Borrelia burgdorferi binds serum amyloid A and modulates subcutaneous adipose tissue immune signaling.

Human ex vivo skin and subcutaneous adipose tissue show B. burgdorferi infection is linked to overall downregulation of immune pathways in adipose cells, alongside inflammatory IL-1β, TNF, and NFKB1 programs.

• Why it matters: Adipose tissue is a dissemination site in Lyme disease, but adipose-specific immune signaling during B. burgdorferi infection is poorly defined.
• What they did: Single-cell sequencing pathway analysis and CellChat mapped immune signaling and intercellular communication in adipose-resident cells; recombinant SAA was tested for direct binding to B. burgdorferi and for effects on viability and phagocytosis in vitro.
• The result: Adipose-specific SAA is downregulated during infection, and SAA directly binds B. burgdorferi, reduces spirochete viability in a dose-dependent manner, and enhances phagocytosis, supporting SAA as a host defense factor.

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