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Examining the Role of Nasopharyngeal-associated Lymphoreticular Tissue (NALT) in Mouse Responses to Vaccines
12:21

Examining the Role of Nasopharyngeal-associated Lymphoreticular Tissue (NALT) in Mouse Responses to Vaccines

Published on: August 1, 2012

The early interferon response of nasal-associated lymphoid tissue to Streptococcus pyogenes infection

Kendra A Hyland1, Robert Brennan, Stephen B Olmsted

  • 1Department of Microbiology, University of Minnesota, Minneapolis, MN 55413, USA. hyla0021@umn.edu

FEMS Immunology and Medical Microbiology
|February 27, 2009
PubMed

Insights

Interferon-gamma (IFN-gamma) is crucial for preventing Streptococcus pyogenes spread from the nasal-associated lymphoid tissue (NALT) to lymph nodes in children. This finding highlights IFN-gamma

Area of Science:

  • Immunology
  • Microbiology
  • Infectious Diseases

Background:

  • Streptococcus pyogenes frequently causes tonsillitis/pharyngitis in children, often leading to recurrent infections despite antibiotic treatment.
  • Persistent S. pyogenes in tonsils contributes to treatment failure and recurring infections.
  • Mouse nasal-associated lymphoid tissue (NALT) models human oropharyngeal lymphoid tissues for studying mucosal immune responses to S. pyogenes.

Purpose of the Study:

  • To investigate the role of interferon-gamma (IFN-gamma) in the innate immune response to Streptococcus pyogenes infection.
  • To characterize the early mucosal immune response, including gene expression and cellular infiltration, following intranasal S. pyogenes challenge.
  • To determine if IFN-gamma is essential for controlling bacterial dissemination within the host.

Main Methods:

  • Intranasal infection of wild-type and IFN-gamma knockout (GKO) mice with wild-type S. pyogenes.
  • Analysis of gene transcription (type I and IFN-gamma-responsive genes, proinflammatory genes, acute-phase proteins) in NALT.
  • Quantification of neutrophil influx into NALT at 24 and 48 hours post-infection.
  • Assessment of bacterial dissemination to draining lymph nodes (LN) and systemic infection.

Main Results:

  • Wild-type S. pyogenes induced type I and IFN-gamma-responsive genes, proinflammatory genes, and acute-phase proteins in NALT.
  • Neutrophil influx into NALT occurred at 24 hours and decreased by 48 hours post-infection.
  • IFN-gamma knockout mice exhibited local dissemination of S. pyogenes to draining lymph nodes, but not systemic infection, and showed increased neutrophil influx.

Conclusions:

  • IFN-gamma-induced immune responses are critical for preventing the local dissemination of Streptococcus pyogenes from NALT to draining lymph nodes.
  • The M protein of S. pyogenes is not essential for NALT invasion or the induction of the interferon response.
  • Understanding the role of IFN-gamma provides insights into host defense mechanisms against streptococcal pharyngitis and potential therapeutic targets.

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