Surfactant protein A modulates neuroinflammation in adult mice upon pulmonary infection.
Central nervous system
Cytokines
Lipopolysaccharide
Neurocognitive impairment
Neuroinflammation
Pseudomonas aeruginosa
Pulmonary infection
Sickness behavior
Surfactant proteins
Journal
Brain research
ISSN: 1872-6240
Titre abrégé: Brain Res
Pays: Netherlands
ID NLM: 0045503
Informations de publication
Date de publication:
02 Jul 2024
02 Jul 2024
Historique:
received:
05
05
2024
revised:
17
06
2024
accepted:
01
07
2024
medline:
5
7
2024
pubmed:
5
7
2024
entrez:
4
7
2024
Statut:
aheadofprint
Résumé
One of the most common entry gates for systemic infection is the lung. In humans, pulmonary infections can lead to significant neurological impairment, ranging from acute sickness behavior to long-term disorders. Surfactant proteins (SP), essential parts of the pulmonary innate immune defense, have been detected in the brain of rats and humans. Recent evidence suggests that SP-A, the major protein component of surfactant, also plays a functional role in modulating neuroinflammation. This study aimed to determine whether SP-A deficiency affects the inflammatory response in the brain of adult mice during pulmonary infection. Adult male wild-type (WT, n = 72) and SP-A-deficient (SP-A SP-A mRNA and histological evidence of protein expression were detected in both the lungs and brains of WT mice, with significantly higher amounts in lung samples. SP-A SP-A is known for its anti-inflammatory role in the pulmonary immune response to bacterial infection. Recent evidence suggests that in an abdominal sepsis model SP-A deficiency can lead to increased cytokine levels in the brain. Our results extend this perception and provide evidence for an anti-inflammatory role of SP-A in the brain of adult WT mice after pulmonary infection.
Sections du résumé
BACKGROUND
BACKGROUND
One of the most common entry gates for systemic infection is the lung. In humans, pulmonary infections can lead to significant neurological impairment, ranging from acute sickness behavior to long-term disorders. Surfactant proteins (SP), essential parts of the pulmonary innate immune defense, have been detected in the brain of rats and humans. Recent evidence suggests that SP-A, the major protein component of surfactant, also plays a functional role in modulating neuroinflammation. This study aimed to determine whether SP-A deficiency affects the inflammatory response in the brain of adult mice during pulmonary infection.
EXPERIMENTAL PROCEDURE
METHODS
Adult male wild-type (WT, n = 72) and SP-A-deficient (SP-A
RESULTS
RESULTS
SP-A mRNA and histological evidence of protein expression were detected in both the lungs and brains of WT mice, with significantly higher amounts in lung samples. SP-A
CONCLUSION
CONCLUSIONS
SP-A is known for its anti-inflammatory role in the pulmonary immune response to bacterial infection. Recent evidence suggests that in an abdominal sepsis model SP-A deficiency can lead to increased cytokine levels in the brain. Our results extend this perception and provide evidence for an anti-inflammatory role of SP-A in the brain of adult WT mice after pulmonary infection.
Identifiants
pubmed: 38964703
pii: S0006-8993(24)00362-7
doi: 10.1016/j.brainres.2024.149108
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
149108Informations de copyright
Copyright © 2024. Published by Elsevier B.V.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.