Article

Interaction of Candida albicans cell wall Als3 protein with Streptococcus gordonii SspB adhesin promotes development of mixed-species communities.

School of Oral and Dental Sciences, University of Bristol, Bristol, United Kingdom.
Infection and immunity (Impact Factor: 4.16). 11/2010; 78(11):4644-52. DOI: 10.1128/IAI.00685-10
Source: PubMed

ABSTRACT Candida albicans colonizes human mucosa and prosthetic surfaces associated with artificial joints, catheters, and dentures. In the oral cavity, C. albicans coexists with numerous bacterial species, and evidence suggests that bacteria may modulate fungal growth and biofilm formation. Streptococcus gordonii is found on most oral cavity surfaces and interacts with C. albicans to promote hyphal and biofilm formation. In this study, we investigated the role of the hyphal-wall protein Als3p in interactions of C. albicans with S. gordonii. Utilizing an ALS3 deletion mutant strain, it was shown that cells were not affected in initial adherence to the salivary pellicle or in hyphal formation in the planktonic phase. However, the Als3(-) mutant was unable to form biofilms on the salivary pellicle or deposited S. gordonii DL1 wild-type cells, and after initial adherence, als3Δ/als3Δ (ΔALS3) cells became detached concomitant with hyphal formation. In coaggregation assays, S. gordonii cells attached to, and accumulated around, hyphae formed by C. albicans wild-type cells. However, streptococci failed to attach to hyphae produced by the ΔALS3 mutant. Saccharomyces cerevisiae S150-2B cells expressing Als3p, but not control cells, supported binding of S. gordonii DL1. However, S. gordonii Δ(sspA sspB) cells deficient in production of the surface protein adhesins SspA and SspB showed >50% reduced levels of binding to S. cerevisiae expressing Als3p. Lactococcus lactis cells expressing SspB bound avidly to S. cerevisiae expressing Als3p, but not to S150-2B wild-type cells. These results show that recognition of C. albicans by S. gordonii involves Als3 protein-SspB protein interaction, defining a novel mechanism in fungal-bacterial communication.

0 Bookmarks
 · 
80 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: C. albicans binds various bacteria, including the oral commensal Streptococcus gordonii. Published reports documented the role of C. albicans Als3 and S. gordonii SspB in this interaction, and the importance of the Als N-terminal domain (NT-Als) in C. albicans adhesion. Here, we demonstrate that Als1 also binds S. gordonii. We also describe use of the NT-Als crystal structure to design mutations that precisely disrupt peptide-binding cavity (PBC) or amyloid-forming region (AFR) function in Als3. C. albicans displaying Als3 PBC mutant proteins showed significantly reduced binding to S. gordonii; mutation of the AFR did not affect the interaction. These observations present an enigma: the Als PBC binds free C termini of ligands, but the SspB C terminus is covalently linked to peptidoglycan and thus unavailable as a ligand. These observations and the predicted SspB elongated structure suggest that partial proteolysis of streptococcal cell wall proteins is necessary for recognition by Als adhesins.
    Frontiers in Microbiology 11/2014; 5:564. · 3.94 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: In polymicrobial biofilms a high level of interspecies interactions occur with often detrimental effect to the host. Many chronic infections are attributed to polymicrobial biofilms which tend to exhibit increased resistance to antimicrobial therapy. Yet despite the gravity of such infections, areas of study in polymicrobial diseases are in their infancy. Thus, much work is needed to promote a better understanding of emerging concepts in the biofilm development process such as interspecies communication and host immune response to microbial biofilms. The key challenges are to design effective therapeutic strategies to impede microbial colonization and prevent development of polymicrobial infections. Therefore, future research directions should focus on designing animal model systems to study in vivo-grown polymicrobial biofilms and infections. This review summarizes our limited knowledge about the nature of these complex communities and examines their role in disease, highlighting the challenges and novel approaches that are being pursued to combat polymicrobial biofilms and infections.
    The Open Mycology Journal 06/2011; 5(1).
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The human microbiome contains diverse microorganisms, which share and compete for the same environmental niches [1, 2]. A major microbial growth form in the human body is the biofilm state, where tightly packed bacterial, archaeal, and fungal cells must cooperate and/or compete for resources in order to survive [3-6]. We examined mixed biofilms composed of the major fungal species of the gut microbiome, Candida albicans, and each of five prevalent bacterial gastrointestinal inhabitants: Bacteroides fragilis, Clostridium perfringens, Escherichia coli, Klebsiella pneumoniae, and Enterococcus faecalis [7-10]. We observed that biofilms formed by C. albicans provide a hypoxic microenvironment that supports the growth of two anaerobic bacteria, even when cultured in ambient oxic conditions that are normally toxic to the bacteria. We also found that coculture with bacteria in biofilms induces massive gene expression changes in C. albicans, including upregulation of WOR1, which encodes a transcription regulator that controls a phenotypic switch in C. albicans, from the "white" cell type to the "opaque" cell type. Finally, we observed that in suspension cultures, C. perfringens induces aggregation of C. albicans into "mini-biofilms," which allow C. perfringens cells to survive in a normally toxic environment. This work indicates that bacteria and C. albicans interactions modulate the local chemistry of their environment in multiple ways to create niches favorable to their growth and survival.
    Current biology : CB. 10/2014;

Preview

Download
1 Download
Available from