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La disfunción de eferocitosis de los macrófagos mediada por la trombospondina-1 exacerba la patología intestinal en
Qiuling Li1, Hanyi Kong1, Qijun Li1
1Pediatric Institute of Soochow University, Children's Hospital of Soochow University, Soochow University, 215025 Suzhou, China; Pediatric Surgery, Children's Hospital of, Soochow University, Soochow University, 215025 Suzhou, China.
International immunopharmacology
|February 12, 2026
Resumen
La trombospondina-1 regulada a la baja (THBS1) afecta la eferocitosis de los macrófagos, provocando inflamación y fibrosis en el estudio de Hirschsprung.
Área de la Ciencia:
- Gastroenterología y Hepatología.
- Inmunología Inmunología.
- Cirugía pediátrica en cirugía pediátrica.
Sus antecedentes:
- La enfermedad de Hirschsprung (HSCR) es una enteropatía pediátrica marcada por inflamación y fibrosis.
- Los mecanismos celulares precisos que impulsan la patología HSCR no se comprenden completamente.
- La trombospondina-1 (THBS1) regula la función de los macrófagos, por lo que es un foco clave para la investigación de la HSCR.
Objetivo del estudio:
- Para investigar el papel de THBS1 en la patogénesis de la enfermedad de Hirschsprung.
- Para aclarar los mecanismos por los cuales THBS1 influye en la función de los macrófagos y la homeostasis intestinal en HSCR.
Principales métodos:
- Secuenciación de ARN unicelular (scRNA-seq) en HSCR y biopsias de colon de control.
- Histopatología, qRT-PCR e inmunofluorescencia para marcadores de inflamación y fibrosis.
- Citometría de flujo e inmunofluorescencia para cuantificar la eferocitosis de los macrófagos; estudios mecanicistas utilizando THBS1 recombinante (rTHBS1) y inhibición de CD36 en los macrófagos.
Principales resultados:
- THBS1 fue regulado a la baja en las células estomales HSCR, correlacionándose con la eferocitosis de los macrófagos deteriorada y la polarización pro-resolvente.
- THBS1 promueve la eferocitosis de los macrófagos a través de la vía CD36/Rac1, crucial para resolver la inflamación y prevenir la fibrosis.
- La deficiencia de THBS1 condujo a un deterioro significativo de la eferocitosis, inflamación no resuelta y fibrosis en modelos de HSCR y muestras humanas.
Conclusiones:
- La señalización estromal THBS1-CD36/Rac1 es crítica para la eferocitosis de los macrófagos y la resolución en HSCR.
- La deficiencia de THBS1 contribuye a la inflamación posquirúrgica persistente y la fibrosis en la HSCR.
- THBS1 representa un objetivo terapéutico potencial y un biomarcador para mejorar los resultados de los pacientes con HSCR.
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