Polysaccharide intercellular adhesin (PIA) protects Staphylococcus epidermidis against major components of the human innate immune system

By C. Vuong, Jovanka M. Voyich, E. Fischer, K. Braughton, Adeline R. Whitney, F. DeLeo, M. Otto. Cellular Microbiology, 2004

645 citations recorded by the source corpus.

The skin commensal and opportunistic pathogen Staphylococcus epidermidis is the leading cause of nosocomial and biofilm‐associated infections. Little is known about the mechanisms by which S. epidermidis protects itself against the innate human immune system during colonization and infection. We used scanning electron microscopy to demonstrate that the exopolysaccharide intercellular adhesin (PIA) resides in fibrous strands on the bacterial cell surface, and that lack of PIA production results in complete loss of the extracellular matrix material that has been suggested to mediate immune evasion. Phagocytosis and killing by human polymorphonuclear leucocytes was significantly increased in a mutant strain lacking PIA production compared with the wild‐type strain. The mutant strain was also significantly more susceptible to killing by major antibacterial peptides of human skin, cationic human β‐defensin 3 and LL‐37, and anionic dermcidin. PIA represents the first defined factor of the staphylococcal biofilm matrix that protects against major components of human innate host defence.

Subfields: Infectious Diseases, Microbiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/675d36bd95227a14c126e90cc008debfdd263075

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Infectious Diseases

In Microbiology

In Molecular Biology

Citations in the corpus

Staphylococcus epidermidis – the “accidental” pathogen (2009, background): “epidermidis from neutrophil killing, complement deposition, immunoglobulins and AMP”
Evolving concepts in biofilm infections (2009, background): “In Staphylococcus epidermidis biofilms, protection from phagocytosis by polymorphic neutrophils (PMNs) and innate immune mechanisms was mediated by the intracellular adhesin, PIA, controlled by the ica locus (Vuong et al., 2004).”
Polymicrobial Interactions: Impact on Pathogenesis and Human Disease (2012, background): “This matrix, often composed of DNA, carbohydrate polymers, and/or proteins, encases the microbial communities, increasing both surface adhesion and protection from host damage and antimicrobial therapy (4, 213).”
Pathogenicity and virulence of Staphylococcus aureus (2021, background): “surface from phagocyte attacks and (ii) contributing to the biofilm network [85,86].”
Bacterial biofilm formation on implantable devices and approaches to its treatment and prevention (2018, background): “epidermidis polysaccharide intercellular adhesion (PIA) antigen plays a role in initial attachment and also protects the proliferating bacteria from polymorphonuclear leukocytes [80].”
Antimicrobial Peptides (2013, background): “These adhesin molecules are polymeric substances and stay on the cell surface after secretion [238].”
Antibiotic resistance and persistence—Implications for human health and treatment perspectives (2020, positive): “…a protective matrix that blocks complement-killing (Domenech et al , 2013), recognition by immune cells (Leid et al , 2002; Jesaitis et al , 2003; Vuong et al , 2004), killing by many antibiotics (Jolivet-Gougeon & Bonnaure-Mallet, 2014) and contains persister cells (Spo-ering & Lewis, 2001;…”
Multidrug tolerance of biofilms and persister cells. (2008, background): “The immune system will be able to mop up remaining planktonic persisters, just as it eliminates nongrowing cells of a population treated with a bacteriostatic antibiotic (Fig. 2 ). However, the biofilm matrix protects against immune cells (Leid et al. 2002; Jesaitis et al. 2003; Vuong et al. 2004 )”
Why chronic wounds will not heal: a novel hypothesis (2008, background): “With regard to antibiotic therapy, there is a lack of evidence concerning optimal regimes or clinical hallmarks for efficient treatment and additionally, biofilm infections are characterized by resistance to the host defenses.(2,19,20) If this is also true for infected chronic wounds, it explains wh”
Persister cells, dormancy and infectious disease (2007, background): “However, the biofilm exopolymer matrix protects against immune cell”
Microbial Biofilm: A Review on Formation, Infection, Antibiotic Resistance, Control Measures, and Innovative Treatment (2023, neutral): “epidermidis polysaccharide intercellular adhesion (PIA) antigen shields the proliferating bacteria against polymorphonuclear leukocytes [51].”
The co-evolution of host cationic antimicrobial peptides and microbial resistance (2006, background): “and the formation of biofilms that are generally refractory to antimicrobial activitie”