Inhibition of IgE production by epsilon (epsilon) chain-specific antisense oligonucleotides (AOs) studied on human myeloma cell line U266 and peripheral blood mononuclear cells of a patient with hypereosinophilia.

Based on cDNA sequence data epsilon chain-specific antisense oligonucleotides were synthesized and checked on in vitro IgE production. Using peripheral blood cells from a hypereosinophilic patient and a human IgE myeloma cell line, U266, marked reduction of in vitro IgE production measured by PRIST was observed. The effect of epsilon antisenses proved to be isotype specific since IgG production by both peripheral blood cells and a lymphoma cell line, CESS, was not affected. Moreover, the expression of other markers on U266 (interleukin-6 receptor and gp130) were not influenced by epsilon-specific antisense oligonucleotides.

IgE-containing cells in gastric mucosa with and without Helicobacter pylori infection.

Gastric mucosa responds with inflammation to Helicobacter pylori (H. pylori) infection. While numerous reports have shown that the immune system produces specific IgG, IgA, and IgM isotype anti H. pylori antibodies, IgE-mediated pathways of H. pylori-associated gastritis are mostly unknown. Our aim was to evaluate whether an increased presence of IgE in the antral gastric mucosa is responsible for the severity of the H. pylori-associated gastritis. The number of IgE-containing cells was estimated in formalin-fixed, paraffin-embedded antral gastric biopsy specimens using immunohistochemistry in three groups of patients: (i) 20 H. pylori-positive cases with moderate inflammation, (ii) 19 H. pylori-negative cases with moderate inflammation, and (iii) 19 H. pylori-negative cases with normal mucosa. In chronic gastritis, the number of IgE-positive cells increased significantly as compared to normal mucosa. In gastritic patients, H. pylori positivity was accompanied by a significant accumulation of IgE-positive cells, mainly plasma cells. These data suggest that IgE-mediated immune response probably plays an important role in the development of H. pylori-associated gastritis.

[Epidemiology of Helicobacter pylori infection in Hungary (comparative sero-epidemiologic study)]. / Helicobacter pylori infekció magyarországi epidemiológiája (szeroepidemiológiai összehasonlító tanulmány).

In the last decade pathogenetical role of Helicobacter pylori infection has been proved in development of gastroduodenal alterations. DNA-RNA hybridisation and protein profile studies proved that Helicobacter pylori is an organism distinct from other bacteria. Therefore serology became a useful method to study the epidemiology of Helicobacter pylori infection in various populations. In Hungary sera were collected from adults aged 20-60 in blood banks (Military Hospital, Tolna County Hospital) in 1993. The samples were classified in 5 year increment groups and questionnaires were filled out. Anti-H. pylori IgG were tested using Cobas Core kit (Roche Diagnostic). The overall rate of seropositivity was 63.3%. The prevalence according to age was the following: 20-24 yrs = 44%, 25-29 yrs = 40%, 30-34 yrs = 52%, 35-39 yrs = 64%, 40-44 yrs = 75%, 45-49 yrs = 73%, 50-54 yrs = 77%, 55-59 yrs = 83%. There were no statistical difference between gender, living in urban or rural areas at the time of collection or in childhood, between the level of education, type of labour or social status. However we found statistical correlation between anti-H. pylori seropositivity and epigastric symptoms. The same characteristics of Helicobacter pylori infection were found in Hungary as well as in other countries. In groups between 20 and 30 years has been proved lower prevalence in Hungary than in Poland, Bulgaria.

[Immune responses of IgG, IgA and anti-CagA IgG to Helicobacter pylori in dyspeptic and peptic ulcer patients]. / Dyspepsiás és pepticus fekélybetegek Helicobacter pylori-ellenes specifikus IgG, IgA és anti-CagA IgG immunválasza.

The anti-H. pylori IgG, IgA, and anti CagA responses in dyspeptic patients have been evaluated. Of 481 patients 76% tested positive for IgG anti-H. pylori, 57% for anti-CagA, and 52% IgA for anti H. pylori. There was a significant age-related increase in IgG anti-H. pylori and IgA anti-H. Pylori prevalence, whereas anti-CagA positives were unreliable in this respect. The IgG seropositivity was the highest (93%) in duodenal ulcers (DU), 82% in antral gastritis and/or bulbitis (AG +/- /B), and 71% in gastric ulcer (GU). GU patients compared with DU and AG +/- /B ones tended to have the highest IgA anti-H. pylori prevalence (78% vs. 66% and 61%). The anti-CagA seropositivity was the most pronounced (80%) in DU followed by GU (72%) and AG +/- /B (68%). It is suggested that the serodiagnosis including IgG, IgA anti-H. pylori and anti-CagA determinations can not replace endoscopy in revealing the exact nature of gastroduodenal lesions. IgA anti-H. pylori determination in female patients with GU can be a valuable diagnostic tool. It is stated that in Hungary the prevalence of CagA positive H. pylori strains in anti-H. pylori IgG positive dyspeptic patients is 85%.

Inhibition of antibody-dependent cellular cytotoxicity (ADCC) by normal and pathological sera from patients with advanced lung cancer.

An improved ADCC assay for the detection of cancer-associated serum blocking factors is described. Inhibition of ADCC by sera was performed without preincubation and washing of effector cells. Effects of individual susceptibility of normal effector cells to serum inhibitors and of the background inhibition by normal sera were also avoided. Based on their inhibitory effect on ADCC, normal and tumour sera from lung cancer patients could be distinguished with 81.4 to 100% accuracy, according to effector cell donors and to concentrations of the sera tested.