Welcome! You have reached the homepage for the laboratory of Dr. Bryan Heit. Our lab is part of the Department of Microbiology and Immunology at Western University, and we are members of the Center for Human Immunology, the lead centre for the CIHR Human Immunology Network.
Our interests surround the function of phagocytes – white blood cells which ingest (phagocytose) pathogens, particles, and dead cells. We focus on the cellular and molecular processes which control the function of these cells during the maintenance of homeostasis, infection and chronic inflammatory disease. Central to most of our studies is the study of efferoctyosis – the phagocytic removal of apoptotic (dying) cells, and how failures in this process lead to inflammation, autoimmunity and infection.
Phagocytes are a class of white blood cells which have the capacity to engulf large particles such as bacterial and fungal pathogens, and subsequently destroy the engulfed material. The term phagocyte literally translates to “cell that eats”, which is an apt description of the primary function of these cells in our bodies. While there are many types of phagocytes, the Heit lab focuses primarily on macrophages, which play key roles in both maintaining our bodies and in fighting infections.
We use a combination of advanced microscopy techniques, gene expression analysis and functional assays to investigate the activity of macrophages. Some examples of the methods we employ can be found on our YouTube channel.
The Heit lab is excited to announce that our newest paper has been accepted for publication in Biochemistry and Cell Biology. This paper presents a method for using fused deposition modelling (3D printing) to produce customized chambers for microscopy-based experiments. This technology allows for scientists to design an imaging chamber that exactly meets the requirements of their experiment while also producing a system optimized for high resolution microscopy.
We have been using this technology extensively in my lab, and have saved literally thousands of dollars in commercial chambers, reduced cell isolation/transfection costs, and reduced reagent usage.
For those without access to Biochemistry and Cell Biology, we have posted the revised version of this paper as a preprint, available over at Biorxiv.
Due to the COVID-19 outbreak, the Heit lab will be closing effective Friday March 20th 2020 at noon. The IDT biobar will not be active during this time, so if you order IDT products via our biobar, please order via another route.
If you need to Contact Dr. Heit, please do so by email. We do not know at this time when normal lab operations will be restored. The MNI Widefield Microscopy Facility remains operational for as long as Western University permits research to continue. However, we cannot offer maintenance, repair or training during this time.
The Heit lab is once again looking to recruit a graduate student to join our diverse and growing team. This position is open to people wishing to complete a MSc or PhD degree, and is focused on the transcriptional control of macrophages during atherosclerosis. Additional details can be found in the attached image.
We are thrilled to announce that our grant on the function of GATA2 and MERTK in early atheroscerlosis has been funded by the Heart and Stroke Foundation of Canada. This 3-year project will continue our earlier work into how the macrophage receptor MERTK, and the transcription factor GATA2, work to enable the onset of atherosclerosis.
Atherosclerosis is the most common cause of heart disease, and is responsible for nearly a third of deaths world-wide. In atherosclerosis, a combination of cholesterol, fats and dead cells accumulate into masses (called plaques) beneath major blood vessels. These plaques are delicate and can easily rupture, forming a blood clot. If the resulting clot blocks circulation in the heart or brain, the patient will suffer a heart attack or stroke.
By understanding the earliest events that occur in disease – events which appear to involve MERTK and GATA2 – we may be able to prevent or reverse the formation of plaques, thereby protecting people from the potentially serious outcomes of a ruptured plaque.