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2018 ; 3
(7
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
The inflammasome potentiates influenza/Staphylococcus aureus superinfection in
mice
#MMPMID29618653
Robinson KM
; Ramanan K
; Clay ME
; McHugh KJ
; Pilewski MJ
; Nickolich KL
; Corey C
; Shiva S
; Wang J
; Muzumdar R
; Alcorn JF
JCI Insight
2018[Apr]; 3
(7
): ä PMID29618653
show ga
Secondary bacterial respiratory infections are commonly associated with both
acute and chronic lung injury. Influenza complicated by bacterial pneumonia is an
effective model to study host defense during pulmonary superinfection due to its
clinical relevance. Multiprotein inflammasomes are responsible for IL-1?
production in response to infection and drive tissue inflammation. In this study,
we examined the role of the inflammasome during viral/bacterial superinfection.
We demonstrate that ASC-/- mice are protected from bacterial superinfection and
produce sufficient quantities of IL-1? through an apoptosis-associated speck-like
protein containing CARD (ASC) inflammasome-independent mechanism. Despite the
production of IL-1? by ASC-/- mice in response to bacterial superinfection, these
mice display decreased lung inflammation. A neutrophil elastase inhibitor blocked
ASC inflammasome-independent production of IL-1? and the IL-1 receptor
antagonist, anakinra, confirmed that IL-1 remains crucial to the clearance of
bacteria during superinfection. Delayed inhibition of NLRP3 during influenza
infection by MCC950 decreases bacterial burden during superinfection and leads to
decreased inflammatory cytokine production. Collectively, our results demonstrate
that ASC augments the clearance of bacteria, but can also contribute to
inflammation and mortality. ASC should be considered as a therapeutic target to
decrease morbidity and mortality during bacterial superinfection.
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