Biology subjects

Oger, C.

Publications and source records attributed to Oger, C..

5 recordsLinked to original sources

bioRxiv2026

Pigment and isoprostanoid responses to cold atmospheric plasma-induced oxidative conditions in a natural epipelic diatom assemblage

Intertidal mudflats hosting diatom-dominated microphytobenthic communities experience strong variability in environmental conditions, which can lead to cellular oxidative stress. These constraints can, in some cases, affect diatom metabolism and photosynthetic performance in the short term, potentially compromising their survival and even leading to cell death. This study investigates pigment, isoprostanoid, and photophysiological changes in a diatom assemblage originating from a natural microphytobenthic biofilm under different durations of helium-oxygen bubbling cold atmospheric plasma experimental treatments, mimicking complex oxidative conditions of the environment. To this end, 2-min and 5-min treatments were applied to the diatom assemblage, and metabolic parameters were monitored over time up to +180 min after plasma treatment cessation. Despite physicochemical changes and slight perturbations in metabolite profiles induced by plasma treatments, photosynthetic capacities of the diatoms remained largely preserved. The duration-dependent effects of plasma treatments induced selective and mostly reversible changes, primarily characterized by an increase in the relative proportions of pheopigments and a decrease in the relative proportions of {beta}-carotenes following the 5-min treatment. A transient decrease in the relative proportions of the isoprostanoids 10-F4t-neuroP and 5-F2t-IsoP was also observed. By exposing natural diatom assemblage to plasma-generated oxidative conditions, this study provides novel insights into how marine microbiome respond to oxidative perturbations, contributing to our understanding of diatom success in fluctuating intertidal environments.

biophysics↗

bioRxiv2024

Delayed viral clearance and altered inflammatory responses resulted in increased severity of SARS-CoV-2 infection in aged mice.

Since the onset of the COVID-19 pandemic, advanced age has emerged as a major predictor of disease severity. Epidemiological investigations consistently demonstrate an overrepresentation of the elderly in COVID-19 hospitalizations and fatalities. Despite this, a comprehensive understanding of the molecular mechanisms explaining how old age constitutes a critical risk factor remains elusive. To unravel this, we designed an animal study, juxtaposing the course of COVID-19 in young adults (2 months) and geriatric (15-22 months) mice. Both groups of K18(hACE2) mice were intranasally exposed to 500 TCID50 of the SARS-CoV-2 Delta variant with a variety of outcomes assessed on days 3, 5, and 7 post-infections (DPI). Analyses included pulmonary cytokines, RNA, viral loads, lipidomic profiles, and histological assessments, with a concurrent evaluation of the percentage of mice reaching humane endpoints. The findings unveiled notable distinctions between the two groups, with aged mice exhibiting impaired viral clearance at 7 DPI, correlating with diminished survival rates together with an absence of weight loss recovery at 6-7 DPI. Additionally, elderly-infected mice exhibited a deficient Th1 response characterized by diminished productions of IFNg, CCL2, CCL3, and CXCL9 relative to younger mice. Furthermore, mass-spectrometry analysis of the lung lipidome indicated altered expression of several lipids with immunomodulatory and pro-resolution effects in aged mice such as Resolvin, HOTrEs, and NeuroP, but also DiHOMEs-related ARDS. Collectively, disease severity implies a dysregulation of the antiviral response in elderly-infected mice relative to younger mice, resulting in compromised viral clearance and a more unfavorable prognosis. This underscores the potential efficacy of immunomodulatory treatments for elderly subjects experiencing symptoms of severe COVID-19. Author summaryIn this study, we investigated why older age is linked to more severe COVID-19 outcomes by comparing the progression of the disease in young (2 months) and elderly (15-22 months) K18(hACE2) mice infected with the SARS-CoV-2 Delta variant. After exposing both groups to the virus, we assessed various factors such as viral loads, immune responses, and lipid profiles in the lungs at different time points. Our findings revealed that elderly mice struggled to clear the virus by day 7 post-infection, leading to higher mortality rates and poorer recovery compared to younger mice. Aged mice showed weaker immune responses, with reduced production of key antiviral proteins like IFNg and certain chemokines. Lipid analysis also highlighted differences in molecules involved in immune regulation and lung protection, such as decreased levels of pro-resolving lipids and increased lipids associated with lung injury. These results suggest that older mice have a compromised antiviral defense, which could inform new therapeutic approaches for elderly patients with severe COVID-19.

microbiology↗

bioRxiv2024

Non-enzymatic oxylipin production in a mudflat microphytobenthic biofilm: evidence of a diatom response to light

