Biology subjects

Faerber, H.

Publications and source records attributed to Faerber, H..

2 recordsLinked to original sources

bioRxiv2026

Reduced antibiotic effect of ciprofloxacin on bacteria in the presence of montmorillonite

Antibiotic residues exceeding selective concentrations for antibiotic-resistant bacteria have been detected in various environments, including manure, wastewater, and effluents from wastewater treatment plants. When these residues come into contact with soils, for instance, due to wastewater irrigation or fertilization with manure, they interact with soil constituents. Soil colloids (1-1000 nm), such as montmorillonite, have been observed to adsorb pharmaceuticals, including antibiotics. We investigated the effect of colloids on the bioavailability of ciprofloxacin and found, that added to bacterial growth medium, montmorillonite reduces, but does not completely prevent, the growth-inhibitory effect of the antibiotic. The bacteria were able to grow at up to roughly double the concentration of ciprofloxacin in the presence of montmorillonite. We show that the incomplete deactivation of ciprofloxacin was most probably caused by medium components that decreased the adsorption of ciprofloxacin to montmorillonite. We conclude that a selective potential of this highly active antibiotic in contaminated soils, which also contain nutrients enabling bacterial growth, cannot be ruled out. Environmental implicationAntibiotics such as ciprofloxacin are frequently detected in water bodies and soils due to wastewater irrigation or manure application. These residues raise concerns about environmental toxicity and antibiotic resistance. This study demonstrates that montmorillonite, a common clay mineral in soils, significantly reduces the antimicrobial efficacy of environmental ciprofloxacin concentrations by sorption. The findings reveal a natural attenuation mechanism that may influence the environmental fate and bioavailability of antibiotics. Understanding such interactions is critical for predicting antibiotic behavior in terrestrial systems and for designing more accurate environmental risk assessments.

microbiology↗

bioRxiv2024

Butyrate and propionate are microbial danger signals that activate the NLRP3-inflammasome in human macrophages in the presence of TLR stimulation

Short chain fatty acids (SCFAs) are immunomodulatory compounds produced by the microbiome through fermentation of dietary fibre. Although they are generally considered beneficial for gut health, patients suffering from inflammatory bowel disease (IBD) have shown poor tolerance to fibre-rich diets, suggesting that SCFAs may have contrary effects under inflammatory conditions. To investigate this, we examined the effect of SCFAs on human macrophages in the presence of toll-like receptor agonists. In contrast to their anti-inflammatory effects under steady state conditions, we observed that the SCFAs butyrate and propionate triggered the activation of the NLRP3 inflammasome when added in conjunction with TLR agonists. Mechanistically, butyrate and propionate activated NLRP3 by inhibiting HDACs 1-3 and 10, leading to an uneven distribution of histone hyperacetylation that resulted in alterations in the transcriptome. Specifically, there was a lack of hyperacetylation at the loci of the CFLAR and IL10 genes, two important inhibitors of NLRP3 inflammasome activation. The concurrent loss of transcription and protein expression of cFLIP and IL-10 enabled caspase-8-dependent NLRP3-inflammasome activation. SCFA-driven NLRP3 activation did not require potassium efflux and did not result in cell death but rather triggered hyperactivation and IL-1{beta} release. Our findings demonstrate that butyrate and propionate are bacterially-derived, viability-dependent danger signals (vita-PAMPs) that regulate NLRP3 inflammasome activation through epigenetic modulation of the inflammatory response. SummaryUnder inflammatory conditions, SCFAs are bacterially-derived, viability-dependent danger signals that, through HDAC inhibition and epigenetic modification, prevent expression of the anti-cell death gene cFLIP to trigger activation of the NLRP3 inflammasome.

immunology↗