Carl Richards

, PhD

Professor
Pathology and Molecular Medicine

Division: Molecular Medicine

McMaster Immunology Research Centre
Institute for Molecular Medicine and Health

McMaster University
4017 Michael DeGroote Centre for Learning & Discovery
905-525-9140 ext. 22472
richards@mcmaster.ca

Assistant: Debra Vanderaar

Education and Professional Standing

• PhD Medical Sciences, McMaster University, 1987
• MSc Medical Sciences, McMaster University, 1984

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Interests

Research Focus

Dr. Richards is one of 14 faculty within the McMaster Immunology Research Centre, housed within state of the art research facilities at the MDCL at McMaster. Richards’  laboratory is investigating the cellular and molecular mechanisms of chronic inflammation, with applications to joint disease (Rheumatoid Arthritis), lung disease (asthma and pulmonary fibrosis) and cardiovascular disease (atherosclerosis). Many studies are integrated with other faculty directions within the McMaster Immunology Research Centre and drive projects that focus on certain cytokines (hormone-like molecules), their cell-receptor complexes, and function in tissues/cells relevant for each of these inflammatory conditions. A number of local, national and international collaborations are geared to specific aspects of these projects.

The lab explores cytokine and receptor regulation, cell signal/gene regulation pathways, mesenchymal precursor cell differentiation and regulation of inflammation in vivo, particularly in response to the gp130 class of cytokines. Certain members of this class are emerging as potentially important targets of new/novel therapy for inflammatory conditions. Links with clinical faculty (at the Firestone Institute for Respiratory Health) integrate analysis of patients with lung disorders. Adenovirus vector systems are used to over-express cytokines in animal models/tissues in vivo, and to examine inflammation in gene-targetted mutant mice, with the goal of developing effective new approaches to treat conditions in joint, lung and cardiovascular inflammatory diseases.

Dr. Richards’ research is currently funded by CIHR, and he has held CIHR and Arthritis Society Research grants for several years.

He has served within national peer-reviewed granting agencies and in administrative positions within McMaster University. Richards has completed terms for CIHR operating grant panels (Scientific Officer), as a grant panel member for Heart and Stroke Foundation and for The Arthritic Society.  He is a member of the Canadian Arthritis Network (CAN), the Canadian Obesity Network (CON), the Spondyloarthritis Research Consortium of Canada (SPARCC) and the International Cytokine Society.   

Academic Interests

Richards has also served two terms (2001-2009) as Associate Dean of Graduate Studies (Health Sciences) at McMaster, and developed the MD/PhD program as well as the BioMedical Engineering graduate programs with colleagues. He continues to instruct in under-graduate and graduate courses in immunology. Dr. Richards has recently been elected as member of McMaster Senate and the Senate Executive Committee.

