Academic onefile – document – microbiota in healthy skin and in atopic eczema hypoxia and anoxia

The italian interest group (IG) on atopic eczema and urticaria is

Member of the italian society of allergology and immunology. The aim of our

IG is to provide a platform for scientists, clinicians, and experts. In this

Review we discuss the role of skin microbiota not only in healthy skin but

Also in skin suffering from atopic dermatitis (AD). A medline and embase

Search was conducted for studies evaluating the role of skin microbiota. We

Examine microbiota composition and its development within days after birth;

We describe the role of specific groups of microorganisms that colonize

Distinct anatomical niches and the biology and clinical relevance of

Antimicrobial peptides expressed in the skin. Specific AD disease states are

hypoxia and anoxia

Characterized by concurrent and anticorrelated shifts in microbial diversity

And proportion of staphylococcus. These organisms may protect the host,

Defining them not as simple symbiotic microbes but rather as mutualistic

Microbes. These findings reveal links between microbial communities and

Inflammatory diseases such as AD and provide novel insights into global

Shifts of bacteria relevant to disease progression and treatment. This review

Also highlights recent observations on the importance of innate immune

Systems and the relationship with normal skin microflora for the maintenance

Of healthy skin.

Every square centimeter of skin contains approximately 1 billion

Bacteria, including hair follicles and sebaceous glands [3].Hypoxia and anoxia these microbial

Communities are intimately involved in human welfare and disease [4-6]. In

2008 the national institutes of health launched the human microbiome project

With the aim of generating the resources and expertise needed to characterize

The human microbiome and analyze its role in health and disease. It focused

On studying the microbes residing in five body areas (skin, nose, mouth,

Stool, and vagina) in 250 normal adult volunteers [7]. Over

11,000 human specimens were obtained. Scientists then purified and sequenced

The DNA from them and used information from the bacterially encoded 16S

Ribosomal RNA gene to identify and quantify the relative abundance of

Bacteria in each sample. In the microbial communities residing at different

hypoxia and anoxia

Body sites four major groups, or phyla, were detected: firmicutes,

Actinobacteria, bacteroidetes, and proteobacteria. Specific groups of

Microorganisms colonize distinct anatomical niches: the most numerous

Microbes are well-defined resident flora. They are constantly present on body

Surfaces and may prevent colonization by pathogens and possible disease,

Restoring the ecological skin niches. Commensal microorganisms are in

Mutualistic symbiosis: they contribute to human health and welfare through

The production of defense molecules or natural antibiotics. Transient skin

Flora can temporarily colonize the skin: these microorganisms are unable to

Remain in the body for a long period of time due to competition from resident

hypoxia and anoxia

Microbes. They persist on the skin for a few hours or days and are not

Pathogenic under normal conditions (normal immune responses, skin barrier

Function intact).

Molecular analysis of the skin bacterial microbiota also revealed

That its temporal variability depends on the body site [16, 17]. In healthy

Individuals the most consistent sites with respect to community membership

And structure are the external auditory canal, inguinal crease, alar crease,

And nare, whereas there is a significant variation on the second sampling of

The popliteal fossa, volar forearm, and buttock, which suggests that

Longitudinal stability of the skin microbiome is site dependent. In general,

Contralateral sites on the same individual are more similar to each other

hypoxia and anoxia

Than to a corresponding site on another individual [18]. Although there was a

Core set of bacterial taxa commonly found on the palm surface, there is a

Pronounced intra- and interpersonal variation in bacterial community

Composition: hands from the same individual shared only 17% of their

Phylotypes, with different individuals sharing a mere 13%. Moreover,

Bacterial population profile analysis showed that the bacterial communities

On human hands were different according to the country considered [19]. Women

Had significantly higher diversity than men and community composition was

Significantly affected by handedness, time since last hand washing, and the

Individual’s sex [20].

3.3. The role of staphylococcus epidermidis.Hypoxia and anoxia the multilayered

Structure of skin reflects the complexity of its multifunctional activities.

The skin is a physical and chemical barrier between the outside environment

And the tissues inside the body; the skin is one of several organ systems

Participating to the maintenance of a core temperature; the skin acquires

Sensory information from the environment and relies on innate defense

Mechanisms inducing the release of antimicrobial peptides (amps) such as

Cathelicidin LL37 orbeta-defensins. These antimicrobial peptides, which are

Synthesized in the skin at sites of potential microbial entry, provide a

Soluble barrier that acts as an impediment to infection. Recent studies have

Revealed that our skin’s innate immune system is not solely of human

hypoxia and anoxia

Origin. The commensal microbes themselves produce antimicrobial peptides

(amps) able to increase the production of amps by keratinocytes. Thus the

Skin helps to maintain homeostasis by suppressing excess cytokine release

After minor epidermal injury [23]. The unique peptides, phenol-soluble

Modulin (PSM)[gamma] and PSM[delta] produced by staphylococcus epidermidis

(S. Epidermidis), could be beneficial to the host and thus serve as

Additional amps on normal skin surface. These peptides possess two opposite

Sides organized by their hydrophobic and cationic amino acids with a

Five-amino acid periodicity, a strategy for the action of both a hydrophilic

And hydrophobic molecule that resembles that of classic amps such as LL-37.Hypoxia and anoxia

These peptides selectively exhibited bactericidal activity against skin

Pathogens, such as staphylococcus aureus (S. Aureus), group A streptococcus

(GAS), and escherichia coli, whereas they are not active against S.

