Introduction Being composed of two primary

Introduction Being composed of two primary layers of mammalian skin—epidermis and dermis—the skin organ represents a formidable barrier providing host skin defense by producing molecules like proteases, lysozymes, and antimicrobial peptides. The skin epidermis forms the outermost layer of the skin which resists microbial penetration and potential toxins inside the body. The dermal skin hosts several substructures like hair follicles, sebaceous glands, apocrine, as well as eccrine sweat glands, thus making the skin surface look uneven, with lines, ridges, and invaginations. The sebaceous glands present in the thick skin produces sebum that spills into the hair follicle. Apocrine sweat glands excrete a fatty substance, whereas eccrine sweat glands produces salty fluid that helps with the maintenance of thermoregulation inside the body. Thus, the skin is predominated by factors such as pH, temperature, moisture, sweat, and sebum content, making it an intricate habitat for a rich tlr inhibitor of microorganisms that outnumbers the human body\'s own cells. Being home to a diverse group of microorganisms, the skin represents a complex ecosystem. From the entire complex microbial diversity of the skin, trillions of bacteria, fungi, and small arthropods have been isolated, identified, and studied using culture-based as well as culture-independent methods. Bacterial species predominating the skin, mainly belong to four phyla: Actinobacteria, Proteobacteria, Bacteroidetes, and Firmicutes out of which over 60% of the bacterial species belong to three genera: Staphylococcus, Corynebacterium, and Propionibacterium. Microbial fluctuations in the skin ecosystem can contribute to perturbation and consequently causes disease. Although microbes protect the human host, they have also been implicated in the pathogenesis of several skin diseases. The pathogenic life cycle of bacteria is mediated by virulence genes encoding virulence factors within their pathogenic islands. The virulence genes, unlike house-keeping genes, are characterized by the production of toxins, adhesins, invasions, or other types of factors, present preferably in the pathogenic microorganisms. These products are directly involved in the pathological damage to the host by promoting interaction between the host and organism and also by damaging and degrading the host tissues. For instance, camp5, gehA, tly, sialidases, neuraminidases, and endoglycoceramidases are some of the virulence factors of Propionibacterium acnes which causes acne vulgaris. Lipases, fatty acid modifying enzyme, polysaccharide intercellular adhesion (PIA), and poly-glutamic acid are the virulence factors in Staphylococcus epidermidis. Adhesins, fibronectin binding protein (FnBp)-A, FnBP-B, proteases, lipases, and hyaluronidases are the virulence factors in Staphylococcus aureus. Thus, each pathogen follows its own pathogenic strategy, with a diverse and unique set of genes/factors operating in a concerted manner to cause disease in the host.
Acne vulgaris Acne vulgaris, a disease affecting the skin\'s oil glands, is one of the most common skin disorders, making a significant number of the human population prone to acne. Although the disease is not life threatening, it affects the quality of life by creating a psychological burden due to the exhibition of diverse lesions on the face, chest, shoulders, and back. The prevalence of acne vulgaris is around 65–75% of teenagers and youths. Accumulation of sebum and dead skin cells within the sebaceous follicle enhances the microbial load, which disrupts the follicular wall resulting in the inflammation of the skin called acne (Figure 1). Sebum production and hormonal changes are the endogenous factors, whereas the change in the activity of the skin microflora is the most contributing factor in the pathogenesis of acne. The microbial flora isolated from acne patients that seems likely to lead to acne pathogenesis includes: P. acnes, S. epidermidis, S. aureus, Klebsiella pneumoniae, Streptococcus, Enterobacter, etc, (Tables 1 and 2).