Journal
SCIENTIFIC REPORTS
Volume 11, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41598-021-01536-4
Keywords
-
Categories
Funding
- Fundacao de Amparo em Pesquisa do Estado da Bahia [JCB0035/2016]
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES), Brazil [001]
Ask authors/readers for more resources
The study investigated the modulating role of citral in inflammation caused by Staphylococcus aureus infection. Citral was found to inhibit inflammation and enhance the expression of anti-inflammatory cytokines, as well as affect multiple immune factors and gene expressions at the cellular level.
Staphylococcus aureus is a Gram-positive bacterium that is considered an important human pathogen. Due to its virulence and ability to acquire mechanisms of resistance to antibiotics, the clinical severity of S. aureus infection is driven by inflammatory responses to the bacteria. Thus, the present study aimed to investigate the modulating role of citral in inflammation caused by S. aureus infection. For this, we used an isolate obtained from a nasal swab sample of a healthy child attending a day-care centre in Vitoria da Conquista, Bahia, Brazil. The role of citral in modulating immunological factors against S. aureus infection was evaluated by isolating and cultivating human peripheral blood mononuclear cells. The monocytes were treated with 4%, 2%, and 1% citral before and after inoculation with S. aureus. The cells were analysed by immunophenotyping of monocyte cell surface molecules (CD54, CD282, CD80, HLA-DR, and CD86) and cytokine dosage (IL-1 beta, IL-6, IL-10, IL-12p70, IL-23, IFN-gamma, TGF-beta, and TNF-alpha), and evaluated for the expression of 84 genes related to innate and adaptive immune system responses. GraphPad Prism software and variables with P values < 0.05, were used for statistical analysis. Our data demonstrated citral's action on the expression of surface markers involved in recognition, presentation, and migration, such as CD14, CD54, and CD80, in global negative regulation of inflammation with inhibitory effects on NF-kappa B, JNK/p38, and IFN pathways. Consequently, IL-1 beta, IL-6, IL-12p70, IL-23, IFN-gamma, and TNF-alpha cytokine expression was reduced in groups treated with citral and groups treated with citral at 4%, 2%, and 1% and infected, and levels of anti-inflammatory cytokines such as IL-10 were increased. Furthermore, citral could be used as a supporting anti-inflammatory agent against infections caused by S. aureus. There are no data correlating citral, S. aureus, and the markers analysed here; thus, our study addresses this gap in the literature.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available