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2019 ; 15
(1
): e1007560
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Influenza-induced immune suppression to methicillin-resistant Staphylococcus
aureus is mediated by TLR9
#MMPMID30682165
Martínez-Colón GJ
; Warheit-Niemi H
; Gurczynski SJ
; Taylor QM
; Wilke CA
; Podsiad AB
; Crespo J
; Bhan U
; Moore BB
PLoS Pathog
2019[Jan]; 15
(1
): e1007560
PMID30682165
show ga
Bacterial lung infections, particularly with methicillin-resistant Staphylococcus
aureus (MRSA), increase mortality following influenza infection, but the
mechanisms remain unclear. Here we show that expression of TLR9, a microbial DNA
sensor, is increased in murine lung macrophages, dendritic cells, CD8+ T cells
and epithelial cells post-influenza infection. TLR9-/- mice did not show
differences in handling influenza nor MRSA infection alone. However, TLR9-/- mice
have improved survival and bacterial clearance in the lung post-influenza and
MRSA dual infection, with no difference in viral load during dual infection. We
demonstrate that TLR9 is upregulated on macrophages even when they are not
themselves infected, suggesting that TLR9 upregulation is related to soluble
mediators. We rule out a role for elevations in interferon-? (IFN?) in mediating
the beneficial MRSA clearance in TLR9-/- mice. While macrophages from WT and
TLR9-/- mice show similar phagocytosis and bacterial killing to MRSA alone,
following influenza infection, there is a marked upregulation of scavenger
receptor A and MRSA phagocytosis as well as inducible nitric oxide synthase
(Inos) and improved bacterial killing that is specific to TLR9-deficient cells.
Bone marrow transplant chimera experiments and in vitro experiments using TLR9
antagonists suggest TLR9 expression on non-hematopoietic cells, rather than the
macrophages themselves, is important for regulating myeloid cell function.
Interestingly, improved bacterial clearance post-dual infection was restricted to
MRSA, as there was no difference in the clearance of Streptococcus pneumoniae.
Taken together these data show a surprising inhibitory role for TLR9 signaling in
mediating clearance of MRSA that manifests following influenza infection.
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