1. Immunological response to Mycobacterium tuberculosis infection in blood from type 2 diabetes patients
- Author
-
Teresa Nebreda-Mayoral, Silvia García-García, Sara Raposo-García, Eduardo López-Fidalgo, Ramiro López-Medrano, Javier Juan-García, José Manuel Guerra-Laso, Cristina Diez-Tascón, and Octavio Miguel Rivero-Lezcano
- Subjects
Male ,Risk ,0301 basic medicine ,Tuberculosis ,Neutrophils ,Immunology ,Type 2 diabetes ,Mycobacterium tuberculosis ,03 medical and health sciences ,0302 clinical medicine ,Immune system ,Phagocytosis ,Diabetes mellitus ,medicine ,Humans ,Immunology and Allergy ,Cells, Cultured ,Aged ,Whole blood ,Aged, 80 and over ,Immunity, Cellular ,Blood Cells ,biology ,Tumor Necrosis Factor-alpha ,business.industry ,Macrophages ,Middle Aged ,medicine.disease ,biology.organism_classification ,030104 developmental biology ,Diabetes Mellitus, Type 2 ,Absolute neutrophil count ,Female ,Tumor necrosis factor alpha ,business ,030215 immunology - Abstract
The convergence of tuberculosis and diabetes represents a co-epidemic that threatens progress against tuberculosis. We have investigated type 2 diabetes as a risk factor for tuberculosis susceptibility, and have used as experimental model whole blood infected in vitro with Mycobacterium tuberculosis. Blood samples from diabetic patients were found to have a higher absolute neutrophil count that non-diabetic controls, but their immune functionality seemed impaired because they displayed a lower capacity to phagocytose M. tuberculosis, a finding that had been previously reported only for monocytes. In contrast, an increased production of TNFα was detected in infected blood from diabetic patients. Despite the altered phagocytic capacity showed by cells from these patients, the antimicrobial activity measured in both whole blood and monocyte derived macrophages was similar to that of controls. This unexpected result prompts further improvements in the whole blood model to analyze the immune response of diabetes patients to tuberculosis.
- Published
- 2017
- Full Text
- View/download PDF