LncRNA CCAT1 is overexpressed in tuberculosis patients and predicts their survival.
Immun Inflamm Dis
; 10(2): 218-224, 2022 02.
Article
en En
| MEDLINE
| ID: mdl-34847295
INTRODUCTION: LncRNA CCAT1 promotes inflammatory responses, which contribute to tuberculosis. Therefore, CCAT1 may participate in tuberculosis. Therefore, we analyzed the involvement of CCAT1 in tuberculosis. METHODS: Plasma samples were donated by a total of 200 patients with newly developed tuberculosis (N-TB), 102 patients with recurrent tuberculosis (R-TB), and 102 healthy controls on the day of admission. Plasma samples were also collected from N-TB and R-TB patients every month after the initiation of treatment for a total of 6 months. CCAT1 expression in these samples was detected by quantitative reverse transcription polymerase chain reaction. Levels of IFN-γ, IL-1ß, iNOS, TNF-α, and IL-10 in plasma were determined by enzyme-linked immunosorbent assay. N-TB and R-TB patients were monitored for 2 months to analyze their survival. RESULTS: On the day of admission, the highest levels of CCAT1, IFN-γ, IL-1ß, iNOS, and TNF-α were detected in N-TB patients, followed by R-TB patients and controls, while the lowest levels of plasma IL-10 were detected in N-TB patients, followed by R-TB patients and controls. Across R-TB and N-TB patients, CCAT1 was inversely correlated with IL-10 but not closely correlated with other inflammatory factors. During the treatment, plasma CCAT1 levels decreased in both N-TB and R-TB patients. High CCAT1 levels were closely correlated with high mortality rates of both N-TB and R-TB patients. CONCLUSION: CCAT1 is overexpressed in tuberculosis patients and predicts their survival. Its function in tuberculosis may be related to IL-10.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Tuberculosis
/
ARN Largo no Codificante
Tipo de estudio:
Prognostic_studies
/
Risk_factors_studies
Límite:
Humans
Idioma:
En
Revista:
Immun Inflamm Dis
Año:
2022
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Reino Unido