificed at different periods from the initial infection and MCP-1 and TNFalpha were quantified in the mouse serum. The level of MCP-1 in the serum of mice infected with 100 larvae increases from 27.5+/-7.0 pg/ml at day 23, to a maximum level of 31.5+/-5.0 pg/ml at day 33, then decreased to 14.6+/-2.0 pg/ml at day 47. When the mice were infected with 200 larvae of T. spiralis the maximum increase was 34.4+/-2.5 pg/ml found on day 23. From day 33 to day 47 MCP-1 levels were decreased. In addition, in infected mice levels of TNFalpha were detectable in the serum as early as day 1. The level of TNFalpha was maximum at day 35 (3812+/-224 pg/ml). Serum from non-infected mice contained no detectable levels of either MCP-1 or TNFalpha. However, even if MCP-1 seems to be implicated in Trichinellosis, its exact role and function in inflammatory parasitic diseases remains to be determined.

Animals↗

PubMed1997

Massive infiltration of basophilic cells in inflamed tissue after injection of RANTES.

Regulated upon activation normal T expressed and secreted (RANTES) is a new inducible protein member of the human C-C branch of chemokines. RANTES is a potent monocyte and lymphocyte chemoattractant and is a mediator of inflammatory responses. In these studies we found that RANTES 10 ng/50 microl chemoattracts basophilic cells in a dose-dependent manner 4 h after an intradermal injection in rat skin sites, as revealed by optic microscopy. Moreover, in biopsy specimens from rat skin injection sites histamine release was significantly higher (P < 0.05) than in controls (PBS 50 microl) after 4 h from RANTES treatment. The presence of basophilic cells in rat skin injection sites after RANTES-treatment was also confirmed by electron microscopy studies. In addition, histidine decarboxylase (HDC) mRNA was increased in rat skin sites injected with RANTES compared to sites injected with PBS (controls). Our report describes additional biological activities for RANTES, suggesting that this human chemoattractant protein may play a fundamental role in histamine and HDC generation, along with basophilic cell recruitment.

Animals↗

PubMed1997

Augmentation of monocyte chemotactic protein-1 and mRNA transcript in chronic inflammatory states induced by potassium permanganate (KMnO4) in vivo.

Monocyte chemotactic protein-1 (MCP-1) is a proinflammatory cytokine that attracts and activates specific types of leucocytes. The purpose of this work was to analyse the generation of MCP-1 and mRNA transcript in a model of chronic inflammation using a granulomatous tissue induced by potassium permanganate (KMnO4; water soluble crystals). The data presented here shows that MCP-1 is generated in granuloma tissue and its level was strongly increased by i.p. injections of lipopolysaccharide (LPS) and inhibited in rats treated with injections of dexamethasone, 18 hr before the animals were killed. In histological studies LPS and dexamethasone increased and decreased, respectively, the recruitment of mononuclear cells in the granuloma tissue compared with the control granulomas from phosphate-buffered saline (PBS)-treated animals. Reverse transcriptase-polymerase chain reaction (RT-PCR) was used for mRNA extraction and cDNA synthesis. mRNA MCP-1 was significantly produced in the granuloma tissue of untreated animals, an effect increased by LPS and inhibited by dexamethasone, compared with the controls. Moreover, MCP-1 protein was found in the supernatant from homogenized granuloma tissues and the levels of MCP-1 were higher in the LPS-treated animals, while they were lower in the dexamethasone group, compared with the granulomas from the PBS-treated groups (control). The generation of MCP-1 was also found in minced granuloma tissue incubated for 18 hr (overnight) from treated (LPS or dexamethasone) and untreated (PBS) rats. When LPS was added in vitro for 18 hr to the controls and treated animals the production of MCP-1 was further increased except in the dexamethasone group (P > 0.05). Analysing blood serum from LPS, dexamethasone or PBS-treated rats, we found that MCP-1 was also present. The level was higher in the LPS group and lower in the dexamethasone group, compared with the control (PBS). In these studies we show for the first time that MCP-1 transcript and translation is generated in chronic experimental inflammatory tissue, an effect inhibited by dexamethasone.

Animals↗

PubMed1996

Human recombinant interleukin-1 beta induces thromboxane A2 release in polymorphonuclear leukocytes, macrophages and platelets: effect of IL-1 receptor antagonist.

Prostaglandins and thromboxanes (Txs) are produced by polymorphonuclears (PMNs) and macrophages (Mphis) in response to various stimuli. PMNs were separated from other human blood cells and Mphis were separated from rat peritoneal lavage. In this paper we show that human recombinant interleukin-1 (hrIL-1) can stimulate the release of thromboxane B2 (TxB2) by PMNs and Mphis. In addition, we have shown that aggregation of PMNs may occur when calcium ions (7 mM) and hrIL-1 (100 ng/ml) are added to the cell preparation, but not when Ca2+ alone, hrIL-1 alone, or first hrIL-1 then calcium are added to the cell preparation. The treatment of human platelets with hrIL-1 shows that after 15 min incubation TxB2 is released. In addition, we compared the aggregation of platelets caused by ADP with that caused by hrIL-1. Human recombinant IL-1 at a concentration of 100 ng/ml also causes little aggregation of platelets, in this case the aggregation is reversible. In conclusion, hrIL-1 beta stimulates TxB2 release in PMNs, Mphis and platelets and this effect increases with addition of Ca2+ ions. The mixture of hrIL-1 and Ca2+ causes little aggregation of PMNs. In monocyte suspensions, pretreated with human recombinant IL-1 receptor antagonist (IL-1ra) 500 ng/ml for 10 min and then treated with LPS or hrIL-1 beta 10 micrograms/ml, the release of TxB2 was partially inhibited. IL-1ra may play a significant role in the control of IL-1 and LPS induction in the release of TxB2.

