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J+Virol
2019 ; 93
(6
): ? Nephropedia Template TP
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Unique Transcriptional Architecture in Airway Epithelial Cells and Macrophages
Shapes Distinct Responses following Influenza Virus Infection Ex Vivo
#MMPMID30626665
Ma JZ
; Ng WC
; Zappia L
; Gearing LJ
; Olshansky M
; Pham K
; Cheong K
; Hsu A
; Turner SJ
; Wijburg O
; Londrigan SL
; Brooks AG
; Reading PC
J Virol
2019[Mar]; 93
(6
): ? PMID30626665
show ga
Airway epithelial cells and macrophages differ markedly in their responses to
influenza A virus (IAV) infection. To investigate transcriptional responses
underlying these differences, purified subsets of type II airway epithelial cells
(ATII) and alveolar macrophages (AM) recovered from the lungs of mock- or
IAV-infected mice at 9?h postinfection were subjected to RNA sequencing. This
time point was chosen to allow for characterization of cell types first infected
with the virus inoculum, prior to multicycle virus replication and the
infiltration of inflammatory cells into the airways. In the absence of infection,
AM predominantly expressed genes related to immunity, whereas ATII expressed
genes consistent with their physiological roles in the lung. Following IAV
infection, AM almost exclusively activated cell-intrinsic antiviral pathways that
were dependent on interferon (IFN) regulatory factor 3/7 (IRF3/7) and/or type I
IFN signaling. In contrast, IAV-infected ATII activated a broader range of
physiological responses, including cell-intrinsic antiviral pathways, which were
both independent of and dependent on IRF3/7 and/or type I IFN. These data suggest
that transcriptional profiles hardwired during development are a major
determinant underlying the different responses of ATII and AM to IAV
infection.IMPORTANCE Airway epithelial cells (AEC) and airway macrophages (AM)
represent major targets of influenza A virus (IAV) infection in the lung, yet the
two cell types respond very differently to IAV infection. We have used RNA
sequencing to define the host transcriptional responses in each cell type under
steady-state conditions as well as following IAV infection. To do this, different
cell subsets isolated from the lungs of mock- and IAV-infected mice were
subjected to RNA sequencing. Under steady-state conditions, AM and AEC express
distinct transcriptional activities, consistent with distinct physiological roles
in the airways. Not surprisingly, these cells also exhibited major differences in
transcriptional responses following IAV infection. These studies shed light on
how the different transcriptional architectures of airway cells from two
different lineages drive transcriptional responses to IAV infection.
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