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Infection and Immunity, March 2008, p. 959-966, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.01455-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Participation of the Serine-Rich Entamoeba histolytica Protein in Amebic Phagocytosis of Apoptotic Host Cells{triangledown}

Jose E. Teixeira1 and Christopher D. Huston1,2*

Departments of Medicine,1 Microbiology and Molecular Genetics, University of Vermont College of Medicine, Burlington, Vermont 054052

Received 30 October 2007/ Returned for modification 28 November 2007/ Accepted 7 December 2007

Entamoeba histolytica is an intestinal ameba that causes dysentery and liver abscesses. Cytotoxicity and phagocytosis of host cells characterize invasive E. histolytica infection. Prior to phagocytosis of host cells, E. histolytica induces apoptotic host cell death, using a mechanism that requires contact via an amebic galactose-specific lectin. However, lectin inhibition only partially blocks phagocytosis of already dead cells, implicating at least one additional receptor in phagocytosis. To identify receptors for engulfment of apoptotic cells, monoclonal antibodies against E. histolytica membrane antigens were screened for inhibition of phagocytosis. Of 43 antibodies screened, one blocked lectin-independent uptake of apoptotic cells, with >90% inhibition at a dose of 20 µg/ml (P < 0.0003 versus control). The same antibody also inhibited adherence to apoptotic lymphocytes and, to a lesser extent, adherence to and killing of viable lymphocytes. The antigen recognized by the inhibitory antibody was purified by affinity chromatography and identified by liquid chromatography-mass spectrometry as the serine-rich E. histolytica protein (SREHP). Consistent with this, the inhibitory antibody bound to recombinant SREHP present in bacterial lysates on immunoblots. The SREHP is an abundant immunogenic surface protein of unclear function. The results of this unbiased antibody screen strongly implicate the SREHP as a participant in E. histolytica phagocytosis and suggest that it may play an important role in adherence to apoptotic cells.

* Corresponding author. Mailing address: Departments of Medicine and Microbiology and Molecular Genetics, Rm. 320, Stafford Hall, University of Vermont, 95 Carrigan Drive, Burlington, VT 05405. Phone: (802) 656-9115. Fax: (802) 847-5322. E-mail: christopher.huston{at}uvm.edu

{triangledown} Published ahead of print on 17 December 2007.

Editor: W. A. Petri, Jr.

Infection and Immunity, March 2008, p. 959-966, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.01455-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Welter, B. H., Temesvari, L. A. (2009). Overexpression of a Mutant Form of EhRabA, a Unique Rab GTPase of Entamoeba histolytica, Alters Endoplasmic Reticulum Morphology and Localization of the Gal/GalNAc Adherence Lectin. Eukaryot Cell 8: 1014-1026 [Abstract] [Full Text]  
  • Baxt, L. A., Baker, R. P., Singh, U., Urban, S. (2008). An Entamoeba histolytica rhomboid protease with atypical specificity cleaves a surface lectin involved in phagocytosis and immune evasion. Genes Dev. 22: 1636-1646 [Abstract] [Full Text]  


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