Staphylococcus aureus Induces Shedding of IL-1RII in Monocytes and Neutrophils

Interleukin 1 (IL-1) β is a critical cytokine that orchestrates host defenses against Staphylococcus aureus and is crucial for the eradication of bacteria. The production and action of IL-1β are regulated by multiple control pathways. Among them, IL-1RII (the type II IL-1 receptor) acts as a decoy r...

Full description

Bibliographic Details
Authors: Giai, Constanza, Gonzalez, Cintia Daniela, Sabbione, Florencia, Garofalo, Ailin Natalia, Ojeda, Diego Sebastian, Sordelli, Daniel Oscar, Trevani, Analía Silvina, Gomez, Marisa Ines
Format: article
Status:Published version
Publication Date:2016
Country:Argentina
Institution:Consejo Nacional de Investigaciones Científicas y Técnicas
Repository:CONICET Digital (CONICET)
Language:English
OAI Identifier:oai:ri.conicet.gov.ar:11336/39003
Online Access:http://hdl.handle.net/11336/39003
Access Level:Open access
Keyword:Adam17#
Il-1rii
Protein A
Shedding
https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
Description
Summary:Interleukin 1 (IL-1) β is a critical cytokine that orchestrates host defenses against Staphylococcus aureus and is crucial for the eradication of bacteria. The production and action of IL-1β are regulated by multiple control pathways. Among them, IL-1RII (the type II IL-1 receptor) acts as a decoy receptor and has been shown to regulate the biological effects of IL-1β. High levels of soluble IL-1RII are present in septic patients; however, the stimuli that regulate the expression and release of IL-1RII in pathological conditions are incompletely elucidated. In the present study, we demonstrated the ability of S. aureus and protein A to induce IL-1RII shedding in myeloid cells. The positive modulation of IL-1RII expression and cleavage was associated with the failure to detect IL-1β in response to S. aureus both in vitro and in vivo, suggesting that the soluble form of the receptor could be masking the availability of IL-1β. The absence of detectable IL-1β was associated with low levels of inflammatory cytokines and chemokines known to be regulated by IL-1β and with increased bacterial persistence. Modulation of decoy receptors during systemic S. aureus infection is proposed as a new strategy used by this bacterium to evade the immune response.