Adenosine Diphosphate↗

PubMed1996

Generation of TNF alpha, IFN gamma, IL-6, IL-4 and IL-10 in mouse serum from trichinellosis: effect of the anti-inflammatory compound 4-deoxypyridoxine (4-DPD).

Infections caused by the nematode Trichinella spiralis is characterized in the host by an inflammatory response with cytokine production. In these studies we have detected TNF alpha, IL-6, IFN gamma, IL-4 and IL-10 in the serum of 10 mice infected with T. spiralis. Moreover, we detected, for the first time, these cytokines in the serum of mice treated with 4-DPD, a potent antagonist of vitamin B6 coenzyme which has anti-inflammatory properties. 4-DPD was used at 100, 400, 800 micrograms/bolus for 20 days, starting one day before the infection. After 15 days of T. spiralis infection, TNF alpha reached a maximum level, while IL-6 was maximal after 7 days, IFN gamma at 20 days and IL-4 at 14 days. IL-10 was not affected by the T. spiralis infection. When the animals were treated with 4-DPD at the reported dosages and infected with T. spiralis the inhibition of TNF alpha and IL-6, were dose-dependent in the first 7 days while IL-4 was reduced only at 400-800 micrograms/bolus. 4-DPD-treated mice did not statistically (P > 0.05) affect the generation of IFN gamma. In healthy animals the production of cytokines were not measurable, just as it was in non-infected animals treated with 4-DPD. The increase of cytokines such as, TNF alpha and IL-6 may be related to the severity of the disease, boosting the host's resistance to the pathogen and inhibiting parasite survival. In addition, the augmentation of IL-4 production enhances T and B cells and macrophage responses and may stimulate T-cell antibody-mediated response to the pathogen. 4-DPD, an inhibitor of IL-1 and inflammatory reactions, proved to be most effective on TNF alpha and IL-6, which are mainly produced by macrophages.

Animals↗

PubMed1995

Immunoglobulin and cytokine profile in murine secondary hydatidosis.

We have investigated specific immune responses in BALB/c mice with experimentally induced secondary hydatidosis. Following intraperitoneal inoculation of brood capsules containing Echinococcus granulosus-protoscoleces, the course of the infection was followed for 513 days. The sera of the mice were screened for the presence of a number of cytokines, and for specific antibodies. During the first 129 days of infection, high levels of cytokines TNF alpha, IL-alpha, IFN gamma, IL-6, and IL-10 and specific IgG1 and IgG3 isotypes were detected, as compared to uninfected controls. The levels of IgM and IgG2a were slightly increased following infection, and remained elevated throughout the period of observation. The levels of IL-1 alpha and specific immunoglobulin of all isotypes except IgM and IgG2a, were significantly decreased 103 days post infection (p.i.), whereas TNF alpha was sharply decreased 129 days p.i. During the period of 129 to 209 days of infection there was an increase in secreted IL-10, and a slow decrease in the levels of IL-6 and IFN gamma. Levels of IgM, IgG, IgG1, and IgG2a plateaued during this period, whereas IgG3 and TNF alpha showed a peak at day 190 p.i. These data suggest the induction of Th2 antibody-mediated immunity with a parallel expansion of Th1-mediated inflammatory responses as important mechanism of host defence against the metacestode.

Animals↗

PubMedDate not supplied

Trichinella spiralis infection is mediated by MCP-1 and MIP-2, while echinococcus granulosus is strongly mediated by MCP-1, but not MIP-2.

The chemokine supergene family are small proteins (8-10 KD) inducible in a number of pathophysiological processes. C-X-C family members are specific largely on neutrophils; whereas C-C chemokines act primarily on monocytes, T-cells, basophils and eosinophils. A wide variety of cell types produce chemokines in response to stimuli, including: infections, mitogens and inflammatory cytokines. Here we found that parasitic diseases, such as Trichinella spiralis and Echinococcus granulosus produce, MCP-1 (beta-chemokine) and MIP-2 (alpha-chemokine), or MCP-1, respectively. The specificity of production of these chemokines in the two parasitic diseases may help to achieve therapeutic strategies in inhibiting inflammation.

Journal Article↗

PubMedDate not supplied

Toxocarosis as zoonosis. A review of literature and the prevalence of Toxocara canis antibodies in 511 serum samples.

A total of 511 serum samples from children aged between 6 months to 15 years old, with different clinical signs-living in the region of Northern Greece - were tested by ELISA (enzyme links immunosorbent assay) technique, for the detection of specific IgG and IgM antibodies against T. canis antigen. The reason IgM was detected was because IgM levels are elevated in the acute phase of toxocara infection, in spite of their notorious non-specificity. In this seroepidemiologic survey of children, a remarkably high percentage (12.5%) reacted positively to this method. Sixteen (3.1%) out of 511 sera showed IgG antibodies, 43 (8.4%) showed IgM, while 5 (1%) showed both IgG and IgM antibodies against T. canis E/S (excretory - secretory) antigen. Females were significantly more infected than males. Seropositivity rate was highest in children over the age of 10.

Journal Article↗