| dc.description.abstract | The bacterium Helicobacter pylori (H. pylori) colonizes the human gastric mucosa and is a recognized causative agent for peptic ulcer disease. The prevalence of H. pylori infection in Zimbabwe is unknown. Treatment requires combination therapies which may predispose to antibiotic resistance. The pathogen is also implicated in development of autoimmune endocrinopathies such as autoimmune thyroiditis, Systemic lupus erythematosus and rheumatoid arthritis. While the prevalence of autoimmune diseases has been increasing in Zimbabwe, there are no studies investigating whether any association exists between H. pylori infection and any
autoimmune disease. Effective treatment regimens to prevent the development of autoimmunity on H. pylori infection are unavailable. It is important to understand the immuno-epidemiology of autoimmunity and H. pylori so as to understand the immune system dynamics that occur during the disease. The aim of the present study was to determine the burden of H. pylori-associated autoimmune conditions and to characterize the cytokines in the affected patients. Methods: Clinical and laboratory records of 1500 patients were reviewed and an analytical crosssectional study on 385 samples was done. Archived samples of patients that warranted an H. pylori and/or autoimmunity test were used for detection of autoantibodies using immunoblot assays. Detection of IgG anti-H. pylori antibodies was done using rapid kits and IgA using ELISA. Flow cytometry was used for detection of cytokines. Ten samples were used in a prospective study where whole blood was stimulated with E. coli antigen, H. pylori antigen and pokeweed mitogen. Cytokines expressed were determined using ELISA. Results& Discussion: The prevalence of co-existing autoimmune autoantibodies and H. pylori infection was 18%. The association of H. pylori infection and expression of autoantibodies was greater among systemic sclerosis patients, SLE and myositis, respectively. The auto antibodies
associated with H. pylori infection are anti-RP155, anti-PM-Scl-100, anti-Th/To, anti- Ku, antidsDNA and anti-PCNA. Of these anti-Th/To and anti-Ku are only found in women. High levels of pro-inflammatory cytokine TNF-α and low INF-γ are associated with H. pylori inflammation while IL-17A was associated with autoimmune inflammation in the patients studied. The immune response to chronic H. pylori infection in the gastric mucosa possibly drives towards autoimmune inflammation. Infection by H. pylori potentially suppresses specific immune cell populations. Conclusion: We conclude that there is an association between H. pylori infection and the expression of auto antibodies in Zimbabwean patients. Immune responses to H. pylori infection in the gastrointestinal tract may potentially drive toward autoimmune inflammation. We recommend investigation of molecular mimicry and B cell compartment studies to further elucidate this association. Key words: H. pylori, infection, autoimmunity, Zimbabwe | en_ZW |
