Dr. Robert Inman - University Health Network. Toronto, ON, CA

Dr. Robert Inman Dr. Robert Inman

Senior Scientist, Krembil Research Institute (Krembil) | University Health Network

Toronto, ON, CA
Dr. Robert Inman is a professor of medicine at the University of Toronto & director of The Spondyloarthritis Research Consortium of Canada.

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Biography

Dr. Robert Inman is a Senior Scientist, Division of Genetics and Development, at the Krembil Research Institute (Krembil). Dr. Inman has held many national and international leadership positions including the member of the Board of Directors of the American College of Rheumatology, Chair of the Medical and Scientific Board of the Spondylitis Association of America, member of the Executive Committee of the Assessment of Spondyloarthritis International Society (ASAS), and Past-President of the Spondyloarthritis Research Consortium of Canada (SPARCC).

The broad research themes in Dr. Robert Inman's lab have been the interaction of infection and autoimmunity, and the environmental-genetic interplay in the pathogenesis of arthritis. This has encompassed translational research into the immunobiology of spondylitis and related forms of arthritis, animal models of infection-induced arthritis and autoimmunity, and the cell biology of host:pathogen interactions.

Industry Expertise (5)

Education/Learning Research Medical/Dental Practice Health and Wellness Writing and Editing

Areas of Expertise (7)

Medicine Immunology Arthritis Spondylitis Higher Education Medical Education Science

Education (5)

Hammersmith Hospital: Research Fellowship, Medicine

Cornell University: Fellowship, Rheumatology

Vanderbilt University: Residency, Internal Medicine

McMaster University: MD, Medicine

Yale: BA, Bachelor of Arts

Affiliations (3)

  • Spondylitis Program UHN : Director
  • Arthritis Center of Excellence UHN : Director
  • Research Committee Arthritis Program UHN : Chair

Media Appearances (1)

From bedridden to Ironman: one man's journey with spinal arthritis

The Globe and Mail  online

2013-11-20

Dr. Inman is featured in this article for the Globe and Mail.

Dr. Robert Inman Media Appearance

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Articles (4)

Tumor necrosis factor inhibitor therapy in ankylosing spondylitis: differential effects on pain and fatigue and brain correlates
Pain

February 2015

Ankylosing spondylitis is associated with back pain and fatigue and impacts mobility but can be treated with tumor necrosis factor inhibitors (TNFi). The differential effects of TNFi treatment on multiple symptoms and the brain is not well delineated. Thus, we conducted a 2-part study. In study 1, we conducted a retrospective chart review in 129 ankylosing spondylitis patients to assess TNFi effects on pain, fatigue, motor function, mobility, and quality of life (QoL). After at least 10 weeks of TNFi treatment, patients had clinically significant improvements (>30%) in pain (including neuropathic pain), most disease and QoL factors, and normalized sensory detection thresholds. However, residual fatigue (mean = 5.3) was prominent. Although 60% of patients had significant relief of pain, only 22% of patients had significant relief of both pain and fatigue. Therefore, the preferential TNFi treatment effect on pain compared with fatigue could contribute to suboptimal effects on QoL. Part 2 was a prospective study in 14 patients to identify TNFi treatment effects on pain, fatigue, sensory and psychological factors, and brain cortical thickness based on 3T magnetic resonance imaging. Centrally, TNFi was associated with statistically significant cortical thinning of motor, premotor, and posterior parietal regions. Pain intensity reduction was associated with cortical thinning of the secondary somatosensory cortex, and pain unpleasantness reduction was associated with the cortical thinning of motor areas. In contrast, fatigue reduction correlated with cortical thinning of the insula, primary sensory cortex/inferior parietal sulcus, and superior temporal polysensory areas. This indicates that TNFi treatment produces changes in brain areas implicated in sensory, motor, affective, and cognitive functions.

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Genetic Dissection of Acute Anterior Uveitis Reveals Similarities and Differences in Associations Observed With Ankylosing Spondylitis
Arthritis & Rheumatology

January 2015

Objective
To use high-density genotyping to investigate the genetic associations of acute anterior uveitis (AAU) in patients with and those without ankylosing spondylitis (AS).

Methods
We genotyped samples from 1,711 patients with AAU (either primary or combined with AS), 2,339 AS patients without AAU, and 10,000 control subjects on an Illumina Immunochip Infinium microarray. We also used data for AS patients from previous genome-wide association studies to investigate the AS risk locus ANTXR2 for its putative effect in AAU. ANTXR2 expression in mouse eyes was investigated by real-time quantitative reverse transcription–polymerase chain reaction.

