Bacterial Adhesion And Invasion
Bacterial Adhesion And Invasion - Related Videos
04:36
Assay for Adhesion and Agar Invasion in S. cerevisiae
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Cited by 17 •
2006
We describe a qualitative assay for yeast adhesion and agar invasion as a measure of invasive and pseudohyphal differentiation. This simple assay can be used to assess the invasive phenotype of various mutants as well as the effects environmental cues and signaling pathways on yeast differentiation.
07:15
Invasion of Human Cells by a Bacterial Pathogen
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Cited by 44 •
2011
A general protocol for the study of invasion of host cells by a bacterial pathogen, focusing on Staphylococcus aureus and human endothelial cells.
05:57
In Vitro Assay of Bacterial Adhesion onto Mammalian Epithelial Cells
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Cited by 81 •
2011
This protocol is a simple bacterial adhesion assay consisting in counting the numbers of bacterial colony forming units that are adhered onto cultured cells. The assay is robust, independent of the adhesin studied, and numerous variations are used in most laboratories working on bacterial pathogenesis.
13:28
Introducing Shear Stress in the Study of Bacterial Adhesion
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Cited by 9 •
2011
During the infection process, a key step is the adhesion of pathogens with host cells. In most instances this adhesion step occurs in the presence of mechanical stress generated by flowing liquid. We describe a technique that introduces shear stress as an important parameter in the study of bacterial adhesion.
02:44
In Vitro Gut Model to Assess Bacterial Adhesion and Internalization
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2026
Source: Calatayud Arroyo, M., et al. Assessing the Viability of a Synthetic Bacterial Consortium on the In Vitro Gut Host-microbe Interface. J. Vis. Exp. (2018).This video demonstrates an in vitro gut host–microbe model to study bacterial viability. A co-culture of Caco-2 and HT29-MTX cells is incubated with bacteria pre-treated under simulated digestive conditions. Epithelial barrier integrity is assessed using transepithelial electrical resistance, and fractions from the medium, solubilized...
FAQs
Surface adhesins influence tissue targeting by binding specific receptors on host cells. This receptor-level matching can determine whether bacteria establish contact with a particular host tissue, making adhesion more than a nonspecific physical attachment. In infection research, examining these interactions helps connect bacterial surface factors with colonization patterns and identifies mechanisms that may be vulnerable to anti-adhesion strategies.
Entry into host cells can depend on more than bacterial contact. Invasion may involve secretion systems, host-cell signaling, and cytoskeletal rearrangement, which together promote uptake or penetration of tissue barriers. Studying these events shows how bacterial factors alter host-cell behavior and helps explain how virulence operates at the cellular level during infection.
Cytoskeletal rearrangement can change the physical behavior of a host cell, helping create conditions that permit bacterial uptake or movement across a tissue barrier. This mechanism links microbial interaction with host-cell structure and function. For immunology and infection research, it provides a way to analyze how bacteria overcome cellular defenses without treating entry as a purely passive process.
These interactions influence what the immune system encounters and where bacteria persist during infection. Adhesion can establish bacteria at host surfaces, while invasion can place them within cells or beyond tissue barriers. The resulting location and host-cell response are relevant to immune recognition, intracellular survival, and the subsequent spread of infection.
Research on these processes can identify bacterial virulence factors and clarify host-pathogen interactions. Examining receptor binding, cellular signaling, cytoskeletal changes, and barrier penetration connects specific bacterial activities with colonization and disease progression. These findings help immunologists and microbiologists explain how infection becomes established and determine which microbial-host interactions may be suitable for intervention.
The mechanisms support approaches that interfere with bacterial establishment rather than depending solely on bacterial killing. Anti-adhesion therapies could disrupt adhesin-receptor interactions, while vaccines may target relevant virulence factors. Antimicrobial strategies can also use knowledge of invasion and host-pathogen interactions to limit establishment, intracellular survival, or infection spread.