RESUMO
Helicobacter pylori is the etiological agent of chronic gastritis, peptic ulcer, and gastric cancer. The duodenal ulcer-promoting gene dupA, which is located in the plasticity region of the H. pylori genome, is homologous to the virB gene which encodes a type IV secretion protein in Agrobacterium tumefaciens. Studies have shown associations between H. pylori dupA-positive strains and gastroduodenal diseases. However, whether dupA acts as a risk factor or protective factor in these diseases remains unclear. Therefore, in this study, we aimed to verify the presence of the dupA gene in infectious H. pylori strains in the Brazilian mid-west and to investigate its association with the clinical outcomes of patients with dyspepsia. Additionally, the phylogenetic origin of the strains was determined. Gastric biopsies from 117 patients with dyspepsia were analyzed using histological and molecular techniques. The hpx gene (16S rRNA) was used to screen for H. pylori infection, and positive samples were then subjected to dupA gene detection and sequencing. The estimated prevalence of H. pylori infection was 64.1%, with the dupA gene being detected in a high proportion of infectious strains (70.7%). Furthermore, a risk analysis revealed that for women, a dupA-positive H. pylori infection increased the chance of developing gastritis by twofold. The partial dupA sequences from isolated infectious strains in this work are similar to those of strains isolated in westerns countries. This study provides useful insights for understanding the role of the H. pylori dupA gene in disease development.
Assuntos
Proteínas de Bactérias , Infecções por Helicobacter , Helicobacter pylori , Fatores de Virulência , Proteínas de Bactérias/genética , Brasil/epidemiologia , Dispepsia/complicações , Dispepsia/epidemiologia , Dispepsia/microbiologia , Feminino , Infecções por Helicobacter/complicações , Infecções por Helicobacter/epidemiologia , Infecções por Helicobacter/microbiologia , Helicobacter pylori/classificação , Helicobacter pylori/genética , Helicobacter pylori/patogenicidade , Humanos , Masculino , Filogenia , Fatores de Proteção , RNA Ribossômico 16S/genética , Fatores de Risco , Fatores de Virulência/genéticaRESUMO
BACKGROUND: Interleukin 32 (IL-32) is a pro-inflammatory cytokine induced in patients with American tegumentary leishmaniasis (ATL) caused by Leishmania braziliensis. Here, we investigated whether IL-32 is also expressed in patient lesions caused by L. amazonensis. In addition, we evaluated experimental L. amazonensis and L. braziliensis infections in C57BL/6 transgenic mice for human IL-32γ (IL-32γTg) in comparison with wild-type (WT) mice that do not express the IL-32 gene. RESULTS: Human cutaneous lesions caused by L. amazonensis express higher levels of IL-32 than healthy control skin. In mice, the presence of IL-32γ promoted the control of cutaneous lesions caused by L. braziliensis, but not lesions caused by L. amazonensis in an ear dermis infection model. In addition, IL-32γTg mice displayed less tissue parasitism and inflammation in IL-32γTg than WT mice during the healing phase of L. braziliensis infection. Production of antigen-specific pro-inflammatory cytokines was higher in IL-32γTg mice than in WT mice during L. braziliensis infection but not during L. amazonensis infection. CONCLUSIONS: Human cutaneous lesions caused by L. amazonensis express high levels of IL-32. In mice, the presence of IL-32γ contributes to the lesion healing caused by L. braziliensis but not by L. amazonensis. Data suggest that despite the ability for both species to induce IL-32 in humans, the connections between this cytokine and other immune players induced by related species of parasites can lead to distinct outcomes of the murine infections.
Assuntos
Interleucinas/metabolismo , Leishmania braziliensis/imunologia , Leishmania mexicana/imunologia , Leishmaniose Cutânea/imunologia , Cicatrização , Animais , Modelos Animais de Doenças , Humanos , Interleucinas/genética , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Pele/parasitologia , Pele/patologiaRESUMO
Interleukin 32 (IL-32) is a proinflammatory cytokine, expressed as 9 distinct isoforms. The most active isoform is the predominantly intracellular-functioning IL-32γ. Involvement of IL-32 in infectious diseases is increasingly being appreciated. Production of IL-32 promotes pathways that serve to control bacterial infection, especially those caused by mycobacteria. A similar role for this cytokine is observed in the cellular response to viral infections. In addition to its protective effects against microorganisms, IL-32 is involved in immunopathogenesis of some infectious diseases. In parasitic diseases, it has been demonstrated that this cytokine is induced by Leishmania infection. In this review, we summarize the present data on the role of IL-32 in infectious diseases, highlighting this cytokine as new target for control of infections.
