Steve LacroixPh.D.

Steve Lacroix is Professor in the Department of Molecular Medicine at the Faculty of Medicine of Laval University. He received his Ph.D. from Laval University in 1998. He was trained as a postdoctoral fellow in the field of spinal cord regeneration at the University of California, San Diego, under the supervision of Dr. Mark H. Tuszynski from 1998 to 2001. From 2001 to 2003, he completed a second postdoctoral training in neuroimmunology at McGill University with Dr. Samuel David. Since 2003, Dr. Lacroix runs a laboratory specialized in neuroimmunology and regenerative medicine at Centre de recherche du CHU de Québec – Université Laval (CRCHUQc-UL). Recent research conducted in his lab has focused on the identification of endogenous danger signals, or damage-associated molecular patterns (DAMPs), initiating neuroinflammation and the role of immune cells and molecules in neural damage and repair in the context of spinal cord and peripheral nerve injury, as well as multiple sclerosis. In 2017, Dr. Lacroix was named the director of the Neurosciences Axis at CRCHUQc-UL, a working group that includes 45 regular and associate researchers.

Manipulating the neuroimmune response to promote spinal cord repair

Research conducted over recent years has greatly contributed to demonstrate the importance of the immune response in the mechanisms of degeneration and regeneration of the central nervous system (CNS). Multiple sclerosis, for example, is a neuroinflammatory disease that results in the attack of nerve cells and myelin sheaths by auto-aggressive immune cells. Paradoxically, immune cells could positively influence regeneration of injured axons in models of peripheral nerve and spinal cord injury. Other studies have however shown that the immune response may also contribute to secondary tissue damage and formation of the glial scar in the injured CNS. While the results of these studies seem diametrically opposed at first sight, recent work in the Lacroix laboratory suggests that these differences could be due to the existence of different subtypes of immune cells with distinct properties (pro- vs. anti-inflammatory, trophic vs. cytotoxic, pro- vs. anti-angiogenic). Hence, a better understanding of the biological roles of the different subtypes of immune cells and mechanisms regulating their functions in the injured/diseased CNS could lead to significant contributions to basic research and even clinical opportunities. Research currently underway in the laboratory focuses on three different disorders:

Spinal cord injury (SCI): Unlike the peripheral nervous system (PNS), the CNS has a very limited capacity to regenerate. Thus, when an injury is inflicted to the spinal cord or brain, permanent deficits are often generated. Current work focuses on harnessing the neuroimmune response to reduce neural tissue loss at the site of lesion and promote functional regeneration of injured axons.

Peripheral nerve lesion (PNL): Despite the ability of peripheral nerves to regenerate, recovery of neurological function after PNL is often incomplete. Peripheral nerve injury can also lead to increased pain sensation. The Lacroix laboratory has recently demonstrated the importance of the immune response in regeneration of injured peripheral axons, recovery of motor function, and the development of neuropathic pain. In years to come, they intend to continue their efforts towards understanding the effects of inflammation in the injured PNS, in an attempt to identify (and eventually manipulate) immune cells and genes regulating neural repair and regeneration.

Multiple sclerosis (MS): In MS, an unknown trigger causes immune cells to transgress the tolerance rule, causing the body’s own immune system to turn against itself and attack the myelin and axons responsible for transmission of nerve impulses. Research conducted in the laboratory over the recent years aims at understanding how the activity and recruitment of immune cells are regulated during MS, with a special focus on cytokines of the interleukin-1 family, in the hope of finding a way to neutralize or stimulate them for therapeutic purposes.