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A Mouse Model for the Transition of Streptococcus pneumoniae from Colonizer to Pathogen upon Viral Co-Infection Recapitulates Age-Exacerbated Illness.
Lenhard, Alexsandra; Joma, Basma H; Siwapornchai, Nalat; Hakansson, Anders P; Leong, John M; Bou Ghanem, Elsa N.
Afiliação
  • Lenhard A; Department of Microbiology and Immunology, University at Buffalo School of Medicine.
  • Joma BH; Department of Molecular Biology and Microbiology, Tufts University School of Medicine; Graduate Program in Immunology, Tufts Graduate School of Biomedical Sciences.
  • Siwapornchai N; Department of Molecular Biology and Microbiology, Tufts University School of Medicine.
  • Hakansson AP; Department of Translational Medicine, Lund University.
  • Leong JM; Department of Molecular Biology and Microbiology, Tufts University School of Medicine; Stuart B. Levy Center for the Integrated Management of Antimicrobial Resistance, Tufts University.
  • Bou Ghanem EN; Department of Microbiology and Immunology, University at Buffalo School of Medicine; elsaboug@buffalo.edu.
J Vis Exp ; (187)2022 09 28.
Article em En | MEDLINE | ID: mdl-36279528
ABSTRACT
Streptococcus pneumoniae (pneumococcus) is an asymptomatic colonizer of the nasopharynx in most individuals but can progress to a pulmonary and systemic pathogen upon influenza A virus (IAV) infection. Advanced age enhances host susceptibility to secondary pneumococcal pneumonia and is associated with worsened disease outcomes. The host factors driving those processes are not well defined, in part due to a lack of animal models that reproduce the transition from asymptomatic colonization to severe clinical disease. This paper describes a novel mouse model that recreates the transition of pneumococci from asymptomatic carriage to disease upon viral infection. In this model, mice are first intranasally inoculated with biofilm-grown pneumococci to establish asymptomatic carriage, followed by IAV infection of both the nasopharynx and lungs. This results in bacterial dissemination to the lungs, pulmonary inflammation, and obvious signs of illness that can progress to lethality. The degree of disease is dependent on the bacterial strain and host factors. Importantly, this model reproduces the susceptibility of aging, because compared to young mice, old mice display more severe clinical illness and succumb to disease more frequently. By separating carriage and disease into distinct steps and providing the opportunity to analyze the genetic variants of both the pathogen and the host, this S. pneumoniae/IAV co-infection model permits the detailed examination of the interactions of an important pathobiont with the host at different phases of disease progression. This model can also serve as an important tool for identifying potential therapeutic targets against secondary pneumococcal pneumonia in susceptible hosts.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Vírus da Influenza A / Infecções Pneumocócicas / Pneumonia Pneumocócica / Infecções por Orthomyxoviridae / Coinfecção Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: J Vis Exp Ano de publicação: 2022 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Vírus da Influenza A / Infecções Pneumocócicas / Pneumonia Pneumocócica / Infecções por Orthomyxoviridae / Coinfecção Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: J Vis Exp Ano de publicação: 2022 Tipo de documento: Article