Pneumocystis carinii infection drives upregulation of Fn1 expression that causes pulmonary fibrosis with an inflammatory response.
Fibrosis pulmonar
Fn1
Infección
Infection
Inflamación
Inflammation
Pneumocystis carinii
Pulmonary fibrosis
Journal
Revista iberoamericana de micologia
ISSN: 2173-9188
Titre abrégé: Rev Iberoam Micol
Pays: Spain
ID NLM: 9425531
Informations de publication
Date de publication:
26 Sep 2024
26 Sep 2024
Historique:
received:
04
05
2023
revised:
15
03
2024
accepted:
09
04
2024
medline:
28
9
2024
pubmed:
28
9
2024
entrez:
27
9
2024
Statut:
aheadofprint
Résumé
Pneumocystis carinii is an opportunistic fungal pathogen that may cause pneumonia and lead to pulmonary fibrosis. This study attempted to investigate the role of P. carinii infection-related genes in regulating lung fibrosis in mice. A screening of P. carinii infection-related differential mRNAs was performed using the GEO database, followed by protein-protein interaction (PPI) network construction using the STRING website in order to obtain P. carinii infection-related key genes. The development of a mouse model with gene aberrant expression was achieved by utilizing mice carrying the Cre-LoxP recombinase system. Dexamethasone was employed to induce tracheal infection in order to develop a model of pulmonary fibrosis, and the magnitude of lung injury was assessed by performing hematoxylin-eosin (H&E) staining and Masson staining. Lung coefficient and hydroxyproline level were assessed on sections of lung tissue as well. Finally, the magnitude of lung fibrosis and inflammation in mice was determined based on immunofluorescence and on the expression of genes associated with lung fibrosis and inflammation. Fn1 was found by PPI with the highest connectivity in the PPI network associated with immunity and inflammation. Besides, Fn1 was significantly highly expressed in P. carinii-infected mice samples. The P carinii pneumonia (PCP)+Fn1 P. carinii infection may promote the upregulation of Fn1, which causes pulmonary fibrosis with an inflammatory response.
Sections du résumé
BACKGROUND
BACKGROUND
Pneumocystis carinii is an opportunistic fungal pathogen that may cause pneumonia and lead to pulmonary fibrosis.
AIMS
OBJECTIVE
This study attempted to investigate the role of P. carinii infection-related genes in regulating lung fibrosis in mice.
METHODS
METHODS
A screening of P. carinii infection-related differential mRNAs was performed using the GEO database, followed by protein-protein interaction (PPI) network construction using the STRING website in order to obtain P. carinii infection-related key genes. The development of a mouse model with gene aberrant expression was achieved by utilizing mice carrying the Cre-LoxP recombinase system. Dexamethasone was employed to induce tracheal infection in order to develop a model of pulmonary fibrosis, and the magnitude of lung injury was assessed by performing hematoxylin-eosin (H&E) staining and Masson staining. Lung coefficient and hydroxyproline level were assessed on sections of lung tissue as well. Finally, the magnitude of lung fibrosis and inflammation in mice was determined based on immunofluorescence and on the expression of genes associated with lung fibrosis and inflammation.
RESULTS
RESULTS
Fn1 was found by PPI with the highest connectivity in the PPI network associated with immunity and inflammation. Besides, Fn1 was significantly highly expressed in P. carinii-infected mice samples. The P carinii pneumonia (PCP)+Fn1
CONCLUSIONS
CONCLUSIONS
P. carinii infection may promote the upregulation of Fn1, which causes pulmonary fibrosis with an inflammatory response.
Identifiants
pubmed: 39332977
pii: S1130-1406(24)00006-8
doi: 10.1016/j.riam.2024.04.002
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright © 2024 Asociación Española de Micología. Publicado por Elsevier España, S.L.U. All rights reserved.