Epidermidis. This selective activity is likely to be an important part of a

Normal microbial defense strategy against colonization and in maintaining the

Normal microbial ecosystem [24].

Staphylococcus epidermidis is a gram-positive bacterium and it

Comprises more than 90% of the aerobic resident flora. Recent studies can be

Interpreted to suggest that S. Epidermidis is a mutualistic organism, much

Like the bacteria in the gut [25]: the bacteria primarily infect compromised

Patients. Many strains of S.Hypoxia and anoxia epidermidis produce lantibiotics, which are

Lanthionine containing antibacterial peptides, also known as bacteriocins.

The several identified bacteriocins include epidermin, epilancin K7,

Epilancin 15X, pep5, and staphylococcin 1580 [26-28]. The host epidermis

Permits S. Epidermidis growth as the bacterium may provide an added level of

Protection against certain common pathogens, making the host-bacterium

Relationship one of mutualism. Many strains of S. Epidermidis produce

Antibacterial peptides (10 KE) that amplify the keratinocyte response to

Pathogens via TLR2. In fact, S. Epidermidis plays an additional protective

Role by influencing the innate immune response of keratinocytes through

Toll-like receptors (tlrs) signaling maintenance of the skin barrier function

hypoxia and anoxia

And integrity. Activation of TLR-2 by S. Epidermidis enhances the expression

Of tight junctions and decreases the production of proinflammatory cytokines

Via TLR3 in the keratinocyte cultures [29, 30]. Through cell

Priming, keratinocytes are able to respond more effectively and

Efficiently to pathogenic insults [31].

Biological control might be a new possible way of controlling

Staphylococcus aureus in body surfaces. Colonization of body surfaces

(especially in the nose) by S. Epidermidis impairs the establishment of S.

Aureus. It was discovered that there are two different strains of S.

Epidermidis, one that inhibits biofilm formation by S. Aureus, S. Epidermidis

Strain JK16 (inhibitory type), and one that does not (noninhibitory type), S.Hypoxia and anoxia

Epidermidis strain JK11 [32, 33]. In vivo studies have shown that

Esp-secreting S. Epidermidis eliminates S. Aureus nasal colonization [34]. In

Fact, the serine protease esp [35-37] secreted by a subset of S. Epidermidis,

A commensal bacterium, inhibits biofilm formation and nasal colonization by

S. Aureus, a human pathogen. Epidemiological studies have demonstrated that

The presence of esp-secreting S. Epidermidis in the nasal cavities of human

Volunteers correlates with the absence of S. Aureus. Purified esp inhibits

Biofilm formation and destroys preexisting S. Aureus biofilms. Furthermore,

Esp enhances the susceptibility of S. Aureus in biofilms to immune system

Components through human beta-defensin2 (hbd2).Hypoxia and anoxia this is due to an

Amensalistic relationship between these microorganisms, the inhibitory strain

Of S. Epidermidis and S. Aureus [38].

The biology of nasal colonization with S. Aureus is not fully

Understood. A variety of bacterial factors have been deemed important for the

Maintenance of colonization of the human nasal cavity by S. Aureus. In

Addition, environmental factors, as well as host factors of the immune

Status, are thought to play a pivotal role in determining the S. Aureus nasal

Carrier state. Several glucocorticoid receptor (GR) gene polymorphisms are

Thought to be functional and have been described as associated also with

Variation in glucocorticoid sensitivity. Consequently, changes in

Glucocorticoid sensitivity may predispose to or protect from microbial

hypoxia and anoxia

Colonization or infection on the one hand or autoimmune disease on the other.

For example, homozygous presence of haplotype 3 conferred a 68% lower risk of

Persistent S. Aureus nasal carriage. Carriers of haplotype 5 were at an

Increased risk of persistent S. Aureus carriage. People with the genotypic

Combination of haplotype 1 and this haplotype allele had an 80% higher risk

Of persistent S. Aureus carriage than all other genotypes [41]. Syed et al.

Demonstrated a novel environmental factor that can influence the ability of

S. Aureus to bind to surfaces altering S. Aureus nasal colonization. In fact,

They showed that the biocide triclosan is commonly found in the nasal

Secretions of healthy adults and the presence of triclosan has a positive

hypoxia and anoxia

Trend with nasal colonization by S. Aureus [42].

Atopic dermatitis is a chronic, relapsing, and intensely pruritic

Inflammatory skin disorder; specific AD disease states are characterized by

Concurrent and anticorrelated shifts in microbial diversity and proportion of

Staphylococcus. There is a strong association between worsening disease

Severity and lower skin bacterial diversity. AD flares are characterized by

Low bacterial diversity in the absence of recent treatment. In contrast,

Intermittent or active treatment is associated with higher bacterial

Diversity. S. Aureus is observed during disease flares; the use of AD

Treatments modifies microbial diversity and proportions of staphylococcus.

Antimicrobial or anti-inflammatory medications decreased S.Hypoxia and anoxia aureus

Predominance, affecting bacterial diversity during flares. Consistent and

Continued treatment over a period of time is required to induce the resolving

Flare stage, which transides into a restoration of full microbial diversity

And low population levels of staphylococcus, typical of a true postflare.

Increases in the proportion of staphylococcus and reductions in microbial

Diversity precede the worsening of AD disease severity as observed in

No-treatment flares [49].