Involvement of β2-integrin in ROS-mediated neutrophil apoptosis induced by Entamoeba histolytica

Seobo Sim, Soon Jung Park, Tai Soon Yong, Kyung Il Im, Myeong Heon Shin

Research output: Contribution to journalArticlepeer-review

28 Citations (Scopus)


Cellular adhesion through β2-integrin (CD18) is an important step in signal transduction leading to apoptosis of human neutrophils, and NADPH oxidase-derived reactive oxygen species (ROS) are essential for neutrophil apoptosis induced by Entamoeba histolytica. Therefore, we investigated the role of β2-integrin-mediated signals in ROS-dependent neutrophil apoptosis induced by E. histolytica. Entamoeba-induced apoptosis was inhibited by pre-incubation of cells with mAb to CD18, but not CD29, suggesting that β2-integrin plays an important role in this response. Moreover, Entamoeba-induced ROS generation in neutrophils was inhibited by mAbs against CD18 or CD11b, but not by mAbs against CD11a, CD11c, or CD29. A combination of d-galactose plus anti-CD18 mAb had a larger inhibitory effect than d-galactose alone on Entamoeba-induced apoptosis and ROS generation. Furthermore, Entamoeba-induced apoptosis and ROS generation were inhibited by pre-treatment of cells with an inhibitor of phosphatidylinositol-3-kinase (PI-3-kinase). These results indicate that β2-integrin and PI-3-kinase are crucial signaling molecules in ROS-dependent apoptosis of neutrophils induced by E. histolytica.

Original languageEnglish
Pages (from-to)1368-1375
Number of pages8
JournalMicrobes and Infection
Issue number11
Publication statusPublished - 2007 Sept

Bibliographical note

Funding Information:
This study was supported by the Yonsei University Research Fund of 2004 (6-2004-0056).

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Infectious Diseases


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