What does this research mean for the field?

Targeting the Candida albicans Als3 adhesin offers a unique therapeutic strategy capable of simultaneously disrupting both the fungal and bacterial components of recalcitrant oral polymicrobial biofilms. Novelty: ClaimNovelty.SYNTHESIS. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To review the structural and regulatory mechanisms governing Candida albicans Als3-mediated polymicrobial biofilm formation and evaluate therapeutic strategies targeting this adhesin.

September 10, 2026Critical Reviews in Microbiology

Targeting the Candida albicans agglutinin-like sequence 3 adhesin to disrupt oral polymicrobial bacterial–fungal biofilms: mechanisms and therapeutic strategies

View Full Paper

Ask AI

Bookmark

Authors

AJAqib Javaid NTNazia Tabassum YSYashfeen Munib Siddiqui

Discussion

Member takes

Overview

Narrative review reveals Als3-driven co-aggregation in oral polymicrobial biofilms, highlighting targeted anti-adhesin therapies as a dual-action approach against antimicrobial tolerance.

Key Points

To review the structural and regulatory mechanisms governing Candida albicans Als3-mediated polymicrobial biofilm formation and evaluate therapeutic strategies targeting this adhesin.
Analyzed the molecular architecture, domain organization, and regulatory pathways of the Als3 hypha-specific adhesin.
Examined molecular binding mechanisms between Als3 and bacterial adhesins, including staphylococcal MSCRAMMs, streptococcal antigen I/II, and Porphyromonas gingivalis InlJ.
Synthesized preclinical and clinical evidence for anti-Als3 interventions, including vaccines, monoclonal antibodies, competitive peptides, and small-molecule inhibitors.
Als3 serves as the primary structural scaffold facilitating bacterial–fungal co-aggregation via its N-terminal peptide-binding cavity and amyloid-forming region.
Co-biofilms dependent on Als3 exhibit amplified antimicrobial tolerance, architectural complexity, and interkingdom metabolic cooperation compared to single-species biofilms.
Interventions targeting Als3, including the NDV-3A vaccine and peptide or small-molecule inhibitors, simultaneously disrupt fungal adhesion and bacterial colonization within oral biofilms.

Cite This Study

Javaid et al. (2026) studied this question.

synapsesocial.com/papers/6aa27ab158559d80afc736d1 https://doi.org/10.1080/1040841x.2026.2727092

View Full Paper

Ask AI

Bookmark

September 10, 2026Critical Reviews in Microbiology

Targeting the Candida albicans agglutinin-like sequence 3 adhesin to disrupt oral polymicrobial bacterial–fungal biofilms: mechanisms and therapeutic strategies

View Full Paper

Ask AI

Bookmark

Authors

AJAqib Javaid NTNazia Tabassum YSYashfeen Munib Siddiqui

Discussion

Member takes

Overview

Narrative review reveals Als3-driven co-aggregation in oral polymicrobial biofilms, highlighting targeted anti-adhesin therapies as a dual-action approach against antimicrobial tolerance.

Key Points

To review the structural and regulatory mechanisms governing Candida albicans Als3-mediated polymicrobial biofilm formation and evaluate therapeutic strategies targeting this adhesin.
Analyzed the molecular architecture, domain organization, and regulatory pathways of the Als3 hypha-specific adhesin.
Examined molecular binding mechanisms between Als3 and bacterial adhesins, including staphylococcal MSCRAMMs, streptococcal antigen I/II, and Porphyromonas gingivalis InlJ.
Synthesized preclinical and clinical evidence for anti-Als3 interventions, including vaccines, monoclonal antibodies, competitive peptides, and small-molecule inhibitors.
Als3 serves as the primary structural scaffold facilitating bacterial–fungal co-aggregation via its N-terminal peptide-binding cavity and amyloid-forming region.
Co-biofilms dependent on Als3 exhibit amplified antimicrobial tolerance, architectural complexity, and interkingdom metabolic cooperation compared to single-species biofilms.
Interventions targeting Als3, including the NDV-3A vaccine and peptide or small-molecule inhibitors, simultaneously disrupt fungal adhesion and bacterial colonization within oral biofilms.

Cite This Study

Javaid et al. (2026) studied this question.

synapsesocial.com/papers/6aa27ab158559d80afc736d1 https://doi.org/10.1080/1040841x.2026.2727092

View Full Paper

Ask AI

Bookmark