Cross-talk between E. coli strains and a human colorectal adenocarcinoma-derived cell line

Abstract

Although there is great interest in the specific mechanisms of how gut microbiota modulate the biological processes of the human host, the extent of host-microbe interactions and the bacteria-specific metabolic activities for survival in the co-evolved gastrointestinal environment remain unclear. Here, we demonstrate a comprehensive comparison of the host epithelial response induced by either a pathogenic or commensal strain of Escherichia coli using a multi-omics approach. We show that Caco-2 cells incubated with E. coli display an activation of defense response genes associated with oxidative stress. Indeed, in the bacteria co-culture system, the host cells experience an altered environment compared with the germ-free system that includes reduced pH, depletion of major energy substrates, and accumulation of fermentation by-products. Measurement of intracellular Caco-2 cell metabolites revealed a significantly increased lactate concentration, as well as changes in TCA cycle intermediates. Our results will lead to a deeper understanding of acute microbial-host interactions.

Gastrointestinal Microbes Interact with Canine Adipose-Derived Mesenchymal Stem Cells In Vitro and Enhance Immunomodulatory Functions

“…L. monocytogenes EDGe behaved similarly to Salmonella, but the two E. coli strains exhibited opposite MSC association patterns. Of the total associated E. coli K12, 78.5% of the bacteria invaded MSCs while E. coli O157:H7 exclusively adhered to and did not invade MSCs, which was also observed by He et al [44].…”

EspFu-Mediated Actin Assembly Enhances Enteropathogenic Escherichia coli Adherence and Activates Host Cell Inflammatory Signaling Pathways

“…Actin pedestal formation induced by EPEC activates inflammation-related pathways on epithelial cells. Transcriptomic analysis has provided valuable insights on bacterial-host interactions, as well on the processes leading to disease, including several studies using pathogenic E. coli infections (36)(37)(38). To investigate how different actin assembly pathways affect transcription of host cells, we performed RNA-Seq analysis using total mRNA purified from HeLa monolayers infected with the WT and the engineered BA320 strains for 6 h. This time point was chosen because after 6 h of infection, the effectors have been delivered, and actin has been rearranged into pedestals.…”

Pore-forming Activity of the Escherichia coli Type III Secretion System Protein EspD

“…In the intestinal tract, it is conceivable that a localized acidic environment required for EspD membrane insertion may be generated by the following: (i) the metabolism of pathogenic E. coli microcolonies attached to epithelial cells (70); (ii) upregulating the activity of the sodium-hydrogen exchanger 2 antiporter, which may cause a decrease in the cell surface pH (70,71), and (iii) down-regulation of the monocarboxylate transporter 1 activity, which would result in the extracellular accumulation of short chain fatty acid metabolites and a decreased pH at the apical surface of the gut epithelial cells (72). It is also possible that contacts with EspA and EspB may be instrumental in driving EspD membrane insertion and pore assembly (28,30).…”