Human skin can be an inhospitable environment that is characterized by large desiccated regions, acidic pH, and continual shedding of superficial skin cells. Host skin defense includes molecules such as proteases, lysozymes, and antimicrobial peptides [26
]. Despite these protective mechanisms, microorganisms survive and thrive.
The topography of human skin varies at a microscopic as well as a macroscopic level (). The skin surface is uneven with lines, ridges, and invaginations from skin appendages. Appendageal structures such as hair follicles, sebaceous glands, nails, and apocrine and eccrine sweat glands result in skin infoldings of differing depths beneath the top skin layer. Sebaceous glands produce sebum that spills into hair follicles and coats hair and adjacent skin. Apocrine sweat glands are localized to the scalp, armpits, and groin and excrete a fatty substance that is broken down by bacteria to cause an odor. Eccrine sweats glands are ubiquitous with especially high density on the scalp, palms, and soles. Eccrine sweat is a salty fluid that upon evaporation helps cool the body. Each invagination provides a distinct reservoir where bacteria flourish and repopulate the skin surface.
Figure 2 Representation of human skin. The topographical surface of human skin is irregular and consists of multiple skin appendageal structures including hair follicles, sebaceous (oil) glands, and sweat glands and ducts. Each of the skin appendages provides (more ...)
On a macroscopic level, the human skin surface is comprised of a variety of unique regions: plateaus such as forearm and back, prominences including elbow and shoulder, and crevices (e.g. ear canal and toe web). Additionally, the distribution of skin appendages is non-uniform over the skin surface. For example, there is variable hair density on the scalp, nose, and forearms; greater humidity in the armpit; and increased sebaceous (oily) skin on the face, chest, and upper back. The thickness of the epidermis and dermis also varies over the body surface and affects skin texture and pliability. The irregular topography and additional different skin site characteristics provide distinctive habitats for bacteria.
Many other elements potentially contribute to the composition of the microbial communities residing on and in skin. External factors such as ambient humidity, seasonal weather conditions, prior antibiotic treatments, clothing types, use of lotions/creams, cleansers, or deodorants/antiperspirants, hygiene frequency, and other environmental surfaces [27
] interact with and can influence cutaneous bacteria. Intrinsic factors such as age, genetic makeup, and host immune system also influence the composition of skin microorganisms. These factors may result in interindividual skin microbiome differences. A challenge for metagenomics will be to determine how much interpersonal variation of skin microbiomes differentially impacts human hosts. A portion of the variance observed in skin microbiomes may result from the presence of different species of skin microorganisms that exhibit functional redundancy.
Bacterial skin populations can be categorized as transient (contaminant, non-reproducing), temporary resident (not typically resident, yet can colonize), and resident (growing, reproducing) flora [28
]. The ‘normal’ resident skin flora includes Propionibacteriumacnes, Staphylococcus epidermis
, Staphylococcus aureus, Corynebacterium diphtheria
, Corynebacterium jeikeium
, and Pseudomonas aeruginosa
, as determined by traditional cultivation methods [26
]. The roles of resident bacteria on human skin are highly varied and incompletely understood.
Resident skin bacteria can be beneficial to humans; some are thought to defend against pathogenic bacteria [30
]. Staphylococcus aureus
is a common pathogen -- approximately 20-30% of healthy individuals are asymptomatic nasal carriers [31
] -- that can cause both localized and systemic infections. Some bacteria, including Staphylococcus epidermis
] and Corynebacterium
spp., can inhibit or reverse S. aureus
colonization of human nares. A subset of S. epidermis
, which secrete the serine protease Esp, inhibited S. aureus
when introduced into the nasal cavities of carriers [3
]. Furthermore, a small molecule produced by S. epidermidis
induced antimicrobial peptide expression in mice with associated reduction in susceptibility to group A Streptococcus
skin infections [35
In addition to protecting human hosts, microbes have been implicated in the pathogenesis and/or clinical course of several skin diseases, including seborrheic dermatitis (Malassezia spp.) and atopic dermatitis (Staphylococcus aureus). Although not considered skin infections, clinical management of such disorders routinely includes the use of antimicrobial agents. Skin disease in general may result from a resident microorganism becoming pathogenic under particular conditions or from newly established colonization by a typically pathogenic microbe. Cutaneous disorders often present in a specific distribution pattern which can aid in diagnosis. For example, seborrheic dermatitis is characterized as greasy white-yellow scales affecting oily areas such as the scalp, creases of the nose, and the external ear canal. In contrast, atopic dermatitis typically presents with scaly and itchy red rashes on the antecubital (inner bend of the arm) and popliteal (behind the knees) creases as well as the folds behind the ears. It is possible that skin diseases presenting at particular anatomical sites are related to the skin physiologic characteristics, such as whether it is oily or moist, or even the bacteria that preferentially reside at those specific skin sites. Understanding how microbes contribute to skin diseases requires a greater understanding of the human skin microbiome, and much recent work has been done in the area of the bacterial microbiome.