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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
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Age-associated inflammation and toll-like receptor dysfunction prime the lungs for pneumococcal pneumonia

Ernesto Hinojosa1, Angela R Boyd, Carlos J Orihuela

  • 1Department of Microbiology and Immunology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229-3900, USA.

The Journal of Infectious Diseases
|July 10, 2009
PubMed
Abstract

Insights

Aging increases pneumonia risk due to chronic inflammation and impaired immune responses. Aged mice showed higher susceptibility to Streptococcus pneumoniae infection, linked to reduced lung immune receptor function.

Area of Science:

  • Immunology
  • Aging Research
  • Infectious Diseases

Background:

  • Aging is linked to heightened inflammation and increased risk of community-acquired pneumonia.
  • Streptococcus pneumoniae utilizes NFkB-regulated proteins (polymeric immunoglobulin receptor [pIgR] and platelet-activating factor receptor [PAFr]) for cellular attachment and invasion.
  • The study investigated the association between aging, chronic inflammation, and elevated pIgR/PAFr levels in the lungs, alongside susceptibility to S. pneumoniae.

Purpose of the Study:

  • To determine if aging and chronic inflammation increase lung polymeric immunoglobulin receptor (pIgR) and platelet-activating factor receptor (PAFr) levels.
  • To assess the impact of aging and chronic inflammation on susceptibility to Streptococcus pneumoniae infection.
  • To explore the underlying mechanisms, including NFkB activation and Toll-like receptor (TLR) function, in aged mice during S. pneumoniae infection.

Main Methods:

  • Quantification of lung protein and messenger RNA (mRNA) levels using Western blot and quantitative polymerase chain reaction (qPCR).
  • Measurement of NFkB activation via electrophoretic mobility shift assay (EMSA).
  • Assessment of cytokine levels using cytometric bead analysis and modeling of chronic inflammation in mice via tumor necrosis factor-alpha (TNF-α) infusion.

Main Results:

  • Aged mice and those with tumor necrosis factor-alpha (TNF-α) infusion exhibited increased lung pIgR and PAFr levels and greater susceptibility to S. pneumoniae.
  • During pneumonia, aged mice displayed reduced pIgR and PAFr levels and diminished NFkB activation, despite a higher bacterial load.
  • Aged mice showed decreased levels of lung Toll-like receptors 1, 2, and 4 (TLR1, TLR2, TLR4) and a blunted proinflammatory cytokine response to S. pneumoniae.

Conclusions:

  • Aging and chronic inflammation contribute to increased pneumonia susceptibility in mice.
  • Dysfunction of Toll-like receptors (TLRs) and a 'priming effect' from chronic inflammation may underlie increased pneumonia risk in aged individuals.
  • Findings suggest potential implications for elderly human populations regarding pneumonia risk and immune response.

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