Table 1.

Members of the microbiome have both beneficial and detrimental effects on cutaneous homeostasis, which dictates their role as a commensal microorganism or pathogen in uninjured skin or a wound microenvironment

Bacteria	Good	Bad	Effects of Stress Mediators
Staphylococcus epidermidis	Stimulates keratinocyte production of host AMPs, such as hBD2 and hBD3, and produces its own AMPs, including PSMγ and PSMδ.10,18	Causative agent of hospital-acquired infections associate with medical devices.3,53	Glucocorticoids decrease the effects of super antigen activated T cells and inhibit staphylococcal exotoxin-induced T-cell proliferation, cytokine release.3
Propionibacterium acnes	Fatty acids generated by lipase activities may slow/inhibit growth of other microorganisms.49,67	Associated with pathogenesis of acne and a number of other opportunistic infections.67	Cortisol and steroids significantly exacerbate inflammation associated with P. acnes via TLR2 stimulation.2,49
Pseudomonas aeruginosa	Produces pseudomonic acid A, which kills staphylococcal and streptococcal pathogens.2	Most common cause of chronic and acute burn wound infections.6	Norepinephrine increases expression of the attachment factor PA-1 of P. aeruginosa and increases biofilm formation.2,7
	Accelerates epithelialization and neovascularization in acute wounds.6,36
Staphylococcus aureus	Produces bacteriocins such as staphylococcin 462, which can inhibit growth of other.	Commonly associated with infectious skin conditions, such as folliculitis and abscesses.	Norepinephrine increases ability to steal iron from host and therefore increases ability to form biofilms.2,55
	S. aureus strains.67	Produces superantigen toxins that can trigger staphylococcal toxic shock syndrome.67
Corynebacterium jeikeium	Manganese acquisition inhibits Mg-dependent superoxide dismutase, which may function to prevent oxidative damage to epidermal tissue.68	Causes infections in immune-compromised patients, in conjunction with underlying malignancies, on implanted medical devices and in skin-barrier defects.68	Reduced expression of transcriptional regulators involved in C. jeikeium carbohydrate metabolism due to a less versatile sugar metabolism; variations in the number of metalloregulatory sensors such that pathogenic C. jeikeium predominantly import metal ions directly from host during hypoglycemic or ionic stress responses.2,68
Group A Streptococcus	Surface-expressed streptokinase sequesters and activates host plasminogen in the epidermis, which leads to keratinocyte chemotaxis, suppression of cell proliferation, and potential re-epithelialization of wounds.68	Associated with numerous infections, such as “strep throat,” impetigo, cellulitis, erysipelas, and necrotizing fasciitis.59	Catecholamines enhance growth likely by increasing iron availability.2,68

Stress mediators can alter bacterial physiology and increase virulence. This shift from a nonpathogenic to a pathogenic state can result in delayed or stalled wound healing responses and infection.

AMP, antimicrobial peptide; hBD, human β-defensin; PSM, phenol-soluble modulin; TLRs, toll-like receptors.