Microbial barrier, skin

Narang et al. (2003) reported that 2-octylcyanoacyrlate-based films are excellent microbial barriers. Dermabond Topical Skin Adhesive and Liquid BandageR are... 

Propionibacterium acnes, commonly isolated from the skin, is the most frequently found anaerobe. Factors and conditions such as blepharitis, dry eye syndrome, meibomian gland dysfunction, and contact lens use may influence the composition of the normal flora or cause disruption to normal epithelial microbial barriers, either of which can lead to disease in susceptible patients. Although immunocompromised individuals may harbor Candida albicans, fungi are considered opportunistic pathogens. Little evidence supports the existence of any indigenous fungi in the normal conjunctival flora. 

Bhende, S., Rothenburger, S., Spangler, D.J., Dito, M., 2002. In vitro assessment of microbial barrier properties of Dermabond topical skin adhesive. Surg. Infect. 3, 251-257. 

Beyond physical barrier protection, several natural processes lead to skin surface conditions unfavorable to microbial growth. Both sebaceous and eccrine secretions are acidic, lowering the surface pH of the skin below that welcomed by most pathogens. This acid mantle (pH 5) [16] is moderately bacteriostatic. Sebum also contains a number of short-chain fungistatic and bacteriostatic fatty acids, including propanoic, butanoic, hexanoic, and heptanoic acids [17]. That the skin s surface is dry also offers a level of protection. It comes as no surprise that fungal infections and other skin infections are more prevalent in the skin s folds... 

In AD increased S. aureus colonization plays a fundamental role therefore, antistaphylococcal therapy is part of a successful management of the disease. Epidermal lipid deficiencies and barrier dysfunction contribute to enhanced S. aureus attachment to the skin and mediate immunological and inflammatory effects including the release of superantigens, additional exotoxins, and exoenzymes, and perhaps bacterial DNA-triggered mechanisms. Therapeutic possibilities include the use of topical antiseptics in cases of microbial-laden atopic eczema, corticosteroids, and specific antibiotic-antiseptic combinations in cases of localized superinfected atopic eczema and systemic antibiotics in cases of generalized superinfected atopic eczema.48... 

The strongest trigger of inflammation, however, is microbial stimulation. We often forget that the human body carries ten times more bacteria than own cells. The gut contains 1-2 kg of bacteria containing about 50 g of endotoxin (Ernst Rietschel, Borstel, personal communication). Many, especially topical toxicities, include breakdown of skin and mucosal barriers, allowing translocation of bacteria and LPS among others. The contribution to manifestation of irritation by chemicals has to the best of the author s knowledge not been addressed. 

I have already shown several syntheses of sphingolipids as microbial metabolites or marine natural products. Sphingolipids are building blocks of the plasma membrane of eukaryotic cells. Their function is to anchor lipid-bound carbohydrates to cell surfaces, and to construct the epidermal water permeability barrier. The chemistry of sphingolipids is therefore closely related to dermatology or the science of skin. This section first treats sphingolipid in human epidermis. 

The skin is an excellent barrier to microbial and parasitic infections. The most superficial layer of the skin is composed of flattened squamous cells, which are highly keratinized. Beneath this is the epidermal layer composed of cells tightly interconnected by desmosomes and other intercellular structures. These, in turn, are attached to the basement membrane composed of covalently bound or interwoven macromolecules. Between the basement membrane and a target blood vessel is an extracellular matrix rich in type I collagen, elastin and proteoglycan. Elastin and type I collagen are both interwoven fibrillar molecules, whereas the carbohydrate-rich proteoglycan behaves like a hydrated gel. For details of these macromolecular interactions, the reader is referred to reviews on the structure of skin. 

The wall of the small intestine and colon is composed of a columnar epithelial cell layer, often producing a thick mucus coat. This mucus coat can be a barrier to microbial or parasitic invasion from the gut lumen (25). As in the skin, this epithelium... 

Before we discuss how to test removal and destruction of the microbial skin flora, we must determine where the bacteria reside and how bacterial populations are maintained on the skin [6,7]. Gibbs and Stuttard [8] have described the skin as uneven in topology and thickness (Table 1), ridged, with openings of pores and ducts (Fig. 1). The skin may act as a physical barrier, though not as a chemical barrier. Both apocrine and eccrine secretions are vital to the microbial population, as well as repopulation after the removal of superficial flora. 

Topical application of compositions comprising sphingolipids, such as ceramides, improves the barrier function and moisture-retaining properties of the skin. Moreover, sphingoid bases exhibit anti-inflammatory and anti-microbial activities, making sphingolipids valuable active ingredients in cosmetic formulations. " ... 

Adopting a non-leaching antimicrobial that doesn t pose the risk of crossing the skin barrier or negatively affecting the normal microbial flora of the skin If it creates a zone of inhibition or must integrate into the all to have function, it leaches or moves and has the potential to cause problems to people and the environment. 

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