Contribution of Choline-Binding Proteins to Cell Surface Properties of
            <i>Streptococcus pneumoniae</i>

Swiatlo, Edwin; Champlin, Franklin R.; Holman, Steven C.; Wilson, W. William; Watt, James

doi:10.1128/iai.70.1.412-415.2002

Cited by 78 publications

(62 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We hypothesize that the incorporation of positive charges on the bacterial cell surface promotes interaction with the negatively charged host cell surface. An analogous situation may exist in Streptococcus pneumoniae, where removal of surface choline-binding proteins was associated with a net increase in negative charge on the bacterial surface and decreased adherence to eukaryotic cells (47).…”

Section: Discussionmentioning

confidence: 99%

d -Alanylation of Teichoic Acids Promotes Group A Streptococcus Antimicrobial Peptide Resistance, Neutrophil Survival, and Epithelial Cell Invasion

Kristian

Datta

Weidenmaier³

et al. 2005

J Bacteriol

222

228

View full text Add to dashboard Cite

Group A streptococcus (GAS) is a leading cause of severe, invasive human infections, including necrotizing fasciitis and toxic shock syndrome. An important element of the mammalian innate defense system against invasive bacterial infections such as GAS is the production of antimicrobial peptides (AMPs) such as cathelicidins. In this study, we identify a specific GAS phenotype that confers resistance to host AMPs. Allelic replacement of the dltA gene encoding D-alanine-D-alanyl carrier protein ligase in an invasive serotype M1 GAS isolate led to loss of teichoic acid D-alanylation and an increase in net negative charge on the bacterial surface. Compared to the wild-type (WT) parent strain, the GAS ⌬dltA mutant exhibited increased susceptibility to AMP and lysozyme killing and to acidic pH. While phagocytic uptake of WT and ⌬dltA mutants by human neutrophils was equivalent, neutrophil-mediated killing of the ⌬dltA strain was greatly accelerated. Furthermore, we observed the ⌬dltA mutant to be diminished in its ability to adhere to and invade cultured human pharyngeal epithelial cells, a likely proximal step in the pathogenesis of invasive infection. Thus, teichoic acid D-alanylation may contribute in multiple ways to the propensity of invasive GAS to bypass mucosal defenses and produce systemic infection.

show abstract

Section: Discussionmentioning

confidence: 99%

d -Alanylation of Teichoic Acids Promotes Group A Streptococcus Antimicrobial Peptide Resistance, Neutrophil Survival, and Epithelial Cell Invasion

Kristian

Datta

Weidenmaier³

et al. 2005

J Bacteriol

222

228

View full text Add to dashboard Cite

show abstract

“…For example, increasing the positive charge of the membrane by D-alanylation of lipoteichoic acids, catalysed by the dlt operon, [20,45] decreases AMP susceptibility. Similarly, deletion of choline-binding proteins, such as LytA, increases pneumococcal susceptibility to AMPs [47]. In addition, pneumococcus can alter its gene-expression as a result of exposure to AMPs and can physiologically increase resistance [48].…”

Section: Discussionmentioning

confidence: 99%

Variation in Streptococcus pneumoniae susceptibility to human antimicrobial peptides may mediate intraspecific competition

2012

View full text Add to dashboard Cite

Streptococcus pneumoniae is a facultative pathogen inhabiting the nasopharynx of humans where it is exposed to a range of antimicrobial peptides (AMPs) of the innate immune response. It is possible therefore that the susceptibility of strains to AMPs plays a role in determining their ability to colonize, and furthermore, that AMPs could mediate competitive interactions between co-colonizing genotypes. However, little is known about patterns of natural variation in AMP susceptibility of S. pneumoniae, and it is unclear whether the susceptibilities of an isolate to multiple human AMPs are correlated. We tested this by characterizing the susceptibility of 31 S. pneumoniae natural isolates to human neutrophil peptide (HNP-1) (a-defensin) and LL-37 (cathelicidin). We observed significant variation in susceptibility between isolates to both AMPs, and in the majority of isolates, susceptibilities to HNP-1 and LL-37 were uncorrelated. Clinical isolates were more susceptible to AMPs than were carriage isolates. The polysaccharide capsule of S. pneumoniae is thought to protect cells against AMPs. However, serotype alone could not explain the observed variation in susceptibility suggesting that genetic background plays an equally important role. We tested directly whether AMPs could mediate competition between isolates using competition experiments in the presence and absence of AMPs. These experiments demonstrated that AMPs could indeed reverse the outcome of competition between selected isolates. AMP-mediated competition could therefore contribute to the maintenance of intraspecific genetic diversity in S. pneumoniae.

show abstract

“…This was confirmed by the results of the CLSM analysis. The cell surface hydrophobicity of microorganisms plays an important role in bacterium-host cell interactions (Swiatlo et al, 2002). Any strategy responsible for reducing the cell surface hydrophobicity and EPS synthesis may affect the development of infection, making the cells more susceptible to antibiotics.…”

Section: Discussionmentioning

confidence: 99%

Lactic acid bacteria protect human intestinal epithelial cells from Staphylococcus aureus and Pseudomonas aeruginosa infections

Affhan¹,

Dachang²,

Xin³

et al. 2015

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT. Staphylococcus aureus and Pseudomonas aeruginosa are opportunistic pathogens that cause nosocomial and food-borne infections. They promote intestinal diseases. Gastrointestinal colonization by S. aureus and P. aeruginosa has rarely been researched. These organisms spread to extra gastrointestinal niches, resulting in increasingly progressive infections. Lactic acid bacteria are Gram-positive bacteria that produce lactic acid as the major end-product of carbohydrate fermentation. These bacteria inhibit pathogen colonization and modulate the host immune response. This study aimed to investigate the effects of Lactobacillus acidophilus and Lactobacillus rhamnosus on enteric infections caused by the paradigmatic human pathogens S. aureus ATCC25923 and P. aeruginosa ATCC27853. The effect of whole cells and neutralized cell-free supernatant (CFS) of the lactobacilli on LoVo human carcinoma enterocyte (ATCC CCL-229) infection was analyzed by co-exposure, pre-exposure, and post-exposure studies. Simultaneous application of whole cells and CFS of the lactobacilli significantly eradicated enterocyte infection (P < 0.05); however, this effect was not seen when the whole cells and CFS 17044-17058 (2015) were added after or prior to the infection (P > 0.05). This result could be attributed to interference by extracellular polymeric substances and cell surface hydrophobicity, which resulted in the development of a pathogen that did not form colonies. Furthermore, results of the plate count and LIVE/ DEAD BacLight bacterial viability staining attributed this inhibition to a nonbacteriocin-like substance, which acted independently of organic acid and H 2 O 2 production. Based on these results, the cell-free supernatant derived from lactobacilli was concluded to restrain the development of S. aureus and P. aeruginosa enteric infections.

show abstract

Contribution of Choline-Binding Proteins to Cell Surface Properties of Streptococcus pneumoniae

Cited by 78 publications

References 27 publications

d -Alanylation of Teichoic Acids Promotes Group A Streptococcus Antimicrobial Peptide Resistance, Neutrophil Survival, and Epithelial Cell Invasion

d -Alanylation of Teichoic Acids Promotes Group A Streptococcus Antimicrobial Peptide Resistance, Neutrophil Survival, and Epithelial Cell Invasion

Variation in Streptococcus pneumoniae susceptibility to human antimicrobial peptides may mediate intraspecific competition

Lactic acid bacteria protect human intestinal epithelial cells from Staphylococcus aureus and Pseudomonas aeruginosa infections

Contact Info

Product

Resources

About