scholarly journals A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection

Author(s):  
Leif S. Anderson ◽  
Mack B. Reynolds ◽  
Kathryn R. Rivara ◽  
Lloyd S. Miller ◽  
Scott I. Simon
Proceedings ◽  
2019 ◽  
Vol 22 (1) ◽  
pp. 72
Author(s):  
Lena Trifonov ◽  
Vadim Nudelman ◽  
Michael Zhenin ◽  
Guy Cohen ◽  
Krzysztof Jozwiak ◽  
...  

TLR4, a member of the toll-like receptors (TLRs) family, serves as a pattern recognition receptor in the innate immune response to different microbial pathogens. [...]


2012 ◽  
Vol 4 ◽  
pp. 405-409 ◽  
Author(s):  
Adrianna Pawlik ◽  
Grażyna Sender ◽  
Rafał Starzyński ◽  
Agnieszka Korwin-Kossakowska

2006 ◽  
Vol 2 ◽  
pp. S97-S97
Author(s):  
Kathleen S. Montine ◽  
Izumi Maezawa ◽  
Mary Nivison ◽  
Nobuyo Maeda ◽  
Thomas J. Montine

2019 ◽  
Vol 87 (4) ◽  
Author(s):  
Talib Alboslemy ◽  
Bing Yu ◽  
Tara Rogers ◽  
Min-Ho Kim

ABSTRACT Staphylococcus aureus infections associated with the formation of biofilms on medical implants or host tissue play a critical role in the persistence of chronic infections. One critical mechanism of biofilm infection that leads to persistent infection lies in the capacity of biofilms to evade the macrophage-mediated innate immune response. It is now increasingly apparent that microorganisms exploit the negative regulatory mechanisms of the pattern recognition receptor (PRR)-mediated inflammatory response to subvert host cell functions by using various virulence factors. However, the detailed molecular mechanism, along with the identity of a target molecule, underlying the evasion of the macrophage-mediated innate immune response against S. aureus infection associated with biofilm formation remains to be elucidated. Here, using an in vitro culture model of murine macrophage-like RAW 264.7 cells, we demonstrate that S. aureus biofilm-conditioned medium significantly attenuated the capacity for macrophage bactericidal and proinflammatory responses. Importantly, the responses were associated with attenuated activation of NF-κB and increased expression of Kruppel-like factor 2 (KLF2) in RAW 264.7 cells. Small interfering RNA (siRNA)-mediated silencing of KLF2 in RAW 264.7 cells could restore the activation of NF-κB toward the bactericidal activity and generation of proinflammatory cytokines in the presence of S. aureus biofilm-conditioned medium. Collectively, our results suggest that factors secreted from S. aureus biofilms might exploit the KLF2-dependent negative regulatory mechanism to subvert macrophage-mediated innate immune defense against S. aureus biofilms.


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