FABP7 is increased in progressive multiple sclerosis and induces a pro-inflammatory phenotype in monocytes through a glycolytic switch

Rohit Patel, Devin King, Brenna LaBarre, Hrishikesh Lokhande, Danielle Caefer, Johnna F. Varghese, Keturah Warner, Marc A. Bouffard, Shrishti Saxena, Alena Zhirova, Rohit Bakshi and Tanuja Chitnis ()
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Rohit Patel: Brigham and Women’s Hospital
Devin King: Brigham and Women’s Hospital
Brenna LaBarre: Brigham and Women’s Hospital
Hrishikesh Lokhande: Brigham and Women’s Hospital
Danielle Caefer: Brigham and Women’s Hospital
Johnna F. Varghese: Brigham and Women’s Hospital
Keturah Warner: Brigham and Women’s Hospital
Marc A. Bouffard: Mass General Brigham
Shrishti Saxena: Brigham and Women’s Hospital
Alena Zhirova: Brigham and Women’s Hospital
Rohit Bakshi: Brigham and Women’s Hospital
Tanuja Chitnis: Brigham and Women’s Hospital

Nature Communications, 2025, vol. 16, issue 1, 1-18

Abstract: Abstract Multiple sclerosis (MS) involves dysregulation of innate immune cells including monocytes, especially in progressive MS. Fatty acid binding proteins (FABP) are essential for fatty acid transport and metabolism in multiple cell types. FABP7, a brain-FABP, maintains metabolic function in astrocytes and neural stem cells, but the effect of FABP7 on monocytes is unknown. Here we find elevated levels of FABP7 in the serum and cerebrospinal fluid of patients with secondary progressive MS. Elevated serum FABP7 levels positively correlate with higher disability scores, brain lesion volumes, and lower brain volumes. FABP7 levels are increased in astrocytes from MS postmortem brain lesion. Mechanistically, in vitro treatment of FABP7 induces CD16, CD80 and IL-1β expression in monocytes via increased glycolysis. FABP7-induced gene expression reflects enhanced inflammation, chemotaxis and glucose metabolism in monocytes. In conclusion, we find that FABP7 induces pro-inflammatory profiles in monocytes, correlates with disability and represents a potential biomarker and therapeutic target for progressive MS.

Date: 2025
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DOI: 10.1038/s41467-025-60747-9

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