Staphylococci: Colonizers and Pathogens of Human Skin

Rosanna Coates; Josephine Moran; Malcolm J Horsburgh

Disclosures

Future Microbiol. 2014;9(1):75-91. 

In This Article

Antimicrobial Fatty Acids Protect Human Epidermis

In addition to AMPs, antimicrobial fatty acids (AFAs) protect skin against invasion by pathogenic bacteria. AFAs, together with lactic acid and amino acids in sweat, contribute to establishing and maintaining the acid mantle, by producing the acid pH that is a signature of the surface of the human epidermis. The acid mantle is important for the maintenance of the cohesion and integrity of the stratum corneum and contributes to the permeability homeostasis of the outer layers of the skin.[92] Enzymes required for the production of ceramides, the lipids integral to barrier homeostasis, function optimally at acidic pH;[93] whereas serine proteases, capable of degrading corneodesmosomes and compromising the integrity of the epidermis, are inhibited.[94]

Structural organization studies recently demonstrated a highly regular 1:1:1 arrangement of fatty acid, sphingosine and cholesterol into multilamellar structures.[23] AFAs, including sapienic acid (16:1Δ9) and linoleic acid (18:2Δ9,Δ12), are abundant on healthy mammalian skin. An apparent inverse correlation between levels of staphylococcal colonization and AFAs[6,95] supports an AFA contribution to colonization inhibition. Atopic dermatitis sufferers have lower AFA levels than normal on their skin, and while S. aureus is isolated from <5% of individuals with healthy skin, it is routinely isolated from atopic dermatitis patients.[96–98] This indicates that AFAs are potentially important contributing factors in the differential survival of S. epidermidis and S. aureus on human skin.

The range and proposed mechanisms of AFA activity were recently reviewed elsewhere.[99] AFAs have a broad range of activity owing to their lipophilic properties, interacting with most organisms bearing lipid bilayer structures. Most theorized antimicrobial mechanisms of AFAs derive from their ability to insert into membranes, whereby unsaturated long chain fatty acids cause increased membrane disorder (fluidity) due to their shape reducing packing density. In S. aureus, inhibitory concentrations of linoleic acid (18:2Δ9,Δ12) cause protein leakage and interfere with metabolic pathways, such as the electron transport chain and nutrient uptake.[100,101] Recent studies have confirmed this observation and demonstrated that, while oleic acid (18:1Δ9) was a substrate for phospholipid biosynthesis, the AFA sapienic acid (16:1Δ9) required elongation for its incorporation into cellular pathways.[102] Arsic et al. determined that in some S. aureus strains AFAs, in addition to other long chain unsaturated fatty acids tested, variably induced protease expression.[103]

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