In vitro study reveals that Streptococcus suis disrupts the histamine axis in human brain endothelial cells, indicating a metabolic driver of blood-brain barrier invasion.
Key Points
To determine how Streptococcus suis infection alters host endothelial cell metabolism to increase blood-brain barrier permeability and facilitate central nervous system invasion.
Infected human brain microvascular endothelial cells (hBMECs) with Streptococcus suis type 2 strain HA9801.
Conducted non-targeted metabolomics to assess changes in cellular metabolic profiles with a focus on histidine metabolism.
Quantified HDC and HNMT expression, endogenous histamine accumulation, tight junction gene expression (TJP1, OCLN, and CLDN5), and bacterial translocation rates across the endothelial barrier.
Streptococcus suis infection significantly altered the hBMEC metabolic profile, showing pronounced enrichment of the histidine metabolism pathway alongside altered HDC and HNMT expression.
Host metabolic reprogramming resulted in significant endogenous histamine accumulation, which was accompanied by reduced expression of tight junction protein genes TJP1, OCLN, and CLDN5.
Elevated histamine levels correlated directly with compromised blood-brain barrier integrity and increased translocation of S. suis across the endothelial barrier.