The Journal of infectious diseases · 2026
Signal Transducers and Activators of Transcription 1 (STAT1), STAT2, and T Cells Mediate Interferon-Dependent Protection Against Neurobrucellosis.
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Moley Charles R, Abushahba Mostafa F N, Ponzilacqua-Silva Bárbara, Kochetkova Irina, Jackson Christa D, Skyberg Jerod A
Аннотация
BACKGROUND: Brucellosis is a significant zoonotic disease throughout the world. Human brucellosis patients develop flu-like symptoms and focal complications including arthritis and neurobrucellosis, which is the most morbid complication of Brucella infection.
METHODS: In this study, we employed murine models to uncover the role of T-cell-mediated immunity, interferons, and signal transducers and activators of transcription (STAT) signaling in the development of neurobrucellosis caused by Brucella melitensis.
RESULTS: Through adoptive transfer experiments, we discovered that T cells are recruited to the brains of Brucella-infected mice and are able to prevent central nervous system infection in an interferon-γ (IFN-γ)-dependent manner. Transferred T cells were also able to reduce established colonization of the brain by Brucella. In addition, we found that STAT1 plays a protective role against colonization of the brain by Brucella and the progression of neurobrucellosis, and that IFN-γ signaling is not entirely essential for these protective effects. While STAT2 deficiency alone did not affect Brucella burdens, a combined deficiency of STAT2 and the IFN-γ receptor led to elevated Brucella burdens in brains and blood, and a higher likelihood of developing neurologic symptoms relative to animals lacking the IFN-γ receptor alone.
CONCLUSIONS: Our findings indicate that T cells and IFN signaling through both STAT1 and STAT2 play complex and important roles in protecting against bacterial colonization and development of neurologic symptoms following infection by Brucella.
METHODS: In this study, we employed murine models to uncover the role of T-cell-mediated immunity, interferons, and signal transducers and activators of transcription (STAT) signaling in the development of neurobrucellosis caused by Brucella melitensis.
RESULTS: Through adoptive transfer experiments, we discovered that T cells are recruited to the brains of Brucella-infected mice and are able to prevent central nervous system infection in an interferon-γ (IFN-γ)-dependent manner. Transferred T cells were also able to reduce established colonization of the brain by Brucella. In addition, we found that STAT1 plays a protective role against colonization of the brain by Brucella and the progression of neurobrucellosis, and that IFN-γ signaling is not entirely essential for these protective effects. While STAT2 deficiency alone did not affect Brucella burdens, a combined deficiency of STAT2 and the IFN-γ receptor led to elevated Brucella burdens in brains and blood, and a higher likelihood of developing neurologic symptoms relative to animals lacking the IFN-γ receptor alone.
CONCLUSIONS: Our findings indicate that T cells and IFN signaling through both STAT1 and STAT2 play complex and important roles in protecting against bacterial colonization and development of neurologic symptoms following infection by Brucella.