Effects of SOCS1-overexpressing dendritic cells on Th17- and Treg-related cytokines in COPD mice.
BMC Pulm Med
; 22(1): 145, 2022 Apr 15.
Article
en En
| MEDLINE
| ID: mdl-35428280
ABSTRACT
BACKGROUND:
In this study, we established a chronic obstructive pulmonary disease (COPD) model by stimulating mice with cigarette smoke, and observed the effects of dendritic cells (DCs) overexpressing SOCS1 on Th17, Treg and other related cytokines in peripheral blood, bronchoalveolar lavage fluid and lung tissues of COPD mice.METHODS:
After successfully transfecting DCs with overexpressing SOCS1 (DC-SOCS1), the mice were injected with DC-SOCS1 (1 × 106), DC-SOCS1 (2 × 106) and immature DCs (1 × 106) via tail vein on days 1 and 7 of COPD fumigation modeling. After day 28 of modeling, the peripheral blood, BALF and lung tissue samples were extracted from the mice, and the changes of DCs, Th17 and Treg cells and related cytokines were detected by immunohistochemistry, immunofluorescence, HE staining, flow cytometry and ELISA.RESULTS:
The results showed that DC-SOCS1 was able to reduce the secretion of pro-inflammatory factors and increase the anti-inflammatory factors in the COPD mice, and the effect of high concentration (2 × 106 DC-SOCS1) was better than low concentration (1 × 106 DC-SOCS1). Moreover, the intervention effect was significant on day 1 compared with day 7. In the mice injected with DC-SOCS1, the expression of CD83, IL-4, Foxp3, and CCR6 was increased on day 1 than those on day 7, while IL-17 and IFN-γ was decreased.CONCLUSIONS:
Intervention of COPD mice with high concentrations of DCs-SOCS1 reduced pro-inflammatory factor secretion and attenuated the inflammatory response in COPD. Trial registration Not applicable.Palabras clave
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Células Dendríticas
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Citocinas
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Linfocitos T Reguladores
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Enfermedad Pulmonar Obstructiva Crónica
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Células Th17
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Proteína 1 Supresora de la Señalización de Citocinas
Tipo de estudio:
Prognostic_studies
Idioma:
En
Revista:
BMC Pulm Med
Año:
2022
Tipo del documento:
Article