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Channel-induced apoptosis of infected host cells-the case of malaria

Florian Lang1, Philipp A Lang, Karl S Lang

  • 1Physiologisches Institut der Universität Tübingen, Gmelinstrasse 5, 72076 Tübingen, Germany. florian.lang@uni-tuebingen.de

Pflugers Archiv : European Journal of Physiology
|March 26, 2004
PubMed

Insights

Malaria infection activates erythrocyte channels, allowing pathogen growth via calcium and sodium entry. These channels also trigger erythrocyte "apoptosis," a host defense mechanism to eliminate infected cells.

Area of Science:

  • Cell Biology
  • Infectious Diseases
  • Malariology

Background:

  • Malaria infection by Plasmodium falciparum induces oxidative stress in erythrocytes.
  • This oxidative stress activates specific anion and cation channels in the erythrocyte membrane.
  • Similar channels can be activated by oxidative stress in non-infected erythrocytes.

Purpose of the Study:

  • To investigate the role of erythrocyte ion channels in malaria pathogenesis.
  • To understand how these channels contribute to pathogen survival and host defense.

Main Methods:

  • Analysis of ion channel activity in infected and non-infected erythrocytes under oxidative stress.
  • Investigation of cation (Ca2+, Na+) influx and its consequences on erythrocyte membrane phospholipid asymmetry.
  • Assessment of the role of phosphatidylserine exposure in erythrocyte phagocytosis.

Main Results:

  • Activation of a non-selective, Ca2+-permeable cation channel allows Ca2+ and Na+ entry, crucial for Plasmodium falciparum growth.
  • Ca2+ influx triggers scramblase activity, leading to phosphatidylserine exposure on the erythrocyte surface.
  • Phosphatidylserine exposure promotes phagocytosis of infected erythrocytes by macrophages, potentially eliminating the pathogen.
  • Absence of these channels inhibits pathogen growth, while enhanced activity accelerates erythrocyte apoptosis, a host defense mechanism.

Conclusions:

  • Erythrocyte ion channels play a dual role in malaria: facilitating pathogen survival and enabling host defense.
  • Targeting these channels could be a therapeutic strategy against malaria.
  • Erythrocyte apoptosis induced by channel activity represents a critical host defense against malaria infection.

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