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.

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Meylan F, Hawley ET, Barron L, Barlow JL, Penumetcha P, Pelletier M, Sciume G, Richard AC, Hayes ET, Gomez-Rodriguez J, Chen X, Paul WE, Wynn TA, McKenzie AN, Siegel RM

The TNF-family cytokine TL1A promotes allergic immunopathology through group 2 innate lymphoid cells.

Journal Article

Mucosal Immunol, 7 (4), pp. 958-68, 2014, ISSN: 1933-0219.

Abstract | Links:

Pelletier M, Billingham LK, Ramaswamy M, Siegel RM

Extracellular flux analysis to monitor glycolytic rates and mitochondrial oxygen consumption.

Journal Article

Methods Enzymol, 542 , pp. 125-49, 2014, ISSN: 0076-6879.

Abstract | Links:

Pelletier M, Lepow TS, Billingham LK, Murphy MP, Siegel RM

New tricks from an old dog: mitochondrial redox signaling in cellular inflammation.

Journal Article

Semin Immunol, 24 (6), pp. 384-92, 2012, ISSN: 1044-5323.

Abstract | Links:

Cassatella MA, Mosna F, Micheletti A, Lisi V, Tamassia N, Cont C, Calzetti F, Pelletier M, Pizzolo G, Krampera M

Toll-like receptor-3-activated human mesenchymal stromal cells significantly prolong the survival and function of neutrophils.

Journal Article

Stem Cells, 29 (6), pp. 1001-11, 2011, ISSN: 1066-5099.

Abstract | Links:

Bulua AC, Simon A, Maddipati R, Pelletier M, Park H, Kim KY, Sack MN, Kastner DL, Siegel RM

Mitochondrial reactive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1-associated periodic syndrome (TRAPS).

Journal Article

J Exp Med, 208 (3), pp. 519-33, 2011, ISSN: 0022-1007.

Abstract | Links:

Costantini C, Calzetti F, Perbellini O, Micheletti A, Scarponi C, Lonardi S, Pelletier M, Schakel K, Pizzolo G, Facchetti F, Vermi W, Albanesi C, Cassatella MA

Human neutrophils interact with both 6-sulfo LacNAc+ DC and NK cells to amplify NK-derived IFN{gamma}: role of CD18, ICAM-1, and ICAM-3.

Journal Article

Blood, 117 (5), pp. 1677-86, 2011, ISSN: 0006-4971.

Abstract | Links:

Pelletier M, Micheletti A, Cassatella MA

Modulation of human neutrophil survival and antigen expression by activated CD4+ and CD8+ T cells.

Journal Article

J Leukoc Biol, 88 (6), pp. 1163-70, 2010, ISSN: 0741-5400.

Abstract | Links:

Pelletier M, Maggi L, Micheletti A, Lazzeri E, Tamassia N, Costantini C, Cosmi L, Lunardi C, Annunziato F, Romagnani S, Cassatella MA

Evidence for a cross-talk between human neutrophils and Th17 cells.

Journal Article

Blood, 115 (2), pp. 335-43, 2010, ISSN: 0006-4971.

Abstract | Links:

Pelletier M, Siegel RM

Wishing away inflammation? New links between serotonin and TNF signaling.

Journal Article

Mol Interv, 9 (6), pp. 299-301, 2009, ISSN: 1534-0384.

| Links:

Ratthe C, Pelletier M, Chiasson S, Girard D

Molecular mechanisms involved in interleukin-4-induced human neutrophils: expression and regulation of suppressor of cytokine signaling.

Journal Article

J Leukoc Biol, 81 (5), pp. 1287-96, 2007, ISSN: 0741-5400.

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Active projects

  • 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
  • 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
  • Développement d’une méthode fiable pour la détection d’anticorps contre Malassezia, Subvention, Fondation de l'Université Laval, from 2020-04-01 to 2021-03-31
  • 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

  • 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
  • Étude de la réponse immune contre Malassezia dans la maladie de Crohn, Subvention, Fondation de l'Université Laval, from 2018-11-01 to 2020-10-31
  • Projet de recherche sur les maladies auto-inflammatoires, Subvention, Fondation du CHU de Québec, from 2019-04-01 to 2020-03-31
  • Réponse immunitaire contre le champignon Malassezia dans la prostate, Subvention, Fondation de l'Université Laval, from 2019-11-01 to 2020-10-31
Data provided by the Université Laval research projects registery