Regulatory RNA Controls for Virulence in Staphylococcus aureus
By Zachary Baker
Introduction
Staphylococcus aureus is a gram-positive bacteria that is naturally found in the nasal cavity of many individuals as a commensal member of the nose microbiome. On certain occasions, most notably in clinical settings in which patients may have weakened immune systems or have recently experienced medical procedures, S. aureus may abnormally enter other parts of the body and cause dangerous infections [1]. S. aureus is the most common cause of Staphylococcal infections and the primary treatment to combat infection with S. aureus is the use of antibiotics such as methicillin [2]. A growing concern regarding the treatment of infection by S. aureus and other bacteria is the increasing presence of antibiotic resistant strains of bacteria in medical settings, an issue that can be partially and temporarily addressed through the development of novel antibiotics [3]. In order to develop effective antibiotics and better control bacterial infections, we must understand the mechanisms that control and contribute to the virulence of bacteria such as S. aureus. One such method of virulence control is the use of regulatory RNA molecules to control the expression and activity of virulence factors in bacteria.
Virulence in Staphylococcus aureus
Staphylococcus aureus infections are characterized by a number of virulence factor proteins that contribute to its pathogenic success. Adherence factors, or adhesins, facilitate the attachment of S. aureus to the host extracellular matrix. Adherence factors related to S. aureus infections are known as microbial surface components recognizing adhesive matrix molecules and are thus a part of the MSCRAMM family of protein adhesins (4). A much broader group of proteins known as exoproteins are also produced by S. aureus to be secreted during infection; such proteins include exotoxins and enzymes that tend to assist in the infection cycle while harming the host organism. Cytolytic proteins released by S. aureus lead to pore formation in host cells, causing cell leakage and eventually cell lysis (5). Another notable group of exotoxins produced by S. aureus is the superantigens: antigenic molecules that bypass the typical immune system antigen recognition process, leading to an influx in T cell proliferation and cytokine release that leads to an immune system overresponse and thus toxic shock (6). S. aureus also produces a number of exoproteins, such as the FLIPr and CHIPS proteins, that inhibit the immune system’s ability to respond to the S. aureus infection (7).
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References
- ↑ [Staphylococcus aureus in Healthcare Settings. (2011, January 17). Centers for Disease Control and Prevention. Retrieved March 16, 2021, from https://www.cdc.gov/hai/organisms/staph.html]
- ↑ [Staphylococcal Infections. (2016, August 25). MedlinePlus. Retrieved March 16, 2021, from https://medlineplus.gov/staphylococcalinfections.html]
- ↑ [Cohen, M. (1992). Epidemiology of Drug Resistance: Implications for a Post-Antimicrobial Era. Science, 257(5073), 1050-1055. Retrieved March 16, 2021, from http://www.jstor.org/stable/2879831l]
- ↑ 4.0 4.1 Hodgkin, J. and Partridge, F.A. "Caenorhabditis elegans meets microsporidia: the nematode killers from Paris." 2008. PLoS Biology 6:2634-2637.
- ↑ Bartlett et al.: Oncolytic viruses as therapeutic cancer vaccines. Molecular Cancer 2013 12:103.
Authored for BIOL 238 Microbiology, taught by Joan Slonczewski, 2021, Kenyon College.
