Microbiology and Immunology 6400 Oral Intermicrobial Interactions Practice Test

Antagonizing ZEB2 expression in host epithelial cells means dampening the signals that push epithelial cells to undergo epithelial–mesenchymal transition, a process linked to loss of barrier function and increased invasiveness. ZEB2 is a transcription factor that promotes this EMT state, so organisms that suppress ZEB2 help keep epithelial cells in a stable, barrier-friendly phenotype.

Streptococcus gordonii fits this role because it’s a commensal early colonizer known for modulating host signaling in a way that maintains epithelial integrity. By downregulating ZEB2 expression in epithelial cells, it reduces EMT-promoting cues and supports a more epithelial, less invasive state. This contrasts with other oral bacteria that tend to disrupt barrier function or promote EMT-like changes; for example, Porphyromonas gingivalis and Fusobacterium nucleatum are more often associated with EMT activation and upregulation of EMT transcription factors, which would elevate ZEB2 levels rather than suppress them. Streptococcus mutans is primarily linked to caries and shared inflammatory responses rather than directly antagonizing ZEB2.

In short, the best-fitting organism reduces the EMT-driving factor ZEB2, helping maintain the epithelial barrier, which aligns with the protective, homeostatic role attributed to Streptococcus gordonii in this context.