Biofilm exopolysaccharides alter sensory-neuron-mediated sickness during lung infection.
Cell
; 187(8): 1874-1888.e14, 2024 Apr 11.
Article
en En
| MEDLINE
| ID: mdl-38518773
ABSTRACT
Infections of the lung cause observable sickness thought to be secondary to inflammation. Signs of sickness are crucial to alert others via behavioral-immune responses to limit contact with contagious individuals. Gram-negative bacteria produce exopolysaccharide (EPS) that provides microbial protection; however, the impact of EPS on sickness remains uncertain. Using genome-engineered Pseudomonas aeruginosa (P. aeruginosa) strains, we compared EPS-producers versus non-producers and a virulent Escherichia coli (E. coli) lung infection model in male and female mice. EPS-negative P. aeruginosa and virulent E. coli infection caused severe sickness, behavioral alterations, inflammation, and hypothermia mediated by TLR4 detection of the exposed lipopolysaccharide (LPS) in lung TRPV1+ sensory neurons. However, inflammation did not account for sickness. Stimulation of lung nociceptors induced acute stress responses in the paraventricular hypothalamic nuclei by activating corticotropin-releasing hormone neurons responsible for sickness behavior and hypothermia. Thus, EPS-producing biofilm pathogens evade initiating a lung-brain sensory neuronal response that results in sickness.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Polisacáridos Bacterianos
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Pseudomonas aeruginosa
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Infecciones por Pseudomonas
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Escherichia coli
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Infecciones por Escherichia coli
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Pulmón
Límite:
Animals
Idioma:
En
Revista:
Cell
Año:
2024
Tipo del documento:
Article
País de afiliación:
Canadá