Sensitivity of staphylococci to fatty acids: novel inactivation of linolenic acid by serum

Abstract

SUMMARY.The inhibition of coagulase-negative staphylococci and Staphylococcus aureus of human or animal origin by most free fatty acids was similar, but coagulase-positive staphylococci were sensitive and coagulase-negative cultures were resistant to linolenic acid. Animal strains of S. aureus were more sensitive to linolenic acid than were human strains. These differences were reflected in the relative abilities of the three categories of strains to survive on human skin.The antibacterial effects of 20 mg of linolenic acid were inactivated by 1 ml of serum in vitro. A test organism seeded on to skin also survived better if first suspended in serum. The mechanism of the interaction between serum and linolenic acid may be due to a detergent effect of the serum and could account for colonisation of diseased skin with S. aureus.Cultures of S. aureus seeded on to human skin were rapidly killed after the skin has been covered with linolenic acid. The possibility of therapeutic use of linolenic acid as an antibacterial agent should be explored.

Resistance to desiccation and skin fatty acids in outbreak strains of methicillin-resistant Staphylococcus aureus

“…aureus. 12 Strains from the SCBU, where survival on hands was presumably important, were not more resistant than those from elsewhere, or than controls, by the methods we used. Others have also found only a narrow range of sensitivity of staphylococci to skin fatty acids.…”

Staphylococcus aureus Strain Newman Photoinactivation and Cellular Response to Sunlight Exposure

“…The carotenoid protects S. aureus from oxidative stress by scavenging radicals (42). Staphyloxanthin may also provide resistance to other stresses like desiccation and light exposure (43,44). Previous field and laboratory studies on photoinactivation of Enterococcus spp.…”

Nutrient Signaling: Evolutionary Origins of the Immune-Modulating Effects of Dietary Fat

“…Pathogens that failed to show inhibition by either category of FA included Pseudomonas aeruginosa and Escherichia coli (Zheng et al 2005) and Listeria monocytogenes (Reiner et al 1986). (Gutteridge et al 1974;Butcher et al 1976;Altenbern 1977b;Kondo and Kanai 1977;Heczko et al 1979;Lacey and Lord 1981;Knapp and Melly 1986;Rohrer et al 1986;Hogan et al 1988;Thompson et al 1990;Ababouch et al 1992;Wang and Johnson 1992;Thompson et al 1994;Petrone et al 1998;Sun et al 2003) C18:3 Kabara et al 1972;Raychowdhury et al 1985;Reiner et al 1986;Mbandi et al 2004;Zheng et al 2005)** Note: When the lipid number fails to distinguish between similar FA, common names of fatty acids are given in parentheses.…”

“…In pooled data from 20 of 22 studies, most comparisons showed greater pathogen inhibition by omega-3 FA than by omega-6 FA (Figure 4c). Two studies, excluded from Figure 4c because they did not provide the exact identification of pathogen strains, also showed stronger bacterial inhibition by omega-3 FA (Heczko et al 1979;Lacey and Lord 1981). Heczko et al showed that of 242 strains of Staphylococcus aureus, most strains were sensitive to the omega-3 linolenic acid (C18:3) at a minimum concentration of 0.19 mmol/L while most strains were inhibited by the omega-6 linoleic acid at a minimum concentration of 6.25 mmol/L (Heczko et al 1979).…”

“…Additional anti-inflammatory effects of shorter-chain FA occur because these FA are ligands for G-protein receptors that tend to elicit anti-inflammatory signaling functions (Cavaglieri et al 2003;Hamer et al 2008). Galbraith et al 1971;Salanitro and Wegener 1971;Kabara et al 1972;Fay and Farias 1975;Altenbern 1977a;Miller et al 1977;Beuchat 1980;Lacey and Lord 1981;Hogan et al 1988;van der Kooij and Hijnen 1988;Ababouch et al 1992;Wang and Johnson 1992;Wang et al 1993;Petschow et al 1996;Petrone et al 1998;Sprong et al 1999;Bergsson et al 2001;Sprong et al 2001;Bergsson et al 2002;Lee et al 2002;Marounek et al 2003;…”