RESUMO
We studied the prevalence of Helicobacter pylori in patients with leprosy and the effects of co-infection on the immune response to Helicobacter antigens in the polar groups of leprosy (lepromatous and tuberculoid). We showed that there is no difference in the prevalence of H. pylori in patients with leprosy as compared to a non-leprosy population. We also demonstrated that the immune response to low molecular weight H. pylori antigens (35, 26 and 19 kDa) differs in patients with lepromatous as compared to those with tuberculoid leprosy. In lepromatous leprosy, we show that there is a higher prevalence of the 35 and 26 kDa antigens, but a lower prevalence of the 19 kDa antigen. These immunological results are consistent with previous histopathological studies illustrating a more severe gastrointestinal inflammation in lepromatous patients; importantly, a response to the 35 kDa antigen is recognized as a marker for the development of ulcerative disease.
Assuntos
Antígenos de Bactérias/imunologia , Gastrite/microbiologia , Infecções por Helicobacter/imunologia , Helicobacter pylori/imunologia , Imunomodulação/imunologia , Hanseníase Virchowiana/imunologia , Hanseníase Tuberculoide/imunologia , Adulto , Idoso , Anticorpos Antibacterianos/análise , Anticorpos Antibacterianos/imunologia , Western Blotting , Estudos de Casos e Controles , Ensaio de Imunoadsorção Enzimática , Feminino , Gastrite/complicações , Gastrite/imunologia , Infecções por Helicobacter/complicações , Infecções por Helicobacter/microbiologia , Humanos , Hanseníase Virchowiana/complicações , Hanseníase Virchowiana/microbiologia , Hanseníase Tuberculoide/complicações , Hanseníase Tuberculoide/microbiologia , Masculino , Pessoa de Meia-Idade , EspanhaRESUMO
We studied the prevalence of Helicobacter pylori in patients with leprosy and the effects of co-infection on the immune response to Helicobacter antigens in the polar groups of leprosy (lepromatous and tuberculoid). We showed that there is no difference in the prevalence of H. pylori in patients with leprosy as compared to a non-leprosy population. We also demonstrated that the immune response to low molecular weight H. pylori antigens (35, 26 and 19 kDa) differs in patients with lepromatous as compared to those with tuberculoid leprosy. In lepromatous leprosy, we show that there is a higher prevalence of the 35 and 26 kDa antigens, but a lower prevalence of the 19 kDa antigen. These immunological results are consistent with previous histopathological studies illustrating a more severe gastrointestinal inflammation in lepromatous patients; importantly, a response to the 35 kDa antigen is recognized as a marker for the development of ulcerative disease.