The microphytobenthos (MPB) is a diatom dominated microbial community of primary producers inhabiting the mudflat sediments. In one hand, the benthic diatoms display photo-protective strategies to face extreme light variations susceptible to generate cellular oxidative stress. In the other hand, oxidative stress induces the production of reactive oxygen species (ROS) that generate oxylipins, oxygenated metabolites of polyunsaturated fatty acids (PUFAs), which are among the known chemical mediators in diatoms. However, non-enzymatically generated oxylipins known as isoprostanoids or isofuranoids are poorly studied in diatoms. To better understand the roles of the latter in migrational MPB light response, we investigated the effect of different light irradiances corresponding to dark (D), low light (LL, 50 and 100 {micro}mol. photons. m-2. s-1PAR), medium light (ML, 250 {micro}mol. photons. m-2. s-1 PAR), high light (HL, 500, 750 and 1000 {micro}mol. photons. m-2. s-1PAR), on the isoprostanoids production by the biofilms organisms. The PUFAs precursors of the varying oxylipins evidenced a diatoms response to light irradiance. Under 1000 PAR condition, the total amount of isoprotanoids increased, indicating an oxidative stress response. Isoprostanes (IsoPs) and prostaglandins (PGs) characterized the HL conditions and evidenced lipid peroxidation probably linked to the higher generation of ROS by the photosynthesis. On the contrary, the phytoprostanes (PhytoPs) characterized the LL and ML where the de-epoxidation state was low and ROS scavengers probably not overwhelmed. This first investigation of non-enzymatic oxylipin production by a microphytobenthic biofilm under different light irradiances highlighted the interest to explore their potential signaling roles related to MPB light responses.

microbiology↗

bioRxiv2022

Activation of hTREK-1 by polyunsaturated fatty acids does not only involve membrane tension

TREK-1 is a mechanosensitive channel also activated by polyunsaturated fatty acids (PUFAs). In this study, we compared the effect of multiple fatty acids and ML402. First, we showed a variable TREK-1 activation by PUFAs related to the variable constitutive activity of TREK-1. Then, we observed no correlation between TREK-1 activation and acyl chain length or number of double bonds suggesting that the bilayer-couple hypothesis cannot explain by itself the activation of TREK-1 by PUFAs. The membrane fluidity measurement is not modified by PUFAs at 10 {micro}M. The spectral shift analysis in TREK-1-enriched microsomes indicates a KD,TREK1 at 44 {micro}M of C22:6 n-3. PUFAs display the same activation and reversible kinetics than the direct activator ML402 and activate TREK-1 in both whole-cell and inside-out configurations of patch-clamp suggesting that the binding site of PUFAs is accessible from both sides of the membrane, as for ML402. Finally, we proposed a two steps mechanism for TREK-1 activation by PUFAs: first, insertion into the membrane, without fluidity or curvature modifications, and then interaction with TREK-1 channel to open it.

biophysics↗

bioRxiv2019

Oxidized products of α-linolenic acid negatively regulate cellular survival and motility of breast cancer cells

BackgroundCancer is a major cause of death in the world, and more than six million new cases are reported every year. Despite recent advances in our understanding of the biological processes leading to the development and progression of cancer, there is still a need for new and effective agents to treat this disease. Phytoprostanes (PhytoPs) and phytofurans (PhytoFs) are non-enzymatically oxidized products of -linolenic acid that are present in seeds and vegetable oils. They have been shown to possess anti-inflammatory and apoptosis-promoting activities in macrophages and leukemia cells, respectively.\n\nMethodsIn this work, seven PhytoPs (PP1-PP7) and one PhytoFs (PF1) were evaluated for their cytotoxic, chemosensitization and anti-migratory activities using the MCF-7 and MDA-MB-231 breast cancer cell lines.\n\nResultsAmong the compounds tested, only three PhytoPs had a significant effect on cell viability compared to the control group: Ent-9-L1-PhytoP (PP6) decreased cell viability in both cell lines, while 16-F1t-PhytoP (PP1) and 9-L1-PhytoP (PP5) decreased viability in MCF-7 and MDA-MB-231 cells, respectively. When combined with a sub-cytotoxic dose of doxorubicin, these three PhytoPs significantly enhanced the cytotoxic effect on MCF-7 cells while the chemotherapeutic drug alone had no effect. In cellular motility assays, Ent-9-(RS)-12-epi-ST-{Delta}10-13-PhytoF could significantly inhibit cellular migration of MDA-MB-231 cells in a wound-healing and a transwell assays. In addition, Ent-9-(RS)-12-epi-ST-{Delta}10-13-PhytoF also enhanced cellular adhesion of MDA-MB-231 cells.\n\nConclusionsThis study shows for the first time that the plant-derived compounds PhytoPs and PhytoFs could be further exploited alone or in combination with chemotherapy to improve the arsenal of therapies available against breast cancer.

cancer biology↗