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Team Members

Technicians

Christine Demers, Rebecca Rodriguez

Graduate Students

(Sept 2010) Jessica Guerette,  Sean Lauber, David Schnittker

Selected Publications

• Fritz DK, Kerr C, Fattouh R, Llop-Guevara A, Khan WI, Jordana MJ, Richards CD. A mouse model of airway disease: Oncostatin-M induced pulmonary eosinophilia, goblet cell hyperplasia and airway hyperresponsiveness are STAT6 dependent and interstitial pulmonary fibrosis is STAT6 independent. J Immunol. 2011;186(2):1107-1118.
• Guihard P, Brounais B, David E, Brion R, Delecrin J, Danger Y, Gascan H, Richards CD, Rédini F, Heymann D, Blanchard F. Induction of bone formation by activated monocytes/macrophages depends on Oncostatin M signaling. Stem Cells. [Epub ahead of print]. Jan 20 2012.
• Hirota JA, Ask K, Fritz D, Ellis R, Wattie J, Richards CD, Kolb M, Inman MD. Role of STAT6 and SMAD2 in a model of chronic allergen exposure: A mouse strain comparison study.Clin Exp Allergy 39:147-158, 2009
• Fritz DK, Kerr C, Botelho F, Stampfli M, Richards CD.  Oncostatin M (OSM) primes  IL-13 and IL-4 induced  eotaxin responses in fibroblasts: regulation of the type-II IL-4 receptor chains IL-4Rα and IL-13α1. Exp Cell Res. 2009; 315(20):3486-3499.
• N Barra, S Reid, R MacKenzie, G Werstuck, B Trigatti, C Richards, A Holloway, A Ashkar. Interleukin-15 contributes to the regulation of murine  adipose tissue and human adipocytes. Obesity. [advanced online publication] doi:10.1038/oby.2009.445.
• Hirota JA, Ask K, Fritz D, Ellis R, Wattie J,Richards CD, Kolb M, Inman MD. Role of STAT6 and SMAD2 in a model of chronic allergen exposure: A mouse strain comparison study.  Clinical and Experimental Immunology. 2009; 39(1):147-158.
• Brounais B, Chipoy C, Kanji M, Charrier C, Battaglia S, Richards C, Pilet P, Heymann D, Redini F, Blanchard F. Oncostatin M induces bone loss and sensitizes rat osteosarcoma to the anti-tumor effect of  Midostaurin in vivo. Clinical Cancer Research. 2008;14(17):5400-5409.
• Smyth DC, Kerr C, Li Y, Tang D, Richards CD. Oncostatin M induction of eotaxin-1 expression requires the convergence of P13'K and ERK1/2 MAPK signal transduction pathways. Cellular Signalling 2008;20:1142-1150.
• Barksby HE, Wui W, Wappler I, Peters HH, Milner JM, Richards CD, Cawston TE, Rowan AD. Interleukin-1 in combination with Oncostatin M up-regulates multiple genes in chondrocytes: implications for cartilage destruction and repair. Arthritis Rheum 2006; 54:540-50.
• Fritz DK, Kerr C, Tong L, Smyth D, Richards CD. Oncostatin-M Up-Regulates VCAM-1 and synergizes with IL-4 in Eotaxin Expression: Involvement of STAT6. J Immunol 2006; 176: 4352-4360.
• Barksby HE, Milner JM, Patterson AM, Peake NJ, Hui W, Robson T, Lakey R, Middleton J, Cawston TE, Richards CD, Rowan AD. Matrix metalloproteinase 10 promotion of collagenolysis via procollagenase activation: implications for cartilage degradation in arthritis. Arthritis Rheum, 2006;54:3244-53.
• Smyth DC, Kerr C, Richards CD. Oncostatin M induced IL-6 expression in murine fibroblasts requires the activation of protein kinase Cδ. J Immunol 2006;177:8740-7.
• Hui W, Cawston T, Richards CD, et al. A model of inflammatory arthritis highlights a role for oncostatin M in pro-inflammatory cytokine-induced bone destruction via RANK/RANKL. Arthritis Res Ther. 2005;7:R57-R64.
• Richards CD. Matrix catabolism in arthritis: priming the guns with oncostatin M. J. Rheumatol. 2004;31:2326-8.
• Langdon C, Kerr C, Tong L, Richards CD. Oncostatin M regulates eotaxin expression in fibroblasts and eosinophilic inflammation in C57BL/6 mice. J Immunol. 2003;170: 548-55.
• Rowan AD, Hui W, Cawston TE, Richards CD. Adenoviral gene transfer of interleukin-1 in combination with oncostatin M induces significant joint damage in a murine model. Am J Pathol. 2003;162:1975-84.
• de Hooge ASK, van de Loo FAJ, Bennink MB, Arntz OJ, Fiselier TJ, Franssen MJ, Joosten LAB, van Lent PL, Richards CD, van den Berg WB. Growth plate damage, a feature of juvenile idiopathic arthritis, can be induced by adenoviral gene transfer of Oncostatin M:a comparative study in gene-deficient mice. Arthritis Rheum. 2003; 48:1750-61.
• Hui W, Rowan AD, Richards CD, Cawston TE. Oncostatin M in combination with tumour necrosis factor α induces cartilage damage and matrix metalloproteinase expression in vitro and in vivo. Arthritis Rheum. 2003;48:3404-18.