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Characterization of Inflammatory Responses During Intranasal Colonization with Streptococcus pneumoniae
09:12

Characterization of Inflammatory Responses During Intranasal Colonization with Streptococcus pneumoniae

Published on: January 17, 2014

[Ca2+ signaling pathways associated with the invasion of Streptococcus pneumoniae to type II pneumocytes]

Yibing Yin1, Banglao Xu, Jinyong Luo

  • 1Department of Clinical Biochemistry, Faculty of Laboratory Medicine, Chongqing University of Medical sciences, Chongqing 400016, China. yibingyin@21cn.com

Wei Sheng Wu Xue Bao = Acta Microbiologica Sinica
|November 10, 2005
PubMed

Insights

Streptococcus pneumoniae adhesion triggers F-actin rearrangements and calcium signaling in lung cells, facilitating bacterial invasion. Calcium inhibitors block these rearrangements, suggesting a pathway for therapeutic intervention.

Area of Science:

  • Microbiology
  • Cell Biology
  • Biochemistry

Context:

  • Streptococcus pneumoniae adhesion to type II pneumocytes (A549 cells) involves cytoskeletal changes.
  • Bacterial invasion mechanisms are not fully understood, particularly the role of host cell actin dynamics.

Purpose:

  • To investigate the role of F-actin rearrangements and calcium signaling in Streptococcus pneumoniae invasion of A549 cells.
  • To determine if calcium inhibitors can block F-actin rearrangements and subsequent bacterial invasion.

Summary:

  • Streptococcus pneumoniae adhesion induced F-actin rearrangements in A549 cells, visualized using FITC-phalloidin.
  • Cytochalasin D pretreatment prevented bacterial invasion, while datrollene (a Ca2+ inhibitor) dose-dependently blocked F-actin rearrangements.
  • Bacterial adhesion increased cytosolic free calcium levels in A549 cells, indicating calcium signaling involvement.

Impact:

  • Findings suggest Streptococcus pneumoniae utilizes Ca2+ signaling pathways to provoke F-actin rearrangements, promoting cell invasion.
  • This research highlights potential therapeutic targets for combating pneumococcal infections by modulating host cell calcium signaling.

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