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Los macrófagos alveolares que patrullan ocultan las bacterias del sistema inmunológico para mantener la homeostasis

Arpan Sharma Neupane¹, Michelle Willson¹, Andrew Krzysztof Chojnacki²

¹Department of Physiology and Pharmacology, University of Calgary, Calgary, AB T2N 4N1, Canada; Calvin, Phoebe, and Joan Snyder Institute for Chronic Diseases, University of Calgary, Calgary, AB T2N 4N1, Canada.

|September 5, 2020

Resumen

Los macrófagos alveolares se arrastran activamente dentro de los pulmones, limpiando eficientemente las bacterias inhaladas. La interrupción de este movimiento conduce a una inflamación dañina y a una mayor susceptibilidad a infecciones secundarias.

Área de la Ciencia:

Inmunología
Biología pulmonar
Microbiología

Sus antecedentes:

Los humanos inhalamos grandes cantidades de aire todos los días, exponiendo los alvéolos pulmonares a posibles patógenos.
Los macrófagos alveolares (AM) son superados en número por los alvéolos, lo que plantea dudas sobre su papel protector si son sessiles.
La invasión de patógenos sin una defensa eficaz de los macrófagos podría conducir a una inflamación crónica.

Objetivo del estudio:

Investigar el comportamiento in vivo y las capacidades de eliminación de patógenos de los macrófagos alveolares (AM).
Determinar el papel de la motilidad AM y la quimiotaxis en la inmunidad pulmonar.
Explorar cómo las infecciones virales afectan la función AM y las infecciones bacterianas secundarias.

Principales métodos:

Desarrollo de técnicas de imagen intravital en tiempo real para los alvéolos pulmonares.
Observación del comportamiento de la AM, incluido el rastreo y la fagocitosis de las bacterias.
Manipulación experimental de la quimiotaxis AM y evaluación de las respuestas inflamatorias resultantes.
Modelado de la infección por el virus de la influenza A para estudiar su efecto en las AM y las infecciones secundarias.

Principales resultados:

Las AM son móviles, utilizan los poros de Kohn para navegar por los alvéolos.
Los AM detectan eficientemente, quimiotaxan hacia y fagocitosan las bacterias inhaladas (por ejemplo, P. aeruginosa, S. aureus).
El deterioro de la quimiotaxis AM da lugar a un reclutamiento excesivo de neutrófilos, causando inflamación y lesiones.
La infección por el virus de la gripe A dificulta el rastreo de la AM a través de la señalización de interferón tipo II, aumentando las co-infecciones bacterianas secundarias.

Conclusiones:

Las AM son células inmunes dinámicas y móviles cruciales para la defensa pulmonar contra patógenos bacterianos.
La motilidad AM y la quimiotaxis son esenciales para prevenir la inflamación inadecuada y mantener la homeostasis pulmonar.
Las infecciones virales pueden comprometer la función AM, aumentando la susceptibilidad a infecciones bacterianas secundarias.

Palabras clave:

Los macrófagos alveolares Los alvéolos Migración celular quimiotaxis La gripe microscopía intravital Inflamación de los pulmones

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