ArticleJournal of Crohn's & colitis2014
In vitro sensitivity assays and clinical response to glucocorticoids in patients with inflammatory bowel disease.
Article in Journal of Crohn's & colitis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Perinatal glucocorticoid sensitivity in the preterm newborn: molecular mechanisms, endogenous determinants, and clinical implications.Frontiers in endocrinology · 2025Review
- Corticosteroid Treatment-Resistance in Myasthenia Gravis.Frontiers in neurology · 2022Review
- Anti-inflammatory effects ofExperimental and therapeutic medicine · 2017Article
- Amelioration of experimental colitis after short-term therapy with glucocorticoid and its relationship to the induction of different regulatory markers.Immunology · 2017Article
- Development and validation of a novel bioassay to determine glucocorticoid sensitivity.Biomarker research · 2016Article
- LPS-Stimulated Whole Blood Cytokine Production Is Not Related to Disease Behavior in Patients with Quiescent Crohn's Disease.PloS one · 2015Article
- Stress induces endotoxemia and low-grade inflammation by increasing barrier permeability.Frontiers in immunology · 2015Review
- Combining genetic and nongenetic biomarkers to realize the promise of pharmacogenomics for inflammatory diseases.Pharmacogenomics · 2014Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundGlucocorticoids (GCs) are steroid hormones used to induce remission in moderate-to-severe inflammatory bowel disease (IBD). A substantial fraction of patients do not respond to GC treatment and require alternate therapies or surgery. At present, non-response can only be assessed empirically by observing continued disease activity.
methodsTo identify potential biomarkers of GC response, we retrospectively identified and recruited 18 GC-responsive and 18 GC-nonresponsive IBD patients. This sample included 14 patients with ulcerative colitis (UC) and 22 patients with Crohn's disease (CD), all previously treated with steroids. In peripheral blood mononuclear cells from each patient, we performed in vitro assays to measure GC inhibition of three different immune stimulants (phytohemagglutinin [PHA], α-CD3/α-CD28, and lipopolysaccharide [LPS]).
resultsIn both diseases, we found that inhibition of PHA-mediated T cell proliferation was significantly associated with clinical GC response (P=0.04). Inhibition of proliferation due to direct T cell receptor stimulation using α-CD3/α-CD28 was also significantly associated with clinical GC response in UC patients (P=0.009), but not in CD patients (P=0.78). Interestingly, inhibition of LPS-mediated cytokine secretion showed the strongest association with clinical GC response across both diseases (P=0.005).
conclusionsWe show that inhibition of LPS stimulation is more strongly associated with clinical GC response in IBD patients than inhibition of PHA and α-CD3/α-CD28-mediated proliferation. These results support an important role of bacterial recognition and innate immunity in the etiology of IBD. This assay could be a powerful predictor of clinical response to GCs.
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