Sodium butyrate modulates chicken macrophage proteins essential for Salmonella Enteritidis invasion.
Actinin
/ genetics
Animals
Avian Proteins
/ genetics
Butyric Acid
/ pharmacology
Chickens
Cytochromes c
/ genetics
Gene Expression Regulation
/ drug effects
Host-Pathogen Interactions
/ genetics
Isoenzymes
/ genetics
Macrophages
/ cytology
Microfilament Proteins
/ genetics
Mitochondrial Proton-Translocating ATPases
/ genetics
Molecular Sequence Annotation
Oxidative Phosphorylation
/ drug effects
Poultry Diseases
/ genetics
Primary Cell Culture
Protein Disulfide-Isomerases
/ genetics
Salmonella Infections, Animal
/ genetics
Salmonella enteritidis
/ growth & development
Vacuolar Proton-Translocating ATPases
/ genetics
Vimentin
/ genetics
Vinculin
/ genetics
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2021
2021
Historique:
received:
29
12
2020
accepted:
02
04
2021
entrez:
28
4
2021
pubmed:
29
4
2021
medline:
29
9
2021
Statut:
epublish
Résumé
Salmonella Enteritidis is an intracellular foodborne pathogen that has developed multiple mechanisms to alter poultry intestinal physiology and infect the gut. Short chain fatty acid butyrate is derived from microbiota metabolic activities, and it maintains gut homeostasis. There is limited understanding on the interaction between S. Enteritidis infection, butyrate, and host intestinal response. To fill this knowledge gap, chicken macrophages (also known as HTC cells) were infected with S. Enteritidis, treated with sodium butyrate, and proteomic analysis was performed. A growth curve assay was conducted to determine sub-inhibitory concentration (SIC, concentration that do not affect bacterial growth compared to control) of sodium butyrate against S. Enteritidis. HTC cells were infected with S. Enteritidis in the presence and absence of SIC of sodium butyrate. The proteins were extracted and analyzed by tandem mass spectrometry. Our results showed that the SIC was 45 mM. Notably, S. Enteritidis-infected HTC cells upregulated macrophage proteins involved in ATP synthesis through oxidative phosphorylation such as ATP synthase subunit alpha (ATP5A1), ATP synthase subunit d, mitochondrial (ATP5PD) and cellular apoptosis such as Cytochrome-c (CYC). Furthermore, sodium butyrate influenced S. Enteritidis-infected HTC cells by reducing the expression of macrophage proteins mediating actin cytoskeletal rearrangements such as WD repeat-containing protein-1 (WDR1), Alpha actinin-1 (ACTN1), Vinculin (VCL) and Protein disulfide isomerase (P4HB) and intracellular S. Enteritidis growth and replication such as V-type proton ATPase catalytic subunit A (ATPV1A). Interestingly, sodium butyrate increased the expression of infected HTC cell protein involving in bacterial killing such as Vimentin (VIM). In conclusion, sodium butyrate modulates the expression of HTC cell proteins essential for S. Enteritidis invasion.
Identifiants
pubmed: 33909627
doi: 10.1371/journal.pone.0250296
pii: PONE-D-20-40856
pmc: PMC8081216
doi:
Substances chimiques
Avian Proteins
0
Isoenzymes
0
Microfilament Proteins
0
Vimentin
0
Butyric Acid
107-92-6
Actinin
11003-00-2
Vinculin
125361-02-6
Cytochromes c
9007-43-6
Vacuolar Proton-Translocating ATPases
EC 3.6.1.-
Mitochondrial Proton-Translocating ATPases
EC 3.6.3.-
Protein Disulfide-Isomerases
EC 5.3.4.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0250296Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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