Biology subjects

Gros, M.

Publications and source records attributed to Gros, M..

3 recordsLinked to original sources

bioRxiv2026

Threshold responses of multi-trophic freshwater communities to browning and eutrophication

Browning and eutrophication strongly influence aquatic ecosystems by altering nutrient dynamics, light availability, and food web structure. To investigate their combined effects on aquatic communities, we conducted a nine-week mesocosm experiment in a clear-water north-temperate lake, crossing dissolved organic carbon (DOC) and total phosphorus plus total nitrogen (TP+TN) enrichment treatments. Multi-trophic plankton communities (bacterioplankton, phytoplankton, and zooplankton) were monitored over time using environmental DNA (eDNA) marker gene amplicon sequencing. Beta-diversity analyses highlighted temporal and treatment-driven community restructuring, while PERMANOVA and Principal Response Curve analyses identified the treatments and taxa driving these changes. Our results show that elevated DOC favoured taxa associated with the microbial loop, while nutrient enrichment and lower DOC promoted the green pathway. Threshold responses across trophic levels were observed at 5-7 mg L-{superscript 1} DOC and 30-70 g L-{superscript 1} TP, marking the levels at which compositional shifts propagated through the food web. Overall, this study demonstrated how aquatic communities respond dynamically to browning and nutrient enrichment, offering insight into the mechanisms shaping multi-trophic interactions under a multiple stressor scenario. HighlightsO_LIBrowning and nutrient pulses drove coordinated shifts across bacterioplankton, phytoplankton, and zooplankton. C_LIO_LITemporal community succession and treatment effects were captured through beta-diversity and multivariate ordination analyses. C_LIO_LIThreshold responses propagated through the food web at 5-7 mg L-{superscript 1} DOC and 30-70 {micro}g L-{superscript 1} TP. C_LI Scientific Significance Statement TopicThis study provides insights into the interactive effects of browning and eutrophication on community composition shifts in freshwater ecosystems. Using a mesocosm experiment, we identified thresholds for dissolved organic carbon and total phosphorus + nitrogen concentrations that drove compositional changes across bacterial, phytoplankton, and zooplankton communities, as determined by environmental DNA amplicon sequencing data. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=133 SRC="FIGDIR/small/719940v1_ufig1.gif" ALT="Figure 1"> View larger version (22K): org.highwire.dtl.DTLVardef@d12f96org.highwire.dtl.DTLVardef@18b4426org.highwire.dtl.DTLVardef@271b94org.highwire.dtl.DTLVardef@183c1d6_HPS_FORMAT_FIGEXP M_FIG C_FIG

ecology↗

bioRxiv2025

Abdominal symptoms of invasive meningococcal disease are associated with the induction of plasminogen activator inhibitor in omental adipocytes

Abdominal symptoms are increasingly reported in invasive meningococcal disease (IMD), but the underlying mechanisms remain unclear. We aimed to explore the pathophysiology of these presentations using an animal model. We utilized a collection of 20 meningococcal isolates that were either associated or not associated with abdominal presentations, which were injected intraperitoneally into transgenic mice expressing human transferrin. We employed histological examination, RNA sequencing (RNAseq) transcriptomic analysis, and reverse transcriptase real-time PCR to analyze tissue preparations of the mices omentum. The 20 tested isolates induced similar levels of bacteremia in mice. However, isolates associated with abdominal presentations (mainly serogroup W isolates of clonal complex 11) caused thrombotic lesions in the blood vessels of the omentum, and they also induced a higher inflammatory response in the omentum with elevated levels of IL-6, TNF-alpha, and KC. Furthermore, these isolates induced higher expression of several genes, some of which are involved in coagulopathy, such as plasminogen activator inhibitor 1 (PAI-1). We also demonstrated that the PAI-1 encoding gene is overexpressed in adipocyte cells of the omentum. Lipopolysaccharide from the isolates associated with abdominal presentations, instead of whole bacteria, induced similar pathological findings. During IMD, thrombosis formation in the omentums blood vessels is associated with a local induction of an inflammatory response and overexpression of the plasminogen activator inhibitor 1 encoding gene. These lesions can lead to thrombosis and hypoperfusion in the omentum, resulting in clinical abdominal presentations Author summaryNeisseria meningitidis, commonly known as meningococci, is a bacterium that is transmitted directly from person to person through respiratory droplets. This bacterium causes invasive meningococcal disease (IMD), which can manifest in various symptoms beyond just meningitis. Notably, abdominal presentations, including abdominal pain and diarrhea, are increasingly being reported. The aim of our investigation was to elucidate the underlying mechanism of these abdominal symptoms. To achieve this, we employed several experimental approaches and provided evidence that these symptoms are caused by the coagulation (clotting) of blood in the microvessels that surround the abdominal organs, such as the intestine. This clotting is triggered by the bacteriums induction of a human enzyme that promotes coagulation. Notably, this is the first study to explore a mechanism underlying an extra-meningeal clinical form of N. meningitidis infection. The enzyme responsible for this coagulation, plasminogen activator inhibitor 1, is a potential target for modulating the host response to IMD. Our findings have significant implications for the understanding of meningococcal pathophysiology and reveal additional potential targets for treatment.

microbiology↗

bioRxiv2020

Small molecule enhancers of endosome-to-cytosol import augment anti-tumour immunity

Efficient cross-presentation of antigens by dendritic cells (DCs) is critical for initiation of anti-tumour immune responses. Yet, several steps of antigen intracellular traffic during cross-presentation are incompletely understood: in particular, the molecular mechanisms and the relative importance of antigen import from endocytic compartments into the cytosol. Here, we asked whether antigen import into the cytosol is rate-limiting for cross-presentation and anti-tumour immunity. By screening 700 FDA-approved drugs, we identified 37 import enhancers. We focused on prazosin and tamoxifen, and generated proteomic organellar maps of drug-treated DCs, covering the subcellular localisations of over 2000 proteins. By combining organellar mapping, quantitative proteomics, microscopy, and bioinformatics, we conclude that import enhancers undergo lysosomal trapping leading to membrane permeation and antigen release into the cytosol. Enhancing antigen import facilitates cross-presentation of both soluble and cell-associated antigens. Systemic administration of prazosin also led to reduced growth of MC38 tumours and to a synergistic effect with checkpoint immunotherapy in a melanoma model. Thus, inefficient antigen import into the cytosol limits antigen cross-presentation, restraining the potency of anti-tumour immune responses and efficacy of checkpoint blockers. HighlightsO_LIQuinazolamine derivatives are potent enhancers of antigen import into the cytosol C_LIO_LIAntigen import enhancement occurs as a consequence of lysosomal trapping C_LIO_LIAntigen import enhancers facilitate cross-presentation and synergise with PD-L1 C_LIO_LIProteomic organellar maps of cDC1s as a tool to detect biological effects of drugs C_LI O_FIG O_LINKSMALLFIG WIDTH=180 HEIGHT=200 SRC="FIGDIR/small/079491v1_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@1d55245org.highwire.dtl.DTLVardef@c3d43org.highwire.dtl.DTLVardef@189fbc8org.highwire.dtl.DTLVardef@1f1280e_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