Biology subjects

Simard, M.

Publications and source records attributed to Simard, M..

3 recordsLinked to original sources

bioRxiv2026

The Vagus Nerve conducts viable translocation of gut flora to the lungs that impacts interstitial lung disease severity in mice

Communication between gut microbiota and extraintestinal organs is increasingly recognized, yet elucidation of relevant translocation mechanism(s) remains enigmatic. Vagus neuroanatomy and reports of vagal protein transfer to extraintestinal organs suggest that this "superhighway" could translocate bacteria. Here we explore whether the vagus superhighway can translocate bacteria to extraintestinal organs. Gavage of green fluorescent protein-expressing Escherichia coli (GFP-E. coli) into germ-free (GF) or specific-pathogen free (SPF) C57BL/6 mice yielded high bacillary loads in the stomach and lungs, followed by the heart, stool and peripheral muscles, despite negative blood cultures. Notably, confocal microscopy and culture revealed GFP-E. coli within the vagus nerve within five minutes of gavage suggesting rapid translocation. Metagenomic analysis of stool, lung, heart, vagus nerve, and muscle from non-gavaged SPF mice demonstrated significant microbial overlap, supporting that bacterial translocation occurs despite the presence of endogenous microflora. Remarkably, subdiaphragmatic vagotomy performed prior to GFP-E. coli gavage resulted in marked reductions of bacterial transduction in the lungs and other extraintestinal organs, except muscle. Furthermore, vagotomy significantly reduced lung fibrosis in SPF mice following intranasal bleomycin administration. In lung cancer patients undergoing lobectomy, vagotomy inhibited postsurgical reductions in forced vital capacity. These findings identify the vagus nerve as a literal gut-lung axis, facilitating viable bacterial translocation and influencing lung severity.

microbiology↗

bioRxiv2025

High-severity fires undermine resilience of black spruce-dominated boreal forests in eastern North America

Climate-induced fire regime shifts may reduce post-fire resilience of black spruce-dominated (BS; Picea mariana) North American boreal forests. While post-fire vulnerability of immature BS stands has been extensively studied, no study has evaluated simultaneous effects of fire severity and seasonality on the post-fire regeneration of mature (> 60-year-old) BS stands. This study aims to quantify post-fire regeneration levels of BS and co-occurring tree species to assess ecosystem recovery and possible loss of resilience due to regeneration failure. We analyzed effects of seed bank conditions, fire regime characteristics (fire severity and seasonality), and seedbed conditions on BS post-fire regeneration in mature forests in Quebec, Canada. Post-fire regeneration density was extensively surveyed across [~]50 400 km2 through a network of 536 plots that were distributed in 21 fires, which burned between 1995 and 2016. One-third of plots failed to regenerate (< 1750 conifer seedlings/ha) at levels adequate to produce closed-crown forest, whereas one-fifth experienced compositional changes, mainly towards jack pine (JP; Pinus banksiana) dominance. Pre-fire basal area of BS and living Sphagnum ground cover increased BS post-fire regeneration, whereas high-severity crown fires and spring fires reduced it. These findings suggest that mature BS-dominated forests may lose resilience in response to high-severity and spring fires. Given the projected increase in fire severity, and the extension towards an early-fire season in response to climate change, our study suggests that post-fire regeneration failure may become more frequent over the coming decades, with potential negative consequences on ecosystem services that are provided by BS-dominated boreal forests.

ecology↗

bioRxiv2021

Traumatic brain injury alters dendritic cell differentiation and distribution in lymphoid and non-lymphoid organs

Pathophysiological consequences of traumatic brain injury (TBI) mediated secondary injury remain incompletely understood. In particular, the impact of TBI on the differentiation and maintenance of dendritic cells (DCs), remains completely unknown. Here, we report that DC-differentiation, maintenance and functions are altered at both early and late phases of TBI. Our studies identify that; 1. frequencies and absolute numbers of DCs in the spleen and BM are altered at both acute and late phases of TBI; 2. surface expression of key molecules involved in antigen presentation of DCs were affected both at early and late phases of TBI; 3. distribution and functions of tissue-specific DC subsets of both circulatory and lymphatic systems were imbalanced following TBI; 4. early differentiation program of DCs, especially the commitment of hematopoietic stem cells to common DC progenitors, were deregulated after TBI; and 5. intracellular ROS levels were reduced in DC progenitors and differentiated DCs at both early and late phases of TBI. Our data demonstrate, for the first time, that TBI affects the distribution pattern of DCs and induces an imbalance among DC subsets in both lymphoid and non-lymphoid organs. In addition, the current study demonstrates that TBI results in reduced levels of ROS in DCs at both early and late phases of TBI, which may explain altered DC differentiation paradigm following TBI. A deeper understanding on the molecular mechanisms that contribute to DC defects following TBI would be essential and beneficial in treating infections in patients with acute central nervous system (CNS) injuries.

immunology↗