br Propionibacterium acnes P acnes an
Propionibacterium acnes P. acnes, an opportunistic pathogen that plays an important role in the progression of inflammatory acne vulgaris, are ubiquitously present within the sebaceous follicles of the human skin. These acne-causing bacteria are usually gram positive, nonmotile, fat splitting microorganisms, having the ability to grow under different oxygen tensions. Being an exclusive occupant of the follicular canal, when clogging of hair follicle happens the bacterium aids in the rupturing of the follicular walls, using their secretory enzymes with degradative properties (Figure 1). These bacterium also target other skin cells, namely, keratinocytes and phagocytic beta-lactamase like macrophages, stimulating the cells to produce proinflammatory cytokines, including interleukin (IL)-1β, IL-8, IL-12, and tumor necrosis factor-α, leading in the inflammatory acne disease. The genomic information clearly highlights that the products of the P. acnes have a major impact on the acne process, but not the invasiveness of the organism. The notable virulence genes involved in the pathogenesis of acne are camp5, gehA, tly, sialidases, neuraminidases, endoglycoceramidases, lipases, and hemolysins (Tables 1 and 2). The lipoglycan-based cell envelope and their extracellular secreted lipase, particularly triacylglycerol lipase, encoded by the gehA gene assists in the adherence and the colonization of the bacterium to the sebaceous follicle. The other product which aids in the acne process by destroying the host tissue includes porphyrins, hyaluronate lyase, endoglycoceramidase, sialidases/neuramidase, cardiolipin synthetase, and calicineurin like phosphoesterase (Tables 1 and 2). The organism further possesses several proteins associated with cell invasion, which are secreted by genes, namely PAmce, PAp60, and cell surface antigen, which are produced by htaA and hsp20. These help the pathogen to invade the host cell further and makes it highly immunoreactive, thereby establishing high virulencity. It is logical to think at what point the virulence factors secreted/produced fulfil the functions of the microorganism turn out to be dangerous for the host, which is actually a skin commensal.
Staphylococcus epidermidis S. epidermidis is a facultative anaerobe of cutaneous microbiota harbored in acne lesions. These microbes which are nonpathogenic resident flora of the human skin at some point of life turns into an infectious agent due to extrinsic factors like an immune system deficiency. The first and foremost virulence factor produced by this organism is fatty acid modifying enzyme which esterifies the fatty acids in the skin to cholesterol, as fatty acids are bactericidal for the organism to survive. The bacterium possesses several adhesion factors for its attachment to the skin surface, like surface anchored proteins, fibrinogen binding protein, autolysin protein, PIA, and poly-N-succinyl-glucosamine, helping as a probable attachment factor. The potentially virulent S. epidermidis also has the ability for biofilm formation and is a reservoir of antibiotic resistance genes, which get horizontally transferred to other organisms. In the process of acne development, the lipases (geh1 gene) and the delta-haemolysin (hld gene) are two virulence factors that have an impact in acne inflammation (Tables 1 and 2). Although they have such virulence characteristics, they have been found to rarely damage the keratinocytes in the skin. This has shown that S. epidermidis secreted the exopolysaccharide intercellular adhesin (PIA), which is responsible for biofilm formation and protects them against major components of human innate host defence. This biofilm provides the favorable anaerobic conditions to grow P. acne in an easy manner. According to Pathak et al., the population of S. epidermidis and P. acnes were found to be increased by ∼70% and ∼82%, respectively, in acne patients compared with controls. The microbial load of these microbes was found to be increased simultaneously in the case of acne, which indicates some important role of these two bacterium in the development and regulation of acne disease. On the basis of above evidence, we can say that S. epidermidis plays an important role in acne pathogenesis not in a direct manner but in an indirect manner. Therefore, it might be assumed that S. epidermidis strains secrete virulence factors to a certain extent, but the beneficial activity of the microorganism should also be considered. Being found to occur in massive loads in acne patients compared with normal human skin raises a question whether they are the source of disease or defense. A potential research including RNA sequencing and quantitative whole-cell proteome analysis of S. epidermidis as well as affected tissue at different stages of disease development might help to better understand the role of this bacterium in acne pathogenesis.