title: Staphylococcus aureus Induces Shedding of IL-1RII in Monocytes and Neutrophils.
abstract: 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.
authors.affiliation: Instituto de Investigaciones en Microbiologia y Parasitologia Medica (IMPaM), Consejo Nacional de Investigaciones Cientx00ED;ficas y Tx00E9;cnicas, Universidad de Buenos Aires, Buenos Aires, Argentina.
authors.forename: Constanza
authors.initials: C
authors.lastname: Giai
authors.forename: Cintia D
authors.initials: CD
authors.lastname: Gonzalez
authors.forename: Florencia
authors.initials: F
authors.lastname: Sabbione
authors.forename: Ailin
authors.initials: A
authors.lastname: Garofalo
authors.forename: Diego
authors.initials: D
authors.lastname: Ojeda
authors.forename: Daniel O
authors.initials: DO
authors.lastname: Sordelli
authors.forename: Analía S
authors.initials: AS
authors.lastname: Trevani
authors.forename: Marisa I
authors.initials: MI
authors.lastname: Gómez
mesh_terms: D000818:Animals; D002460:Cell Line; D005786:Gene Expression Regulation; D006801:Humans; D057131:Immune Evasion; D018836:Inflammation Mediators / Q000378:metabolism; D053583:Interleukin-1beta / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D009000:Monocytes / Q000276:immunology* / Q000382:microbiology; D009504:Neutrophils / Q000276:immunology* / Q000382:microbiology; D059748:Proteolysis; D053574:Receptors, Interleukin-1 Type II / Q000235:genetics / Q000378:metabolism*; D018805:Sepsis / Q000276:immunology*; D013203:Staphylococcal Infections / Q000276:immunology*; D013205:Staphylococcal Protein A / Q000276:immunology; D013211:Staphylococcus aureus / Q000276:immunology*
chemical_list: D018836:Inflammation Mediators; D053583:Interleukin-1beta; D053574:Receptors, Interleukin-1 Type II; D013205:Staphylococcal Protein A