Characterization of the immune impairment of patients with tuberculosis and COVID-19 coinfection

•Tumor necrosis factor-α significantly discriminates tuberculosis (TB)-COVID-19 from COVID-19.•SARS-CoV-2-specific response is significantly impaired in patients with TB-COVID-19.•Mycobacterium tuberculosis-specific response is significantly reduced in patients with TB-COVID-19. To characterize the...

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Veröffentlicht in:International journal of infectious diseases Jg. 130; S. S34 - S42
Hauptverfasser: Najafi-Fard, Saeid, Aiello, Alessandra, Navarra, Assunta, Cuzzi, Gilda, Vanini, Valentina, Migliori, Giovanni Battista, Gualano, Gina, Cerva, Carlotta, Grifoni, Alba, Sette, Alessandro, Vaia, Francesco, Palmieri, Fabrizio, Goletti, Delia
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Canada Elsevier Ltd 01.05.2023
Elsevier
Schlagworte:
Coinfection
COVID-19
Immune response
M. tuberculosis
SARS-CoV-2
Tuberculosis
COVID-19
SARS-CoV-2
Tuberculosis
Coinfection
Immune response
M. tuberculosis
ISSN:1201-9712, 1878-3511, 1878-3511
Online-Zugang:Volltext
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Zusammenfassung:•Tumor necrosis factor-α significantly discriminates tuberculosis (TB)-COVID-19 from COVID-19.•SARS-CoV-2-specific response is significantly impaired in patients with TB-COVID-19.•Mycobacterium tuberculosis-specific response is significantly reduced in patients with TB-COVID-19. To characterize the plasma immune profile of patients with tuberculosis (TB)-COVID-19 compared with COVID-19, TB, or healthy controls and to evaluate in vitro the specific responses to SARS-CoV-2 and Mycobacterium tuberculosis (Mtb)-antigens. We enrolled 119 subjects: 14 TB-COVID-19, 47 COVID-19, 38 TB, and 20 controls. The plasmatic levels of 27 immune factors were measured at baseline using a multiplex assay. The specific response to SARS-CoV-2 and Mtb antigens was evaluated using a home-made whole blood platform and QuantiFERON-Plus tubes, respectively. We found an immune signature (tumor necrosis factor [TNF]-α, macrophage inflammatory protein-1β, and interleukin [IL]-9) associated with TB-COVID-19 coinfection compared with COVID-19 (P <0.05), and TNF-α showed the highest discriminant power. We also found another signature (TNF-α, IL-1β, IL-17A, IL-5, fibroblast growth factor-basic, and granulocyte macrophage colony-stimulating factor [GM-CSF]) in coinfected patients compared with patients with TB (P <0.05), and among them, TNF-α and granulocyte macrophage colony-stimulating factor showed a non-negligible discriminating ability. Moreover, coinfected patients showed a significantly reduced SARS-CoV-2-specific response compared with COVID-19 for several pro-inflammatory cytokines/chemokines, anti-inflammatory cytokines, and growth factors (P ≤0.05). Furthermore, coinfection negatively affected the Mtb-specific response (P ≤0.05). We found immune signatures associated with TB-COVID-19 coinfection and observed a major impairment of SARS-CoV-2-specific and, to a lesser extent, the Mtb-specific immune responses. These findings further advance our knowledge of the immunopathology of TB-COVID-19 coinfection.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1201-9712
1878-3511
1878-3511
DOI:10.1016/j.ijid.2023.03.021