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Calcium signaling events in Streptococcus pneumoniae invasion of human type II pneumocytes

Bang-lao Xu1, Yi-bing Yin

  • 1Department of Clinical Laboratory, First Municipal Hospital of Guangzhou, Guangzhou 510180, China. xubanglao@hotmail.com

Di 1 Jun Yi Da Xue Xue Bao = Academic Journal of the First Medical College of PLA
|February 18, 2004
PubMed
Abstract

Insights

Streptococcus pneumoniae (S.pn) triggers filamentous actin (F-actin) changes in lung cells via calcium signaling, promoting bacterial invasion. Blocking calcium pathways inhibits this process, offering potential therapeutic targets.

Area of Science:

  • Cell Biology
  • Microbiology
  • Immunology

Background:

  • Streptococcus pneumoniae (S.pn) is a major cause of bacterial pneumonia.
  • Bacterial invasion of host cells is a critical step in pathogenesis.
  • The role of calcium signaling in S.pn-induced host cell invasion is not fully understood.

Purpose of the Study:

  • To investigate if S.pn induces filamentous actin (F-actin) rearrangements in type II pneumocytes (A549 cells) through calcium signaling pathways.
  • To determine if these F-actin rearrangements contribute to S.pn invasion of A549 cells.

Main Methods:

  • F-actin rearrangements were visualized using FITC-phalloidin labeling after S.pn adhesion to A549 cells.
  • S.pn invasion was assessed by pretreating A549 cells with cytochalasin D.
  • Calcium signaling was studied by measuring cytosolic free calcium levels using Fura-2/AM probe in the presence of S.pn and calcium inhibitors like dantrolene.

Main Results:

  • S.pn adhesion induced F-actin rearrangements in A549 cells.
  • Cytochalasin D effectively blocked S.pn invasion of A549 cells, with no invasion observed at 0.25 microg/ml.
  • Calcium signaling inhibitors partially blocked F-actin rearrangements, and S.pn adhesion significantly increased cytosolic free calcium levels over time.

Conclusions:

  • S.pn provokes F-actin rearrangements in A549 cells via calcium signaling pathways.
  • These F-actin rearrangements are essential for S.pn invasion of lung epithelial cells.
  • Targeting calcium signaling pathways may represent a strategy to prevent S.pn infection.

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