Arachidonic Acid Kills Staphylococcus aureus through a Lipid Peroxidation Mechanism
Year: 2019
Type: article
Abstract: Despite the ability of the human immune system to generate a plethora of molecules to control Staphylococcus aureus infections, S. aureus is among the pathogens with the greatest impact on human health. One class of host molecules toxic to S. aureus consists of polyunsaturated fatty acids. Here, we investigated the antibacterial properties of arachidonic acid, one of the most abundant polyunsaturated fatty acids in humans, and discovered that the mechanism of toxicity against S. aureus proceeds through lipid peroxidation. A better understanding of the molecular mechanisms by which the immune system kills S. aureus , and by which S. aureus avoids host killing, will enable the optimal design of therapeutics that complement the ability of the vertebrate immune response to eliminate S. aureus infections.
Source: mBio
Institutions: Vanderbilt University, Vanderbilt University Medical Center
Language: English
Subfield: Infectious Diseases
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,900
Funders: American Heart Association, National Institutes of Health, National Heart, Lung, and Blood Institute, National Eye Institute, National Cancer Institute, National Institute of Allergy and Infectious Diseases, National Institute of Diabetes and Digestive and Kidney Diseases, National Center for Research Resources
Awards: G1344704808, G290080222, G3872320933, G4462420853, The Vanderbilt Institute for Clinical and Translational Research (VICTR) UL1, Mechanism and function of heme-iron utilization in staphylococcal pathogenesis, G725763919, VANTAGE:Consolidation to create the Vanderbilt Technologies for Advanced Genomics, Interrogating methionine sulfoxide reductases in S. aureus pathogenesis, G836990232, G8434023134, Molecular and Cellular Basis for Digestive Diseases, Vanderbilt Infection Pathogenesis and Epidemiology Research Training Program, Core Grant in Vision Research, G949362299
OpenAlex ID: W2978361963