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Digestive exophagy of bacterial biofilms by parasitic intestinal amoeba and its impact on stress tolerance, antibiotic resistance and cytotoxicity

ABSTRACT: The human protozoan parasiteEntamoeba histolyticais responsible for amebiasis, a disease endemic to developing countries.E. histolyticatrophozoites colonize the large intestine, primarily feeding on bacteria. However, in the GI, as well as in aquatic and soil microenvironments, bacterial cells form aggregates or structured communities, called biofilm, too large for phagocytosis. However, trophozoites are still able to invade and degrade bacteria under biofilm form by a mechanism mimicking digestive exophagy. E.histolytica cysteine proteinase degrade TasA, one of the main component of the biofilm matrix. Biofilm also play an important role protecting trophozoites against oxidative stress. The specific mechanism suggests that amoeba is adapted to biofilm predation and may serve as a new unexplored reservoir of novel therapeutic approaches to treat biofilms. Consistently, amoeba’s products restored antibiotic sensitivity to biofilm cells. Furthermore, our findings here show that probiotic biofilms may serve as a protective shield for mammalian cells, hindering the progression of the parasite towards them.

ORGANISM(S): Entamoeba histolytica

PROVIDER: GSE233645 | GEO | 2023/10/25

REPOSITORIES: GEO

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Project description:Is there a universal genetically programmed defense providing tolerance to antibiotics when bacteria grow as biofilms? A comparison between biofilms of three different bacterial species by transcriptomic and metabolomic approaches uncovered no evidence of one. Single-species biofilms of three bacterial species (Pseudomonas aeruginosa, Staphylococcus aureus, and Acinetobacter baumannii) were grown in vitro for three days then challenged with respective antibiotics (ciprofloxacin, daptomycin, tigecycline) for an additional 24 h. All three microorganisms displayed reduced susceptibility in biofilms compared to planktonic cultures. Global transcriptomic profiling of gene expression comparing biofilm to planktonic and antibiotic-treated biofilm to untreated biofilm was performed. Extracellular metabolites including 18 amino acids, glucose, lactate, acetate, formate, and ethanol were measured to characterize the utilization of carbon sources between biofilms, treated biofilms, and planktonic cells. While all three bacteria exhibited a species-specific signature of stationary phase, no conserved gene, gene set, or common functional pathway could be identified that changed consistently across the three microorganisms. Across the three species, glucose consumption was increased in biofilms compared to planktonic cells and alanine and aspartic acid utilization were decreased in biofilms compared to planktonic cells. The reasons for these changes were not readily apparent in the transcriptomes. No common shift in the utilization pattern of carbon sources was discerned when comparing untreated to antibiotic-exposed biofilms. Overall, our measurements do not support the existence of a common genetic or biochemical basis for biofilm tolerance against antibiotics. Rather, there are likely myriad genes, proteins, and metabolic pathways that influence the physiological state of microorganisms in biofilms contributing to antibiotic tolerance. The Staphylococcus aureus microarray data from the study described above is deposited here.

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Digestive exophagy of bacterial biofilms by parasitic intestinal amoeba and its impact on stress tolerance, antibiotic resistance and cytotoxicity

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