In cats with small cell GI LSA, what cellular markers correlated with higher Fusobacterium numbers?

• A. CD4 T cells
• B. CD11b+ myeloid cells and NF-κB expression
• C. B cells
• D. T regulatory cells

Answer: (B)

This question centers on how gut bacteria relate to the immune environment in feline small cell GI lymphoma. The strongest link is between higher Fusobacterium numbers and activation of the innate immune system, specifically myeloid cells and the NF-κB inflammatory pathway.

CD11b marks myeloid lineage cells—monocytes, macrophages, and neutrophils. When Fusobacterium abundance increases, these cells are often recruited to the gut mucosa and become activated, driving local inflammation. NF-κB is a key transcription factor that turns on pro-inflammatory genes in response to microbial signals; its expression or activity rises as innate immune cells respond to bacteria like Fusobacterium. The combination of elevated CD11b+ myeloid cells and active NF-κB reflects an innate inflammatory milieu tied to the microbiota, making it the best descriptor of higher Fusobacterium numbers in this context.

In contrast, markers associated with adaptive immunity or immune regulation—such as CD4 T cells, B cells, or T regulatory cells—do not specifically capture the direct association with bacterial-driven innate inflammatory signaling, so they’re less aligned with the observed correlation with Fusobacterium abundance.