Humoral and cellular immunity in HIV positive and HIV negative Helicobacter pylori infected patients.
The prevalence of H. pylori associated gastritis seems to be different in HIV positive and HIV negative patients. Therefore a correlation to immunodeficiency can be postulated. The histology of gastritis, status of H. pylori infection and parameters of humoral and cellular immune response were investigated in 41 HIV positive and 47 HIV negative patients, who were subjected to upper endoscopy for the evaluation of gastrointestinal symptoms. In HIV positive patients 37% had active chronic gastritis against 62% of the HIV negative patients. In 73% of HIV positive cases of active chronic gastritis H. pylori was detected by bacteriological culture and/or Warthin-Starry stain. In HIV negative patients active chronic gastritis was always associated to H. pylori infection. Production of antibodies as measured by two commercially available ELISA tests was significant in HIV positive and HIV negative patients; both tests correlated well with H. pylori detection by culture or direct microscopy. Immunoglobulin class specific immunoblots corresponded to the ELISA results in HIV negative patients but to a lesser extent in the HIV positive group which was assumed to be related to unspecific polyclonal activation in these patients. Systemic cellular immunity was investigated by proliferation assays of peripheral blood mononuclear cells (PBMC). Proliferative response to the unspecific mitogen PHA was reduced in HIV positive patients. A sonicated H. pylori antigen failed to induce lymphocyte proliferation. The antimitogenic effect was also seen in case of coincubation with PHA. This observation was independent of H. pylori and HIV infection status. We conclude that in HIV positive as in HIV negative patients active chronic gastritis is predominantly related to H. pylori infection. The prevalence of H. pylori associated gastritis in HIV positive patients is significantly reduced (p < 0.025) compared to HIV negative controls. Decreased susceptibility to H. pylori infection in HIV positive patients may not be explained by the abnormal reactivity of their humoral or cellular immune response.
Benz
J
J
Institut für Medizinische Mikrobiologie und Hygiene, Universität zu Köln, Germany.
Hasbach
H
H
Brenden
M
M
Eidt
S
S
Fätkenheuer
G
G
Schrappe
M
M
Geisel
J
J
Goossens
H
H
Mauff
G
G
D000328:Adult; D000907:Antibodies, Bacterial / Q000096:biosynthesis* / Q000276:immunology; D002478:Cells, Cultured; D005756:Gastritis / Q000150:complications / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D018023:HIV Seronegativity; D006679:HIV Seropositivity / Q000150:complications* / Q000276:immunology; D016481:Helicobacter Infections / Q000150:complications / Q000276:immunology* / Q000473:pathology; D016480:Helicobacter pylori / Q000276:immunology* / Q000302:isolation & purification; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D008213:Lymphocyte Activation; D008875:Middle Aged
D000907:Antibodies, Bacterial