Occurrence of serum class G immunoglobulins interacting with specific antigens of Helicobacter pylori in patients with unstable coronary artery disease and in symptomless individuals.
An impact of Helicobacter pylori on the process of atherogenesis may be related to the intensity of humoral response against selected specific antigens of this bacteria. We performed serological studies in which the recognition of 7 selected antigens was possible. The investigated group consisted of 56 patients hospitalized due to unstable angina pectoris. The control group consisted of 29 symptomless volunteers. The levels of class G serum immunoglobulins interacting with glycine extract (GE) of H. pylori antigens were assessed by ELISA test in both groups. The same sera were tested by the Milenia blot H. pylori IgG system. In this assessment the presence of IgG antibodies interacting with antigens of molecular weight of 120, 87, 64, 35, 30, 26, and 20 kDa was estimated separately for every listed antigen. The results revealed significant differences between investigated groups in the prevalence of anti-GE IgG (unstable angina - 100% vs. controls - 60%) and in the level of such antibodies expressed as total optical density units--OD450 (6.1 +/- 3.0 vs. 3.4 +/- 3.0 respectively, p<0.05). However, anti-GE IgG detected in the sera of patients as well as controls reacted with similar frequency with selected H. pylori antigens: highly specific (120, 87, 64, 30 kDa) and specific (35, 26, and 20 kDa). We conclude, that although H. pylori infection is so common and mainly associated with gastroduodenal symptoms, it is also recognized by serological methods with high prevalence in patients with coronary artery disease, and less frequently in symptomless individuals. The humoral response against H. pylori in class G immunoglobulins in patients with unstable angina is characterized by higher levels of anti-H. pylori IgG but not by the higher prevalence of serum IgG interactions with the highly specific and specific H. pylori antigens. Such infection could be considered as a cofactor for atherogenesis by inducing strong humoral response against surface antigens of this bacteria.
Rechciński
Tomasz
T
Second Chair and Clinic of Cardiology, Medical University of Lódź, ul. Kniaziewicza 1/5, 91-347 Lódź Poland. Tomasz.2336843@pharmanet.com.pl
Grebowska
Aneta
A
Kurpesa
Małgorzata
M
Rudnicka
Wiesława
W
Krzemińska-Pakuła
Maria
M
Chmiela
Magdalena
M
D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000097:blood / Q000276:immunology*; D001426:Bacterial Proteins / Q000097:blood / Q000276:immunology; D003324:Coronary Artery Disease / Q000276:immunology / Q000382:microbiology*; D004797:Enzyme-Linked Immunosorbent Assay; D016481:Helicobacter Infections / Q000276:immunology* / Q000382:microbiology; D016480:Helicobacter pylori / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D014510:Urease / Q000097:blood
D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D007074:Immunoglobulin G; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori; D014510:Urease