ArticleThe Journal of infectious diseases2016
Impaired Recognition of Mycobacterium tuberculosis by Alveolar Macrophages From Diabetic Mice.
Article in The Journal of infectious diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Immune dysregulation in tuberculosis-diabetes comorbidity: mechanistic and translational insights.Frontiers in immunology · 2026Pooled it
- Chemerin Exacerbates Pulmonary Inflammation in Type 2 Diabetes and Mycobacterium Tuberculosis Infection Comorbidity.Inflammation · 2025Article
- Human alveolar macrophage function is impaired in tuberculosis contacts with diabetes.EBioMedicine · 2025Article
- Stopping Tuberculosis at the Gate: The Role ofVaccines · 2025Review
- Inhibition of CYP450 family 1 subfamily B member 1 (CYP1B1) expression in macrophage reduces the inflammatory response in type 2 diabetes mellitus combined with tuberculosis.Frontiers in endocrinology · 2025Article
- Increased circulating Th17 cells and altered CD4 T cell maturation and differentiation in active tuberculosis with type 2 diabetes: a pilot study.Frontiers in immunology · 2025Article
- Interaction between type 2 diabetes and past COVID-19 on active tuberculosis.BMC infectious diseases · 2024Article
- Impact of diabetes mellitus on tuberculosis prevention, diagnosis, and treatment from an immunologic perspective.Exploration (Beijing, China) · 2024Review
- Diabetes and tuberculosis: An emerging dual threat to healthcare.World journal of diabetes · 2024Article
- Intersecting epidemics: deciphering the complexities of tuberculosis-diabetes comorbidity.Frontiers in tuberculosis · 2024Review
- Importance of adjuvant selection in tuberculosis vaccine development: Exploring basic mechanisms and clinical implications.Vaccine: X · 2023Review
- Role of pattern recognition receptors in sensingHeliyon · 2023Review
- Glycerol contributes to tuberculosis susceptibility in male mice with type 2 diabetes.Nature communications · 2023Article
- A multi-center, prospective cohort study of whole blood gene expression in the tuberculosis-diabetes interaction.Scientific reports · 2023Article
- The cause-effect relation of tuberculosis on incidence of diabetes mellitus.Frontiers in cellular and infection microbiology · 2023Review
- Immunologic, metabolic and genetic impact of diabetes on tuberculosis susceptibility.Frontiers in immunology · 2023Review
- Mouse Models forPathogens (Basel, Switzerland) · 2022Review
- Differential Role of Type 2 Diabetes as a Risk Factor for Tuberculosis in the Elderly versus Younger Adults.Pathogens (Basel, Switzerland) · 2022Article
- Review
- A Blunted GPR183/Oxysterol Axis During Dysglycemia Results in Delayed Recruitment of Macrophages to the Lung During Mycobacterium tuberculosis Infection.The Journal of infectious diseases · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundDiabetes mellitus is associated with increased tuberculosis risk and severity. We previously reported that tuberculosis susceptibility in diabetic mice results from a delay in innate immune response to inhaled Mycobacterium tuberculosis, leading to delayed adaptive immune priming and, consequently, a higher plateau lung bacterial burden and greater immune pathology.
methodsWe tested the capacity of alveolar macrophages from diabetic mice to phagocytose M. tuberculosis ex vivo and promote T-cell activation in vivo.
resultsAlveolar macrophages from diabetic mice had reduced expression of CD14 and macrophage receptor with collagenous structure (MARCO), which recognize the bacterial cell wall component trehalose 6,6'-dimycolate (TDM). Diabetic alveolar macrophages exhibited reduced phagocytosis of M. tuberculosis or TDM-coated latex beads. This alveolar macrophage phenotype was absent in peritoneal and bone marrow-derived macrophages. Transfer of infected alveolar macrophages from diabetic mice into nondiabetic recipients confirmed an intrinsic alveolar macrophage defect that hindered T-cell priming. The diabetic alveolar macrophage phenotype depended in part on expression of the receptor for advanced glycation end products.
conclusionsReduced MARCO and CD14 expression contributes to defective sentinel function of alveolar macrophages, promoting tuberculosis susceptibility in diabetic hosts at a critical early step in the immune response to aerosol infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.