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Interleukin-17RA (IL-17RA) and Interleukin-1 receptor (IL-1R) signaling are crucial for controlling Streptococcus pneumoniae (Spn) infections. These pathways ensure sustained neutrophil presence and activity, preventing persistent nasopharyngeal colonization.

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Area of Science:

  • Immunology
  • Microbiology
  • Infectious Diseases

Background:

  • Streptococcus pneumoniae (Spn) is a leading cause of mucosal infections.
  • Primary nasopharyngeal colonization by Spn is the initial step in pathogenesis.
  • The duration of Spn colonization is influenced by host immune responses.

Purpose of the Study:

  • To investigate immune signaling pathways that regulate the duration of Spn nasopharyngeal colonization.
  • To elucidate the roles of IL-17RA and IL-1R signaling in controlling Spn infection.
  • To understand the involvement of neutrophils in Spn clearance.

Main Methods:

  • Utilized wild-type (WT) and knockout mouse models (IL-17RA, IL-1R, dual-knockout).
  • Performed RNA-sequencing (RNA-seq) analysis to identify affected pathways.
  • Quantified Spn colonization duration and assessed neutrophil numbers, activation, and trafficking.

Main Results:

  • Absence of IL-17RA signaling led to persistent Spn colonization (> 6 months).
  • IL-17RA signaling is essential for replenishing neutrophils in nasal tissue and promoting their trafficking via endothelial adhesion molecules.
  • IL-1R signaling is required for neutrophil activation (CD11b expression) and contributes to Spn phagocytosis.
  • IL-17RA and IL-1R pathways are non-redundant and both regulate Cxcl5 chemokine expression, crucial for neutrophil maintenance.

Conclusions:

  • Sustained neutrophil presence and activity are critical for preventing persistent mucosal infection by Spn.
  • IL-17RA signaling supports neutrophil replenishment and trafficking.
  • IL-1R signaling promotes neutrophil activation for pathogen clearance.
  • Combined IL-17RA and IL-1R signaling, along with Cxcl5, ensures effective control of Spn colonization.