Biology subjects

Soulard, C.

Publications and source records attributed to Soulard, C..

2 recordsLinked to original sources

bioRxiv2025

A deeper study on propionic acid-related inhibition during anaerobic digestion: insights on methane production and identification of biomarker candidates for an early warning

Propionic acid (HPr) accumulation is a major indicator of anaerobic digestion (AD) dysfunction, yet the relative contributions of acidity, undissociated HPr, and propionate ions (Pr-) to process inhibition remain poorly understood. We investigated these effects in mesophilic batch AD microcosms fed with municipal sewage sludge, using a comparative design involving HPr, sodium propionate (NaPr), NaCl, and HCl treatments across two series of experiments. While 20 mM HPr caused a 22% reduction in the maximal methane production rate, 81 mM HPr led to complete inhibition, with the initial pH dropping to 5.1. By contrast, 81 mM NaPr reduced methane production rate by only 40%, and 81 mM NaCl caused no inhibition, demonstrating that acidity is the dominant inhibitory factor, with Pr- exerting a secondary concentration-dependent effect. 16S rRNA gene amplicon sequencing revealed strong, compound-specific shifts in microbial community composition, affecting key functional groups including syntrophs and methanogenic archaea. The proportion of methanogens dropped from 2-3% in control reactors to less than 0.2% under 81 mM HPr, consistent with the observed methane production inhibition. Under HPr81, over 100 ASVs were differentially abundant compared to controls, a pattern largely shared with HCl-treated reactors, further confirming the predominant role of acidity. The number of differentially abundant ASVs was negatively correlated with methane production rates (R{superscript 2} = 0.97), underscoring the link between community reshaping and process impairment. These results provide a unifying framework for propionate inhibition in AD and suggest that microbial community profiling could serve as an early warning tool for process imbalance detection.

bioengineering↗

bioRxiv2022

Generation of Functional Human T Cell Development in NOD/SCID/IL2rγnull Humanized Mice Without Using Fetal Tissue: Application as a Model of HIV Infection and Persistence

Generating humanized mice with fully functional T cells currently relies on co-implantation of hematopoietic stem cells from fetal liver and autologous fetal thymic tissue (BLT mouse). However, access to such tissues has ethical and logistical challenges. Herein, we show that NOD/SCID/IL2r{gamma}null mice humanized with cord blood-derived CD34+ cells and implanted in quadriceps with pediatric thymic tissues excised during cardiac surgeries (CCST mice) are an alternative to BLT mice. Our data revealed a strong immune reconstitution in CCST mice, with T cells originating from CD34+ progenitor cells, proliferating efficiently in response to mitogenic stimulation ex vivo and capable of rejecting allogeneic human leukemic cells in vivo. Despite having less T cells than BLT mice, CCST mice were equally susceptible to mucosal or intraperitoneal HIV infection. Importantly, HIV-specific T cell responses were significantly higher in CCST-mice (median: 10.4% vs. 0.7%; p<0.0001 for CD8+cells and 3.9% vs. 0.7%; p<0.01 for CD4+ cells). As well, antiretroviral therapy (ART) robustly suppressed viremia and reduced the frequencies of cells carrying integrated HIV DNA by up to 2 logs in various CCST mouse tissues. As in BLT mice, we observed a complete viral rebound in 67% of the animals by 2-4 weeks following ART interruption, suggesting the presence of HIV reservoirs. In conclusion, CCST mice represent an ethical and practical alternative to BLT mice, broadening the feasibility of utilizing humanized mice for research on HIV and other human diseases. One Sentence SummaryWe herein report a new humanized mouse model implanted with human cord blood hematopoietic stem cells and allogenic pediatric thymic tissue that develops a functional T cell compartment and supports efficient HIV infection and persistence during antiretroviral therapy.

immunology↗