Dr. Martin Pelletier is a researcher in the Division of Infectious and Immune Diseases at the CHU de Québec-Laval University Research Center, and Assistant Professor in the Department of Microbiology-Infectious Diseases and Immunology at Laval University. Author of over 35 publications, he has developed a unique expertise in inflammation, innate immunity, and energy metabolism. His research program focuses on the identification of intrinsic and extrinsic factors involved in triggering, maintaining, and resolving inflammation. Funded by the CIHR, NSERC, Fondation du Grand défi Pierre Lavoie, Crohn & Colitis Canada and Rare Disease Foundation, his work aims at characterizing environmental and host factors that modulate energy metabolism and the functional responses of inflammatory cells in chronic diseases to develop new therapeutic strategies and improve patient care.
Portray the bioenergetic events involved in inflammatory cells’ aberrant activation in chronic diseases such as inflammatory arthritis and inflammatory bowel disease
Pro-inflammatory mediators such as cytokines, actively participate in the progression and severity of inflammatory diseases. These mediators modulate the functional responses of inflammatory cells such as neutrophils and monocytes. Very little is known, however, about the metabolic changes that occur systemically in the patients. The characterization of the molecular mechanisms underlying altered energy metabolism in inflammatory chronic diseases such as gout, rheumatoid arthritis and colitis could provide the foundation for new personalized therapeutic treatments of chronic inflammatory diseases that specifically modulate bioenergetics of pathogenic immune cells.
Characterize the effects of widely used endocrine-disrupting chemicals on the bioenergetics of inflammatory cells
Endocrine-disrupting chemicals are natural or synthetic compounds that can alter endocrine functions, often through mimicking or blocking endogenous hormones, and are linked to cancer, obesity and autoimmune diseases. These chemicals include pesticides, herbicides, plasticizers (bisphenol A and phthalates), pharmaceuticals, and cosmetics. The widespread use of endocrine-disrupting chemicals leads to their distribution in the environment, as well as human exposure, as evidenced by their presence in human tissues and biological fluids, such as blood and urine. Understanding the effects of endocrine-disrupting chemicals on the bioenergetics of the most abundant inflammatory cells in the blood, namely neutrophils and monocytes, could explain their immunomodulatory activities, and how these chemicals can contribute to inflammation or increased susceptibility to infections.
Development of a clinical assay to classify and guide the personalized treatment of rare auto-inflammatory patients
Recurrent fevers, systemic/organ-specific inflammation and hyperreactive innate immune cells linked to abnormal cytokine secretion are characteristics of auto-inflammatory syndromes. While being inherited conditions, mutations in patients with high suspicion for auto-inflammatory syndromes are detected in less than 20% of cases, and patients bear confounding phenotypes with systemic autoimmune rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus. Although anti-cytokine therapeutics are available, auto-inflammatory syndrome treatments are often inefficient because information on the specific cytokines abnormally secreted in each patient is overlooked, leading not only to inappropriate treatment, but also to severe complications, with important repercussions on the patient’s health, his family, and bring about substantial socio-economic costs. The quantification of the cytokines abnormally secreted should not only help the diagnosis, but also provide personalized treatment options to auto-inflammatory syndrome patients.
2705, boulevard Laurier
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- Lachhab, AsmaaDoctoral studentCHUL+1 418-525-4444, extension 42296+1 418-525-4444, extension firstname.lastname@example.org@crchudequebec.ulaval.ca
2705, boulevard Laurier
Canada G1V 4G2
- Pagé, NathalieEmployeeCHUL+1 418-525-4444, extension 47043 / 46113+1 418-654-2765Nathalie.Page@crchudequebec.ulaval.ca
2705, boulevard Laurier
Canada G1V 4G2
The use of leukocytes' secretome to individually target biological therapy in autoimmune arthritis: a case report.Journal Article
Clin Transl Med, 8 (1), pp. 19, 2019, ISSN: 2001-1326.
Anti-mitochondrial autoantibodies in systemic lupus erythematosus and their association with disease manifestations.Journal Article
Sci Rep, 9 (1), pp. 4530, 2019, ISSN: 2045-2322.
Tumor-Associated Macrophages Enhance Tumor Hypoxia and Aerobic Glycolysis.Journal Article
Cancer Res, 79 (4), pp. 795-806, 2019, ISSN: 0008-5472.
Enhanced myelopoiesis and aggravated arthritis in S100a8-deficient mice.Journal Article
PLoS ONE, 14 (8), pp. e0221528, 2019.
Quinoline-3-carboxamides such as tasquinimod are not specific inhibitors of S100A9.Journal Article
Blood Adv, 2 (10), pp. 1170-1171, 2018, ISSN: 2473-9529.
ICAM1+ neutrophils promote chronic inflammation via ASPRV1 in B cell-dependent autoimmune encephalomyelitis.Journal Article
JCI Insight, 2 (23), 2017, ISSN: 2379-3708.
S100A9 induces differentiation of acute myeloid leukemia cells through TLR4.Journal Article
Blood, 129 (14), pp. 1980-1990, 2017, ISSN: 0006-4971.
S100A9 potentiates the activation of neutrophils by the etiological agent of gout, monosodium urate crystals.Journal Article
J Leukoc Biol, 102 (3), pp. 805-813, 2017, ISSN: 0741-5400.
Critical role of fatty acid metabolism in ILC2-mediated barrier protection during malnutrition and helminth infection.Journal Article
J Exp Med, 213 (8), pp. 1409-18, 2016, ISSN: 0022-1007.
Recruitment of A20 by the C-terminal domain of NEMO suppresses NF-κB activation and autoinflammatory disease.Journal Article
Proc Natl Acad Sci U S A, 113 (6), pp. 1612-7, 2016, ISSN: 0027-8424.
- Centre de recherche du CHU de Québec - Université Laval, Subvention, Centre hospitalier universitaire de Québec - Université Laval, Centres de recherche affiliés, from 2017-01-01 to 2099-12-31
- Centre de recherche en arthrite de l'Université Laval, Subvention, Institutionnel - BDR, BDR - Entités de recherche en émergence, from 2019-01-01 to 2020-01-31
- Defining the Effects of Endocrine-Disrupting chemicals on the cellular metabolism of inflammatory cells., Subvention, Conseil de recherches en sciences naturelles et génie Canada, Subventions à la découverte SD (individuelles et d'équipe), from 2015-04-01 to 2021-03-31
- Étude de la réponse immune contre Malassezia dans la maladie de Crohn, Subvention, Fondation de l'Université Laval, from 2018-11-01 to 2019-10-31
- Métabolisme bioénergétique et réponse fonctionnelle des cellules inflammatoires : Étude de facteurs endogènes et environnementaux, Subvention, Fonds de recherche du Québec - Santé, Chercheur-boursier Juniors 1 et 2, Seniors, from 2018-07-01 to 2021-06-30
Recently finished projects
- Characterizing the role of inflammatory cells' bioenergetics in the pathophysiology of colitis, Subvention, Crohn et Colite Canada, Innovations en recherche sur les MII, from 2016-07-01 to 2018-09-30
- Rôle des neutrophiles dans les impacts des édulcorants non caloriques sur le métabolisme : De la souris à l’homme, Subvention, Fonds de recherche du Québec - Santé, Réseaux thématiques de recherche, from 2018-04-01 to 2019-03-31