Helicobacter pylori colonizes half of the human population. Age, ethnicity, and socioeconomic status are factors that influence the prevalence of the infection. This is important in southern Chile, one of the most unequal regions in the world, where a significant difference in the health access of the population occurs due to the existence of two competing health systems. Moreover, in the last few years, current protocols of H. pylori eradication have shown high rates of resistance with reduced therapeutic efficacy. This study reported the epidemiology of infection and attempted to identify divergent points among the population beneficiaries of the two health care schemes in southern Chile. Biopsies from public (n = 143) and private (n = 86) health systems were studied. At the same time, clinical and sociodemographic factors were evaluated. H. pylori strains were obtained from gastric biopsies for culture and molecular testing. Antibiotic susceptibility was determined by the agar dilution method. Differences about ethnicity, rural residence, and education (p ≤ 0.05) were observed between beneficiaries of the two health systems. The prevalence of H. pylori was 45%, with no significant differences regardless of the socioeconomic conditions. The only identified risk factor associated with H. pylori infection was Mapuche ethnicity (OR (odds ratio) = 2.30). H. pylori showed high resistance rates, particularly against clarithromycin (40%), levofloxacin (43.1%), and metronidazole (81.8%). This study highlighted the importance of Mapuche ancestry as a risk factor in southern Chile and emphasized the need to search for new eradication strategies as well as further studies evaluating therapeutic efficacy.

Helicobacter pylori is the main bacteria associated with gastroduodenal diseases. Recent studies have reported that gastric microbiota might be modified by the H. pylori colonization, favoring gastric lesions′ development. In Chile, the region of La Araucanía concentrates a high risk of gastric cancer associated with Helicobacter pylori colonization, rurality, poverty, and Mapuche ethnicity. Hence, we aimed to identify the culturable gastric microbiota and characterize its variability at different stages of epithelial injury, based on its H. pylori colonization in dyspeptic patients from this Chilean region. Microaerophilic bacteria strains were isolated from antrum biopsies of 155 dyspeptic patients′ biopsies and identified using MALDI-TOF MS or 16sRNA gene sequencing for non-pylori species identification, and UreC gene amplification for H. pylori confirmation. We found 48 species from 18 families, mainly belonging to Neisseriaceae (21.3%), Streptococcaceae (20.0%), Actynomicetaceae (9.0%), Enterobacteriaceae, and Lactobacillaceae (4.5%); however, Streptococcaceae and Actinomycetaceae families showed a significant reduction in samples infected with H. pylori, along with a considerably lower diversity of species. Our results revealed a microbiota modification due to H. pylori colonization associated with the gastric epithelial state, suggesting a potential microbiota role for developing and progressing gastric diseases.

Background/Objectives: Helicobacter pylori is a cause of chronic gastric infections and gastrointestinal carcinogenesis, with a prevalence of 20–90% around the world. Its eradication is increasingly challenged by clarithromycin resistance, particularly in regions with high rates of antibiotic resistance. While clarithromycin resistance is primarily attributed to 23S rRNA mutations, secondary mechanisms such as efflux pumps remain understudied. The present study reports a high prevalence of hefA efflux pump overexpression as a main molecular basis of clarithromycin resistance in H. pylori isolates from southern Chile. Materials and Methods: A total of 102 H. pylori isolates were obtained from gastric biopsy cultures. Isolates were analyzed for clarithromycin susceptibility by MIC, the 23S rRNA mutations A2142G/A2143G by PCR-RFLP followed by sequencing, and hefA relative expression by qPCR. Results: Clarithromycin resistance was detected in 38% of isolates. Resistance was significantly associated with therapeutic failure and urban residence. While 44% of resistant isolates harbored A2142G/A2143G mutations, 56% did not, suggesting alternative resistance mechanisms. Mutation C2182T was identified in 11% resistant isolates, and increased hefA expression was observed in resistant strains without 23S rRNA mutations, indicating efflux pump dysregulation as a resistance mechanism. Conclusions: Our findings reveal a shift in epidemiology of clarithromycin resistance mechanisms in H. pylori that extends beyond classical 23S rRNA mutations to include efflux-mediated adaptive resistance as a contributing mechanism. The positive correlation between hefA overexpression and MIC elevation underscores its role in resistance. These findings have important implications for the efficacy of clarithromycin-based therapies and highlight the need to reassess empirical treatment strategies in response to emerging resistance patterns.

(1) Background: Gastric cancer, the fourth most common cause of death from tumors in the world, is closely associated with Helicobacter pylori. Timely diagnosis, therefore, is essential to achieve a higher survival rate. In Chile, deaths from gastric cancer are high, mainly due to late diagnosis. Progranulin has reflected the evolution of some cancers, but has been poorly studied in gastric lesions. Aiming to understand the role of progranulin in H. pylori infection and its evolution in development of gastric lesions, we evaluated the genic expression of progranulin in gastric tissue from infected and non-infected patients, comparing it according to the epithelial status and virulence of H. pylori strains. (2) Methods: The genic expression of progranulin by q-PCR was quantified in gastric biopsies from Chilean dyspeptic patients (n = 75) and individuals who were uninfected (n = 75) by H. pylori, after receiving prior informed consent. Bacteria were grown on a medium Columbia agar with equine-blood 7%, antibiotics (Dent 2%, Oxoid^TM), in a microaerophilic environment, and genetically characterized for the ureC, vacA, cagA, and iceA genes by PCR. The status of the tissue was determined by endoscopic observation. (3) Results: Minor progranulin expression was detected in atrophic tissue, with a sharp drop in the tissue colonized by H. pylori that carried greater virulence, VacAs1m1⁺CagA⁺IceA1⁺. (4) Conclusions: Progranulin shows a differential behavior according to the lesions and virulence of H. pylori, affecting the response of progranulin against gastric inflammation.