Areas of expertise
Immune system disturbances , Apoptosis , Cancer , Genomic stability , Toxic resistance
- Full Professor
The research field of our laboratory focuses on cell death by apoptosis, more specifically, DNA fragmentation by the endonuclease DFF40. Most human cells express DFF40 in a heterodimeric form with the protein DFF45. This subunit is involved both in the maturation and in the repression of the activity of DFF40. We aim to understand new mechanisms responsible for suppressing the activity of DFF40 and find other roles related to this protein in the maintenance of cell homeostasis. We have demonstrated that there is a post-translational control of the DFF40. Serine residues of DFF40 undergo phosphorylation and O-GlcNAcylation. These modifications influence the aggregation of DFF40, as well as its activity. In addition, the inhibition of DFF40 expression by the CRISPR-Cas9 technique produces significant disturbances in the response of cells to toxic or pharmacological agents used in chemotherapy. Cells no longer expressing DFF40 acquire resistance to xenobiotics. A link was established between DFF40 and mitochondrial activity to explain cell survival. Moreover, the absence of expression of this endonuclease influences genomic stability, which therefore suggests a role for DFF40 in neoplastic transformation. This project is essential to better understand the cancer resistance mechanism of DFF40 negative cells to chemotherapy, as well as on the development of specific therapy.
A second research theme of our laboratory regards the role of CD4 + T cells in inflammation. Our work focuses on the inflammatory state of severely burned patients and workers or populations exposed to environmental toxicants. We have an interest on the impact of different toxins interaction with the intracellular aromatic hydrocarbon receptor (AhR) on the development of CD4 + T lymphocytes subpopulations, acquiring an inflammatory (Th1, Th17) or an anti-inflammatory (Th2, Treg) potential. Thus, we have established a relationship between occupational exposure to xenobiotics, activation of the AhR receptor, and the establishment of an inflammatory profile. Our laboratory is also interested in the toxicity of nanoparticles on the functionality of T lymphocytes. These projects are relevant for understanding the impacts of environmental toxicants on the inflammatory status of individuals, and the possible development of pathologies.
Dr. Jacques Bernier received his B.Sc. and M.Sc. in biology from the Université du Québec a Montréal. He then obtained Ph.D. degree in cellular biology from the faculty of medicine of the Université de Sherbrooke.
Following postdoctoral studies at the Institut de recherches cliniques de Montréal in molecular immunology, he joined the research center of Hôtel-Dieu de Montréal as independent researcher, working on the effect of burn injury on the immune response.In 1997 Dr. Bernier became professor at INRS-Armand Frappier Institute while keeping an affiliation as an associate researcher with the Burn Research Center at the Hôtel-Dieu de Montréal.His background is on the immunomodulation induced either by a pathogen, a physical stress or a xenobiotic. He is working on the role of endocrine disruptors on the immune function.
Kulbay M, Johnson B, Bernier J.DNA fragmentation factor 40 expression in T cells confers sensibility to tributyltin-induced apoptosis.Toxicology. 2019 ;426:
Cote-Maurais G,Bernier J Silver and fullerene nanoparticles’ effect on interleukin-2-dependent proliferation of CD4(+) T cells . Toxicol in vitro 2014 ;28(8):1474-81.
Johnson B, Opimba M, Bernier J. Implications of the O-GlcNAc modification in the regulation of nuclear apoptosis in T cells. Bioch Biophys Acta. 2013 1840(1):191-198.
Patenaude J, D’Elia M, Côté-Maurais G,Bernier J. LPS response and endotoxin tolerance in Flt-3L-induced bone marrow-derived dendritic cells. Cell Immunol. 2011;271(1):184-91 (FPQGB).
D’Elia, M., J. Patenaude, C. Dupras, J. Bernier (2010)
T cells from burn-injured mice demonstrate a loss of sensitivity to glucocorticoids.
Am J Physiol Endocrinol Metab. Aug;299(2):E299-307.
Patenaude, J., M. D’Elia, C. Hamelin, J. Bernier(2010)
Selective effect of burn injury on splenic CD11c(+) dendritic cells and CD8alpha(+)CD4(-)CD11c(+) dendritic cell subsets.
Cell Mol Life Sci. 67(8):1315-29.
