The majority of staphylococci produce biofilm on medical devices, which is the main mechanism to infect humans. Staphylococcal biofilms attach to abiotic or biotic surfaces, forming aggregates and protecting themselves against the immune system and the antimicrobial compounds of the host. Few studies on biofilm formation mechanism in Staphylococcus epidermidis and other coagulase-negative staphylococci (CNS) have been performed; however, there is a great interest in studying and controlling biofilm formation of this genus. This chapter exhibits the state of the art on biofilm formation in S. epidermidis and other staphylococcal species. The main goal of this chapter is to recognize the importance of biofilm formation in Staphylococcus. The participating molecules in staphylococcal biofilm formation are described. Currently, biofilm producer strains of Staphylococcus and mainly CNS have been frequently isolated at hospitals, causing significant economic losses. This chapter includes promising solutions in order to prevent medical device-associated infections, as the development of medical devices possessing anti-biofilm materials or surfaces that act against the adhesion or viability of the microorganisms.
Part of the book: Microbial Biofilms
Staphylococcus aureus is a commensal bacterium that causes infections such as sepsis, endocarditis, and pneumonia. S. aureus can express a variety of virulence factors, including surface proteins. Surface proteins are characterized by presence of a Sec‐dependent signal sequence at the amino terminal, and the sorting signal domain. Surface proteins are covalently attached to peptidoglycan and they are commonly known as cell wall–anchored (CWA) proteins. CWA proteins have many functions and participate in the pathogenesis of S. aureus. Furthermore, these proteins have been proposed as therapeutic targets for the generation of vaccines. In this chapter, different topics related to CWA proteins of S. aureus are addressed. The molecular structure of CWA proteins and their role as virulence factors of S. aureus are described. Furthermore, the involvement of CWA proteins in the processes of adhesion, invasion of host cells and tissues, evasion of the immune response, and the formation of biofilm is discussed. In addition, the role of CWA proteins in skin infection and the proposal to use them as potential vaccine antigens are described. The information contained in this chapter will help the readers to understand the biology of CWA proteins and to recognize the importance of surface molecules of S. aureus.
Part of the book: The Rise of Virulence and Antibiotic Resistance in Staphylococcus aureus
Psoriasis is a skin disease mainly developed in humans, although it is also seen in monkeys and dogs. Animal models with psoriasis-like lesions have been a key factor for its understanding. Xenotransplants of human psoriatic skin in immunodeficient mice were the first approach for the association of immunologic problems with the development of psoriasis and have been also useful for the evaluation on new therapeutic agents. Imiquimod-induced murine psoriasis is nowadays one of the most used animal models to study this disease, perhaps because healthy wild-type mice are used, which means that it is an affordable model, easy to generate, and, more importantly, resembles the inflammatory, angiogenic and hyperproliferative characteristics of human psoriasis. Several transgenic (over-expressing VEGF, Tie2, TGFβ, STAT3, IL-36, PPARβ/γ) and knockout (lacking IκBα, JunB, IFNR-2, IL-36RA, CD18, IKK2) mice have been useful for the association of specific molecules for the development of psoriasis. Other approach has been the use of both transgenic/knockout mice and imiquimod treatment, where the importance of βTrCP, IκBζ, IL-35 and Tnip1 for the development of psoriasis was found. In this chapter, some of these animal models are discussed.
Part of the book: Psoriasis