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Background: Helicobacter pylori is an etiologic agent of gastroduodenal diseases. The microorganism, considered a type I carcinogen, affects about 50% of the global population. H. pylori virulence factors are determinant for the clinical outcome of the infection. The outer inflammatory protein A (oipA) gene encodes an outer membrane adhesin and is related to severe gastropathies, such as gastric cancer., Objective: The aim of this study was to evaluate the association of the oipA gene with the severity of gastroduodenal diseases in dyspeptic patients in region Central Brazil., Methods: The polymerase chain reaction (PCR) was used to determine the presence of H. pylori. Samples positives were used for molecular screening of the oipA gene. Gastropathies were categorized as non-severe and severe diseases., Results: Approximately 68% of patients had H. pylori and 36% were infected with H. pylori oipA+ strains. Infection was significantly associated in patients aged over 44 years (P=0.004). However, there was no association between oipA and patients' age (P=0.89). Approximately 46% of patients infected with oipA+ strains had some severe illness. Gastric adenocarcinoma was the most frequent severe gastropathy. The H. pylori oipA genotype was inversely associated with the severity of gastroduodenal diseases (OR=0.247, 95%CI: 0.0804-0.7149 and P=0.007)., Conclusion: The characterization of possible molecular markers will contribute to personalized medicine, impacting the prognosis of patients., Background: • Evidence points to an association between the H. pylori oipA gene and gastropathies., Background: • There is a high prevalence of H. pylori infection with a relevant percentage of oipA+ strains., Background: • More severe gastropathies were observed in those infected with H. pylori oipA+ strains.

The aims of this study were to identify mercury-associated protein spots in the liver tissue of rats exposed to low concentrations of mercury and to elucidate the physiological and functional aspects of the proteins identified in the protein spots. Therefore, proteomic analysis of the liver tissue of Wistar rats exposed to mercury chloride (4.60 μg kg -1 in Hg 2+ ) was performed for thirty days (Hg-30 group) and sixty days (Hg-60 group). The proteomic profile of the liver tissue of the rats was obtained by two-dimensional electrophoresis (2D-PAGE), and the determinations of total mercury in the liver tissue, pellets and protein spots were performed by graphite furnace atomic absorption spectrometry (GFAAS). ImageMaster 2D Platinum 7.0 software was used to identify the differentially expressed mercury-associated protein spots, which were then characterized by liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). The determinations by GFAAS indicated a total mercury bioaccumulation of 2812% in the Hg-30 group and 3298% in the Hg-60 group and 10 mercury-associated protein spots with a concentration range of 51 ± 1.0 to 412 ± 6.00 mg kg -1 in the 2D PAGE gels from the liver tissue of the Hg-60 group. The LC-MS/MS analyses allowed the identification of 11 metal binding proteins in mercury-associated protein spots that presented fold change with upregulation >1.5, downregulation < -1.7 or that were expressed only in the Hg-60 group. Using the FASTA sequences of the proteins identified in the mercury-associated protein spots, bioinformatics analyses were performed to elucidate the physiological and functional aspects of the metal binding proteins, allowing us to infer that enzymes such as GSTM2 presented greater mercury concentrations and downregulation < -3; Acaa2 and Bhmt, which showed expression only in the Hg-60 group, among others, may act as potential mercury exposure biomarkers., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Background: Helicobacter pylori colonizes approximately half of the world's human population. Its presence in the gastric mucosa is associated with an increased risk of gastric adenocarcinoma, gastric lymphoma, and peptic ulcer disease. In Brazil, the high prevalence of H. pylori infection is a serious health problem. H. pylori virulence factors are associated with an increased risk of serious gastrointestinal disorders. The cagA gene encodes a cytotoxin-A-associated antigen (CagA) that is involved in bacterial pathogenicity. H. pylori strains carrying the cag pathogenicity island (cag-PAI) are significantly associated with severe clinical outcomes and histopathological changes., Objective: The present study aims to investigate the prevalence of the cagA gene among H. pylori isolates from patients with different gastric pathologies. Further, the study hopes to verify its association with clinical outcomes. In addition, phylogenetic analysis was performed on cagA-positive H. pylori strains from patients with severe and non-severe diseases., Methods: Gastric specimens were collected through a biopsy from 117 patients with different esogastroduodenal diseases. DNA was extracted from these gastric specimens and the polymerase chain reaction was performed to amplify the gene fragments corresponding to the 16S ribosomal RNA and cagA genes using specific primers. The polymerase chain reaction products of selected samples positive for cagA were sequenced. The sequences were aligned with reference sequences from the National Center for Biotechnology Information (NCBI) (Bethesda/USA), and a phylogenetic tree was constructed., Results: H. pylori was detected in 65.9% (77/117) of Brazilian patients with different gastroduodenal disorders. Overall, 80.5% (62/77) of the strains were cagA-positive. The ages of patients with cagA-positive strains (15 males and 47 females) ranged from 18 to 74 years. The lesions were categorized as non-severe and severe according to the endoscopic and histopathological reports the most prevalent non-severe esogastroduodenal lesion was gastritis 54/77 (70.12%), followed by esophagitis 12/77 (15.58%) and duodenitis 12/77 (15.58%). In contrast, the most prevalent severe lesions were atrophy 7/77 (9.09%), followed by metaplasia 3/77 (3.86%) and gastric adenocarcinoma 2/77 (2.59%). Phylogenetic analyses performed with the partial sequences of the cagA gene obtained from local strains were grouped in the same clade. No differences in phylogenetic distribution was detected between severe and non-severe diseases., Conclusion: The cagA gene is highly prevalent among H. pylori isolates from gastric lesions in Brazilian patients. The presence of the cagA gene was not considered a marker of the severity of esogastroduodenal lesions in the present study. This is the first study to investigate the phylogenetic population structure of H. pylori strains in a Brazilian capital, which may improve our understanding of the clinical outcome of H. pylori infection.

How human macrophages can control the intracellular infection with Leishmania is not completely understood. IL-15 and IL-32 are cytokines produced by monocytes/macrophages that can induce antimicrobial mechanisms. Here, we evaluated the effects of recombinant human IL-15 (rhIL-15) on primary human macrophage infection and response to L. braziliensis. Priming with rhIL-15 reduced the phagocytosis of L. braziliensis and increased the killing of the parasites in monocyte-derived macrophages from healthy donors. rhIL-15 induced TNFα and IL-32 in uninfected cells. After infection, the high levels of rhIL-15-induced TNFα and IL-32 were maintained. In addition, there was an increase of NO and an inhibition of the parasite-induced IL-10 production. Inhibition of NO reversed the leishmanicidal effects of rhIL-15. Although rhIL-15 did not increase L. braziliensis-induced reactive oxygen intermediates (ROS) production, inhibition of ROS reversed the control of infection induced by rhIL-15. Treatment of the cells with rhIL-32γ increased microbicidal capacity of macrophages in the presence of high levels of vitamin D (25D3), but not in low concentrations of this vitamin. rhIL-15 together with rhIL-32 lead to the highest control of the L. braziliensis infection in high concentrations of vitamin D. In this condition, NO and ROS mediated rhIL-32γ effects on microbicidal activity. The data showed that priming of human macrophages with rhIL-15 or rhIL-32γ results in the control of L. braziliensis infection through induction of NO and ROS. In addition, rhIL-32γ appears to synergize with rhIL-15 for the control of L. braziliensis infection in a vitamin D-dependent manner., Competing Interests: Declaration of Competing Interest We declare that we do not have any potential sources of conflict of interest., (Copyright © 2020 Elsevier B.V. All rights reserved.)