Results
A comparison between all patients with AAU and healthy control subjects showed strong association over HLA–B, corresponding to the HLA–B27 tag single-nucleotide polymorphism rs116488202. The association of 3 non–major histocompatibility complex loci, IL23R, the intergenic region 2p15, and ERAP1, reached genome-wide significance (P < 5 × 10−8). Five loci harboring the immune-related genes IL10–IL19, IL18R1–IL1R1, IL6R, the chromosome 1q32 locus harboring KIF21B, as well as the eye-related gene EYS, were also associated, reaching a suggestive level of significance (P < 5 × 10−6). Several previously confirmed AS associations demonstrated significant differences in effect size between AS patients with AAU and AS patients without AAU. ANTXR2 expression varied across eye compartments.

Conclusion
These findings of both novel AAU-specific associations and associations shared with AS demonstrate overlapping but also distinct genetic susceptibility loci for AAU and AS. The associations in IL10 and IL18R1 are shared with inflammatory bowel disease, suggesting common etiologic pathways.

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The Effect of Golimumab Therapy on Disease Activity and Health-related Quality of Life in Patients with Ankylosing Spondylitis: 2-year Results of the GO-RAISE Trial
The Journal of Rheumatology

15 April 2014

Objective
To evaluate the effects of golimumab therapy on achieving inactive disease or major improvement, as assessed by the Ankylosing Spondylitis Disease Activity Score (ASDAS), and improvements in health-related quality of life (HRQOL) and productivity through 2 years in patients with AS.

Methods
In the phase III GO-RAISE trial, 356 patients were randomized to placebo with crossover to golimumab 50 mg at Week 24 (n = 78), golimumab 50 mg (n = 138), or golimumab 100 mg (n = 140) at baseline and every 4 weeks. The proportions of patients with ASDAS major improvement (improvement ≥ 2.0) or inactive disease (score < 1.3) were determined. HRQOL was assessed using the 36-item Medical Outcomes Study Short Form-36 physical/mental component summary (SF-36 PCS/MCS) scores (normal score ≥ 50). The effect of disease on productivity was assessed by visual analog scale (0–10). Regression analyses on the association of disease activity and HRQOL were performed. The final assessment was at Week 104.

Results
Significantly greater proportions of golimumab-treated patients achieved ASDAS major improvement or inactive disease at weeks 14 and 24 versus placebo. Through Week 104, patients who achieved ASDAS inactive disease or major improvement had significantly greater improvements in SF-36 PCS and MCS scores and productivity than did patients not meeting these targets. Among all patients, achieving ASDAS inactive disease at weeks 52 and 104 was associated with normalized SF-36 PCS/MCS scores and significant improvements in work productivity.

Conclusion
Greater proportions of golimumab-treated patients achieved ASDAS major improvement or inactive disease and improved HRQOL versus placebo. Achieving an inactive disease state by ASDAS criteria (< 1.3) was associated with normalized HRQOL through 2 years.

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Intervertebral Disc-Derived Stem Cells: Implications for Regenerative Medicine and Neural Repair
Spine

1 February 2013

Study Design
An in vitro and in vivo evaluation of intervertebral disc (IVD)–derived stem/progenitor cells.

Objective
To determine the chondrogenic, adipogenic, osteogenic, and neurogenic differentiation capacity of disc-derived stem/progenitor cells in vitro and neurogenic differentiation in vivo.

Summary of Background Data
Tissue repair strategies require a source of appropriate cells that could be used to replace dead or damaged cells and tissues such as stem cells. Here we examined the potential use of IVD-derived stem cells in regenerative medicine approaches and neural repair.

Methods
Nonchondrodystrophic canine IVD nucleus pulposus (NP) cells were used to generate stem/progenitor cells (NP progenitor cells [NPPCs]) and the NPPCs were differentiated in vitro into chondrogenic, adipogenic, and neurogenic lineages and in vivo into the neurogenic lineage. NPPCs were compared with bone marrow–derived mesenchymal (stromal) stem cells in terms of the expression of stemness genes. The expression of the neural crest marker protein 0 and the Brachyury gene were evaluated in NP cells and NPPCs.

Results
NPPCs contain stem/progenitor cells and express “stemness” genes such as Sox2, Oct3/4, Nanog, CD133, Nestin, and neural cell adhesion molecule but differ from mesenchymal (stromal) stem cells in the higher expression of the Nanog gene by NPPCs. NPPCs do not express protein 0 or the Brachyury gene both of which are expressed by the totality of IVD NP cells. The percentage of NPPCs within the IVD is 1% of the total as derived by colony-forming assay. NPPCs are capable of differentiating along chondrogenic, adipogenic, and neurogenic lineages in vitro and into oligodendrocyte, neuron, and astroglial specific precursor cells in vivo within the compact myelin-deficient shiverer mouse.

Conclusion
We propose that the IVD NP represents a regenerative niche suggesting that the IVD could represent a readily accessible source of precursor cells for neural repair and regeneration.

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