Virulence of Enterococcus faecalis and Impact of Genome‐wide approaches

2011 ◽  
Vol 1 (1) ◽  
pp. 16-24
Author(s):  
Rakesh Kumar Patidar ◽  
Mithilesh Kumar Gupta ◽  
Vinod Singh
Keyword(s):  
Immune Response ◽  
Enterococcus Faecalis ◽  
Virulence Factors ◽  
Host Immune Response ◽  
Oral Infection ◽  
Bacterial Virulence ◽  
Host Defenses ◽  
Opportunistic Pathogens ◽  
New Therapies

Enterococci are well recognized opportunistic pathogens in human and animal infections. Enterococcus faecalis have attracted much attention in recent times due to their increased recognition as an oral infection. The severity of these infections depends on the host immune response and on the presence of virulence factors. Bacterial virulence factors enable a host to replicate and disseminate within a host in part by subverting or eluding host defenses. Application of genome‐wide approaches has led to the identification of new virulence factors that may serve as targets for new therapies. This review discusses the virulence factors of E. faecalis and impact of genome‐wide approaches.

scholarly journals Enterococcus faecalis Glycolipids Modulate Lipoprotein-Content of the Bacterial Cell Membrane and Host Immune Response

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0132949 ◽  
Author(s):  
Christian Theilacker ◽  
Ann-Kristin Diederich ◽  
Andreas Otto ◽  
Irina G. Sava ◽  
Dominique Wobser ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Membrane ◽  
Enterococcus Faecalis ◽  
Bacterial Cell ◽  
Host Immune Response ◽  
Bacterial Cell Membrane ◽  
Lipoprotein Content

scholarly journals Brucella Hijacks Host-Mediated Palmitoylation To Stabilize and Localize PrpA to the Plasma Membrane

2018 ◽  
Vol 86 (11) ◽  
Author(s):  
Juan M. Spera ◽  
Francisco Guaimas ◽  
María M. Corvi ◽  
Juan E. Ugalde
Keyword(s):  
Immune Response ◽  
Plasma Membrane ◽  
Host Cell ◽  
Virulence Factors ◽  
Cell Activity ◽  
Host Immune Response ◽  
Content Type ◽  
Cell Plasma ◽  
The Individual ◽  
Cellular Immune

ABSTRACT Brucellaceae are a group of pathogenic intracellular bacteria with the ability to modulate the host response, both at the individual cell level and systemically. One of the hallmarks of the virulence process is the capacity of the bacteria to downregulate the adaptive and acquired host immune response through a plethora of virulence factors that directly impact several key signaling cascades. PrpA is one of those virulence factors that alters, via its polyclonal B-cell activity, the humoral and cellular immune responses of the host, ultimately favoring the establishment of a chronic infection. Even though PrpA affects B cells, it directly targets macrophages, triggering a response that ultimately affects B lymphocytes. In the present article we report that PrpA is S-palmitoylated in two N-terminal cysteine residues by the host cell and that this modification is necessary for its biological activity. Our results demonstrate that S-palmitoylation promotes PrpA migration to the host cell plasma membrane and stabilizes the protein during infection. These findings add a new mechanism exploited by this highly evolved pathogen to modulate the host immune response.

scholarly journals On Commensalism of Candida

2020 ◽  
Vol 6 (1) ◽  
pp. 16 ◽  
Author(s):  
Jesus A. Romo ◽  
Carol A. Kumamoto
Keyword(s):  
Immune Response ◽  
Candida Species ◽  
Fungal Pathogens ◽  
Current Knowledge ◽  
Host Immune Response ◽  
Opportunistic Pathogens ◽  
Disease Manifestation ◽  
Pathogenic Potential ◽  
Gastrointestinal Epithelium ◽  
Epithelial Barriers

Candida species are both opportunistic fungal pathogens and common members of the human mycobiome. Over the years, the main focus of the fungal field has been on understanding the pathogenic potential and disease manifestation of these organisms. Therefore, understanding of their commensal lifestyle, interactions with host epithelial barriers, and initial transition into pathogenesis is less developed. In this review, we will describe the current knowledge on the commensal lifestyle of these fungi, how they are able to adhere to and colonize host epithelial surfaces, compete with other members of the microbiota, and interact with the host immune response, as well as their transition into opportunistic pathogens by invading the gastrointestinal epithelium.

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