Dynamic Pneumococcal Genetic Adaptations Support Bacterial Growth and Inflammation during Coinfection with Influenza

Amanda Smith(University of Tennessee Health Science Center), Lindey C. Lane(University of Tennessee Health Science Center), Tim van Opijnen(Boston College), Stacie Woolard(St. Jude Children's Research Hospital), Rob Carter(St. Jude Children's Research Hospital), Amy Iverson(St. Jude Children's Research Hospital), Corinna Burnham(St. Jude Children's Research Hospital), Peter Vogel(St. Jude Children's Research Hospital), Dana Roeber(St. Jude Children's Research Hospital), Gabrielle Hochu(University of Tennessee Health Science Center), Michael D. L. Johnson(University of Arizona), Jonathan A. McCullers(University of Tennessee Health Science Center), Jason W. Rosch(St. Jude Children's Research Hospital), Amber M. Smith(University of Tennessee Health Science Center)
Infection and Immunity
April 14, 2021
Cited by 11Open Access
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Abstract

, but each still grew to high titers in the lungs of mock- and influenza virus-infected hosts. Despite high bacterial loads, mortality was significantly reduced or delayed with all SGD mutants. Time-dependent reductions in pulmonary neutrophils, inflammatory macrophages, and select proinflammatory cytokines and chemokines were also observed. Immunohistochemical staining further revealed altered neutrophil distribution with reduced degeneration in the lungs of influenza virus-SGD mutant-coinfected animals. These studies demonstrate a critical role for specific bacterial genes and for bacterial metabolism in driving virulence and modulating immune function during influenza-associated bacterial pneumonia.


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