ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2018
Patients with type 1 diabetes mellitus have impaired IL-1β production in response to Mycobacterium tuberculosis.
Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
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Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.
- Immune dysregulation in tuberculosis-diabetes comorbidity: mechanistic and translational insights.Frontiers in immunology · 2026Pooled it
- Caring for children and adolescents with type 1 diabetes mellitus: Italian Society for Pediatric Endocrinology and Diabetology (ISPED) statements during COVID-19 pandemia.Diabetes research and clinical practice · 2020Guideline
- Type 1 diabetes alters early macrophage-iScience · 2026Article
- Observational
- Pediatric Tuberculosis: Unraveling Immunity, Clinical Complexities, and Resource-Driven Disparities in the Pursuit of Prevention.Vaccines · 2026Review
- Immune Response to TB Antigen Stimulation in Type 2 Diabetes Mellitus: Insights from a Cross-Sectional Cytokine Profile Analysis.Journal of inflammation research · 2025Article
- Associations between type 1 diabetes and pulmonary tuberculosis: a bidirectional mendelian randomization study.Diabetology & metabolic syndrome · 2024Article
- A nod to the bond between NOD2 and mycobacteria.PLoS pathogens · 2023Review
- Mass cytometry reveals the corneal immune cell changes at single cell level in diabetic mice.Frontiers in endocrinology · 2023Article
- Infectious diseases associated with pediatric type 1 diabetes mellitus: A narrative review.Frontiers in endocrinology · 2022Review
- Dysregulated expression of microRNAs in aqueous humor from intraocular tuberculosis patients.Molecular biology reports · 2022Article
- Tuberculosis endotypes to guide stratified host-directed therapy.Med (New York, N.Y.) · 2021Article
- Hyperglycemia and dyslipidemia: Reduced HLA-DR expression in monocyte subpopulations from diabetes patients.Human immunology · 2021Observational
- Insulin Modulates Inflammatory Cytokine Release in Acute Stages and Augments Expression of Adhesion Molecules and Leukocytes in Lungs on Chronic Stages of Paracoccidioidomycosis.Frontiers in immunology · 2020Article
- Perspective for Precision Medicine for Tuberculosis.Frontiers in immunology · 2020Review
- Gene Expression Analysis of the Pre-Diabetic Pancreas to Identify Pathogenic Mechanisms and Biomarkers of Type 1 Diabetes.Frontiers in endocrinology · 2020Article
- The diabetes pandemic and associated infections: suggestions for clinical microbiology.Reviews in medical microbiology : a journal of the Pathological Society of Great Britain and Ireland · 2019Article
- Infections in children with diabetes.Jornal de pediatriaReview
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Patients with diabetes mellitus have an increased risk of developing tuberculosis. Although the underlying mechanism is unclear, evidence suggests a role for chronic hyperglycaemia. We examined the influence of hyperglycaemia on Mycobacterium tuberculosis-induced cytokine responses in patients with type 1 diabetes mellitus (T1D). Peripheral blood mononuclear cells (PBMCs) from 24 male T1D patients with sub-optimal glucose control [HbA1c > 7.0% (53 mmol/L)] and from 24 age-matched male healthy controls were stimulated with M. tuberculosis lysate. Cytokine analysis, assessment of aerobic glycolysis, receptor recognition and serum cross-over experiments were performed to explore the mechanistic differences. PBMCs from T1D patients produced less bioactive interleukin (IL)-1β in response to M. tuberculosis. IL-6 and interferon (IFN)-γ production trended towards a decrease, whilst other cytokines such as tumour necrosis factor (TNF)-α, IL-17 and IL-1Ra were normal. The decrease in cytokine production was not correlated to HbA1c or plasma glucose levels. Cross-over serum experiments did not alter the cytokine profile of T1D or control patients, arguing for an intrinsic cellular defect. Cellular metabolism and the expression of M. tuberculosis-related pattern recognition receptors (PRRs) such as TLR2, TLR4 and NOD2 did not differ between T1D patients and healthy controls. Compared to matched controls, T1D patients have a reduced capacity to produce pro-inflammatory cytokines in response to M. tuberculosis. The impaired IL-1β production in T1D patients may contribute to the increased susceptibility to tuberculosis. This effect appears not to be related to prevailing glucose levels but to an intrinsic cellular deficit.
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