Dupéré-Minier, G., P. Desharnais, J. Bernier (2010)
Involvement of tyrosine phosphatase CD45 in apoptosis.
D’Elia, M., J. Patenaude, C. Dupras, J. Bernier (2009)
Burn injury induces the expression of cystine/glutamate transporter (x(c)(-)) in mouse T cells.
Immunol Lett. 15;125(2):137-44.
D’Elia, M., J. Patenaude, J. Bernier (2009)
Regulation of glucocorticoid sensitivity in thymocytes from burn-injured mice.
Am J Physiol Endocrinol Metab. 296(1):E97-104.
Fortier, M., F. Omara, J. Bernier, P. Brousseau, M. Fournier (2008)
Effects of physiological concentrations of heavy metals both individually and in mixtures on the viability and function of peripheral blood human leukocytes in vitro.
J Toxicol Environ Health A. 71(19):1327-37.
Desharnais, P., G. Dupéré-Minier, C. Hamelin, P. Devine, J. Bernier (2008)
Involvement of CD45 in DNA fragmentation in apoptosis induced by mitochondrial perturbing agents.
Pillet, S., M. D’Elia, J. Bernier, J.M. Bouquegneau, . Fournier, D.G. Cyr (2006)
Immunomodulatory effects of estradiol and cadmium in adult female rats.
Toxicol Sci. 92(2):423-32.
D’Elia, M., J. Patenaude, C. Hamelin, D.R. Garrel, and J. Bernier (2005)
Corticosterone binding globulin regulation and thymus changes after thermal injury in mice.
Am. J. Physiol. Endocrinol. Metab. 288: E852-E860.
Colombo, M., C. Hamelin, E. Kouassi, M. Fournier, and J. Bernier (2004)
Differential effects of mercury, lead, and cadmium on IL-2 production by Jurkat T cells.
Dupéré-Minier, G., C. Hamelin, P. Desharnais, and J. Bernier (2004)
Apoptotic volume decrease, pH acidification and chloride channel activation during apoptosis requires CD45 expression in HPB-ALL T cells.
D’Elia, M., J. Patenaude, C. Hamelin, D.R. Garrel, and J. Bernier (2003)
No detrimental effect from chronic exposure to buprenorphine on corticosteroid-binding globulin and corticosensitive immune parameters.
Clin. Immunol. 109(2):179-87.
Garrel, D., J. Patenaude, B. Nedelec, L. Samson, J. Dorais, J. Champoux, M. D’Elia, and J. Bernier (2003)
Decreased mortality and infectious morbidity in adult burn patients given enteral glutamine supplements: a prospective, controlled, randomized clinical trial.
Crit. Care Med. 31(10):2444-9.
Rooney, A.A., M. Fournier, J. Bernier, and D.G. Cyr (2003)
Neonatal exposure to propylthiouracil induces a shift in lymphoid cell sub-populations in the developing postnatal male rat spleen and thymus.
Cell Immunol. 223(2):91-102.
Borde, V.D., J. Bernier, and D.R. Garrel (2002)
Effects of dietary fatty acids on burn-induced immunosuppression.
Cell Immunol. 220(2):116-24.
Moisan, E., S. Arbour, N. Nguyen, M.J. Hebert, D. Girard, J. Bernier, M. Fournier, and E. Kouass (2002).
Prolongation of human neutrophil survival by low-level mercury via inhibition of spontaneous apoptosis.
J. Toxicol. Environ. Health A. 25;65(2):183-203.
Jobin, N., D.R. Garrel, J. Champoux, and J. Bernier (2002)
Improved immune functions with administration of a low-fat diet in a burn animal model.
Cell Immunol. 206(2):71-84.
Jobin, N., D.R. Garrel, and Bernier, J. (2000)
Increased burn-induced immunosuppression in LPS-resistant mice.
Cellular Immunology 200:65-75.
DeGuise, S., J. Bernier, P. Lapierre, M. Dufresne, P. Dubreuil, and M. Fournier (1999)
Immune function of bovine leucocytes following in vitro exposure to selected heavy metals.
Am. Vet. Res. 61:339-344.
Jobin, N., D.R. Garrel, and J. Bernier (2000)
Increased serum soluble-interleukine-2 receptor in burn patients: characterization and effects on the immune system.
Hum. Immunol. 61:233-246.