Following a Chlamydia trachomatis infection, the host immune response is characterized by its recognition via Toll-like and Nod-like Receptors, and the subsequent activation of interferon (IFN)-γ-mediated signaling pathways. Recently, the inflammasome-mediated host cell response has emerged to play a role in the physiopathology of C. trachomatis infection. Here we investigated, for the first time, the interaction of IFN-γ and inflammasome in an in vitro model of C. trachomatis-infected primary human synovial cells. Chlamydial replication as well as the expression of caspase-1, IL-1β, as well as IL-18 and IL-6, were assayed. Our results demonstrated the inhibitory activity of IFN-γ by interfering with the inflammasome network through the downregulation of caspase-1 mRNA expression. In addition, the ability of C. trachomatis to hinder the inflammasome pathway favoring its intracellular survival within synovial cells, was observed. Overall, our data suggest a potential mechanism of immune evasion by C. trachomatis in synovial cells, that may be contested by IFN-γ.

Potential IFNγ modulation of inflammasome pathway in Chlamydia trachomatis infected synovial cells / Filardo, Simone; Di Pietro, Marisa; Frasca, Federica; Diaco, Fabiana; Scordio, Mirko; Antonelli, Guido; Scagnolari, Carolina; Sessa, Rosa. - In: LIFE. - ISSN 2075-1729. - 11:12(2021), pp. 1-14. [10.3390/life11121359]

Potential IFNγ modulation of inflammasome pathway in Chlamydia trachomatis infected synovial cells

Simone Filardo
Co-primo
;
Marisa Di Pietro
Co-primo
;
Federica Frasca;Fabiana Diaco;Mirko Scordio;Guido Antonelli;Carolina Scagnolari;Rosa Sessa
Ultimo
2021

Abstract

Following a Chlamydia trachomatis infection, the host immune response is characterized by its recognition via Toll-like and Nod-like Receptors, and the subsequent activation of interferon (IFN)-γ-mediated signaling pathways. Recently, the inflammasome-mediated host cell response has emerged to play a role in the physiopathology of C. trachomatis infection. Here we investigated, for the first time, the interaction of IFN-γ and inflammasome in an in vitro model of C. trachomatis-infected primary human synovial cells. Chlamydial replication as well as the expression of caspase-1, IL-1β, as well as IL-18 and IL-6, were assayed. Our results demonstrated the inhibitory activity of IFN-γ by interfering with the inflammasome network through the downregulation of caspase-1 mRNA expression. In addition, the ability of C. trachomatis to hinder the inflammasome pathway favoring its intracellular survival within synovial cells, was observed. Overall, our data suggest a potential mechanism of immune evasion by C. trachomatis in synovial cells, that may be contested by IFN-γ.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1614125
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