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Biology subjects

OSMAN, D.

Publications and source records attributed to OSMAN, D..

3 recordsLinked to original sources

Isolation of rat and human hepatic cholangiocytes using a peptide derived from a conserved domain of enterobacteria BamA/TamA-like proteins

Using the phage display technology, we identified a novel peptide, P11Chol, which preferentially binds to both human and rat cholangiocytes. Peptide P11Chol alignment with protein databases evidenced strong similarities with a highly conserved peptide motif from BamA/TamA-like outer membrane proteins expressed in enterobacteriaceae belonging to Pseudomonadota phylum including Photorhabdus, Providencia, Acinetobacter, Salmonella enterica and Helicobacter pylori species. In addition, we showed that Providencia stuartii bacteria were able to bind to cholangiocytes-like HepaRG cells in vitro and that P11Chol modulated this interaction suggesting the possible involvement of BamA/TamA-like outer membrane proteins in cell adhesion and/or internalization of Providencia stuartii bacteria. Using fluorescent P11Chol peptide, we next developed a flow cytometry procedure to detect and isolate rat and human liver epithelial cells from hepatic cell suspension obtained after collagenase dissociation of liver parenchyma. Three distinct P11Chol-positive rat liver epithelial cell lines (RLEC) were established, which produced functional cholangiocytes capable to form cyst-like structures in vitro and to maintain expression of specific functions in hepatocytes in coculture. The characterization of these three RLEC lines evidenced functional differences that support the concept of small and large cholangiocytes exhibiting different functional phenotypes within the intrahepatic bile tree.

cell biology↗

Comprehensive investigation of SARS-CoV-2 intestinal pathogenesis in Drosophila

Gastrointestinal (GI) manifestations have been increasingly reported in COVID-19 patients. Here, we use the Drosophila melanogaster midgut model to investigate SARS-CoV-2-induced GI pathogenesis. The fly midgut exhibits susceptibility to orally administered virus, resulting in disrupted epithelial architecture, reduced organ size, and altered visceral muscle dynamics. These effects are accompanied by sustained proliferation of intestinal stem cells alongside decreased replenishment and viability of differentiated cells. Transcriptomic profiling reveals biphasic perturbations in midgut gene expression, particularly in pathways related to lipid metabolism. Intriguingly, SARS-CoV-2 elicits a dichotomous effect on lipid homeostasis, with lipid droplet accumulation in the posterior midgut and depletion in anterior segments. Treatment with Plitidepsin, a COVID-19 drug candidate, mitigates most SARS-CoV-2 pathogenic features in both the Drosophila midgut and human pulmonary cells, while modulating basal lipid droplet homeostasis in uninfected conditions. These findings establish the Drosophila midgut as a potent model for studying SARS-CoV-2 GI pathogenesis and evaluating antiviral compounds.

pathology↗

Bacillus thuringiensis Cry1A toxins divert progenitor cell fate toward enteroendocrine lineage by diminishing cell adhesion with intestinal stem cells

Bacillus thuringiensis subsp. kurstaki (Btk) is a strong pathogen toward lepidopteran larvae thanks to specific Cry toxins causing leaky gut phenotypes. Hence, Btk and its toxins are used worldwide as microbial insecticide and in genetically modified crops, respectively, to fight crop pests. However, Btk belongs to the B. cereus group, some strains of which are well known human opportunistic pathogens. Therefore, ingestion of Btk along with food may threaten organisms not susceptible to Btk infection. Here we show that Cry1A toxins induce enterocyte death and intestinal stem cell (ISC) proliferation in the midgut of Drosophila melanogaster, an organism non-susceptible to Btk. Surprisingly, a high proportion of the ISC daughter cells differentiate into enteroendocrine cells instead of their initial enterocyte destiny. We show that Cry1A toxins weaken the Cadherin-dependent adherens junction between the ISC and its immediate daughter progenitor, leading the latter to adopt an enteroendocrine fate. Hence, though not lethal to non-susceptible organisms, Cry toxins can interfere with conserved cell adhesion mechanisms, thereby disrupting intestinal homeostasis and enteroendocrine functions.

cell biology↗