Anti-capsular immunity to Streptococcus pneumoniae serotype 22F prevents bacterial transmission in murine colonization and influenza virus co-infection models

Schmit, Taylor; Kuntz, Mikale; Patel, Devarshi; Khan, M. Nadeem

doi:10.1016/j.vaccine.2020.11.075

Cited by 1 publication

(2 citation statements)

References 15 publications

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“…Human IAV strain (H1N1) pdm09 strain A/California/04/2009 was purchased from American type culture collection (ATCC). Spn serotype 6A strain BG7322 was provided by Rochester General Hospital Research Institute and has been previously used by us and others [ 22 , 37 , 38 ].…”

Section: Methodsmentioning

confidence: 99%

“…Mock and IAV-infected WT and IL-17RA -/- mice were i.n. infected with 10 μL PBS containing 50xTCID 50 of IAV, and on 3, 7, and 14 dpi, the histology samples of the nasopharynx were prepared as previously described [ 37 ]. Briefly, the skin was removed from the skull, and the anterior nasopharynx was removed and placed in 10% neutral buffered formalin for 24 hours prior to being stored in 70% ethanol.…”

Section: Methodsmentioning

confidence: 99%

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IL-17RA promotes pathologic epithelial inflammation in a mouse model of upper respiratory influenza infection

Navaeiseddighi,

Tripathi,

Guo

et al. 2023

PLoS Pathog

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The upper respiratory tract (nasopharynx or NP) is the first site of influenza replication, allowing the virus to disseminate to the lower respiratory tract or promoting community transmission. The host response in the NP regulates an intricate balance between viral control and tissue pathology. The hyper-inflammatory responses promote epithelial injury, allowing for increased viral dissemination and susceptibility to secondary bacterial infections. However, the pathologic contributors to influenza upper respiratory tissue pathology are incompletely understood. In this study, we investigated the role of interleukin IL-17 recetor A (IL-17RA) as a modulator of influenza host response and inflammation in the upper respiratory tract. We used a combined experimental approach involving IL-17RA-/- mice and an air-liquid interface (ALI) epithelial culture model to investigate the role of IL-17 response in epithelial inflammation, barrier function, and tissue pathology. Our data show that IL-17RA-/- mice exhibited significantly reduced neutrophilia, epithelial injury, and viral load. The reduced NP inflammation and epithelial injury in IL-17RA-/- mice correlated with increased resistance against co-infection by Streptococcus pneumoniae (Spn). IL-17A treatment, while potentiating the apoptosis of IAV-infected epithelial cells, caused bystander cell death and disrupted the barrier function in ALI epithelial model, supporting the in vivo findings.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%