Which organism upregulates ZEB2 in host epithelial cells?

Prepare for the Microbiology and Immunology 6400 Oral Intermicrobial Interactions Test. Study with engaging materials, flashcards, and multiple-choice questions. Each question offers hints and detailed explanations. Ace your exam today!

Multiple Choice

Which organism upregulates ZEB2 in host epithelial cells?

Explanation:
ZEB2 is a transcription factor that drives epithelial–mesenchymal transition (EMT), a program that loosens cell–cell junctions and can make the epithelial barrier more permissive to invasion. Some oral pathogens actively trigger host signaling to push cells into EMT, including upregulating ZEB2. Porphyromonas gingivalis is a key periodontal pathogen known to manipulate gingival epithelial cells through its virulence factors (like fimbriae and gingipains) that engage host receptors and activate signaling pathways such as MAPK and NF-κB. This signaling can lead to EMT-like changes, including increased ZEB2 expression, which helps the bacteria invade and persist by weakening the epithelial barrier. The other organisms listed are primarily associated with adhesion, biofilm formation, or cariogenic processes rather than inducing EMT through ZEB2 upregulation in host epithelial cells.

ZEB2 is a transcription factor that drives epithelial–mesenchymal transition (EMT), a program that loosens cell–cell junctions and can make the epithelial barrier more permissive to invasion. Some oral pathogens actively trigger host signaling to push cells into EMT, including upregulating ZEB2.

Porphyromonas gingivalis is a key periodontal pathogen known to manipulate gingival epithelial cells through its virulence factors (like fimbriae and gingipains) that engage host receptors and activate signaling pathways such as MAPK and NF-κB. This signaling can lead to EMT-like changes, including increased ZEB2 expression, which helps the bacteria invade and persist by weakening the epithelial barrier.

The other organisms listed are primarily associated with adhesion, biofilm formation, or cariogenic processes rather than inducing EMT through ZEB2 upregulation in host epithelial cells.

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