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Pathology, Pathogenesis, and Experimental Amebiasis

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Amebiasis

Abstract

The most important feature of the pathology of human amebiasis is the greatly destructive nature of the anatomical lesions produced by the protozoan Entamoeba histolytica. Recent advances on the knowledge of biochemistry, immunology, cellular and molecular biology, and genetics of this parasite, added to the use of different in vitro, in vivo, and ex vivo models to analyze host–parasite interactions or the production of intestinal and extraintestinal amebic lesions, all have given a better perception of the mechanisms of pathogenesis in amebiasis. The present chapter is divided into three parts: first, a general review of the pathology of human amebiasis; second, a short review of the mechanisms of invasion and production of damage in the host, and third, a review of the different in vivo experimental models currently available to study the mechanisms involved in amebic infection. In reference to pathogenesis, each factor, molecule or gene, or mechanism of target cell damage is reviewed individually in other chapters of this section on “Pathogenesis and Immunity” in the present book. Therefore, the meticulous or probing aspects of the studies are mentioned by each responsible and expert group of researchers. In this review, we mention in general each of the different factors of pathogenesis in amebiasis. The contributions obtained using different techniques and methodologies of experimental models are emphasized, and the subjects that still need to be unraveled to understand how this microscopic parasite has earned its well-deserved “histolytic” name are discussed.

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Abbreviations

ALA:

Amebic liver abscess

CP:

Cysteine proteinase

E-64:

l-trans-Epoxisuccinil-leucylamido-(4-guanidino butane)

Gal:

Galactose

GalNAc:

Acetylgalacosamine

GM-CSF:

Granulocyte macrophage-colony stimulating factor

GTP:

Guanosine triphosphate

IL-1β:

Interleukin-1-beta

INF-γ:

Interferon-gamma

Muc2:

Mucin 2

NF-κb:

Nuclear factor kappa-light-chain-enhancer of activated B cells

SCID:

Severe combined immunodeficiency

TNF:

Tumor necrosis factor

TUNEL:

Terminal deoxynucleotidyl transferase-dUTP nick-end labeling

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Acknowledgments

The authors gratefully acknowledge Ms. Silvia Galindo-Gómez, Angélica Silva-Olivares, Karla Gil-Becerril, and Claudia Pérez-Galindo for their technical assistance. The present work was partially supported by SEP-CONACyT (México), grant No. 128317 to MS.

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Authors and Affiliations

  1. Department of Infectomics and Molecular Pathogenesis, Center for Research and Advanced Studies, National Polytechnic Institute, (CINVESTAV-IPN), Mexico City, Mexico

    Mineko Shibayama & Víctor Tsutsumi

  2. Department of Cell Biology, Center for Research and Advanced Studies, National Polytechnic Institute, (CINVESTAV-IPN), Mexico City, Mexico

    José de Jesús Serrano-Luna

  3. Laboratory of Pathology, MIG Hospital, Mexico City, Mexico

    Jesús Aguirre-García

Authors
  1. Mineko Shibayama
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  2. José de Jesús Serrano-Luna
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  3. Jesús Aguirre-García
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  4. Víctor Tsutsumi
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Correspondence to Víctor Tsutsumi .

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Editors and Affiliations

  1. Department of Parasitology, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo, Japan

    Tomoyoshi Nozaki

  2. Jawaharlal Nehru University, New Delhi, India

    Alok Bhattacharya

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Shibayama, M., de Jesús Serrano-Luna, J., Aguirre-García, J., Tsutsumi, V. (2015). Pathology, Pathogenesis, and Experimental Amebiasis. In: Nozaki, T., Bhattacharya, A. (eds) Amebiasis. Springer, Tokyo. https://doi.org/10.1007/978-4-431-55200-0_23

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