Pathology of human amebiasis

Brandt, Herman; Tamayo, Ruy Pérez

doi:10.1016/s0046-8177(70)80072-7

Cited by 149 publications

(65 citation statements)

References 136 publications

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“…Eosinophilic E. histolytica trophozoites could be seen amidst the necrotic debris (Fig. 3), and were present throughout the abscess cavity, rather than solely at the periphery of the abscess, as has been described in human liver abscesses (21). The intense neutrophilic infiltration seen in hepatic tissue bordering the SCID mouse liver abscesses is not a regular component of hepatic amebiasis in humans, but it has been reported as an early stage of abscess development in animal models (22).…”

Section: Resultsmentioning

confidence: 66%

A severe combined immunodeficient (SCID) mouse model for infection with Entamoeba histolytica.

Cieslak

Virgin

Stanley

1992

The Journal of Experimental Medicine

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SummaryWe used severe combined immunodeficient (SCID) mice to study resistance to invasive infection with Entamoeba histolytica. Seven of seven SCID mice developed liver abscesses when challenged intrahepatically with virulent HMI:IMSS strain 15. histolytica trophozoites. Only one of seven similarly challenged immunocompetent congenic C.B-17 mice developed an abscess. Adoptive transfer of polyclonal rabbit anti-E, histolytica antiserum, but not preimmune rabbit serum, completely protected 7 of 12 SCID mice from intrahepatic challenge with ameba. These results demonstrate that lymphocyte-based immunity is important in protection against amebic liver abscess, and that anti-E, histolytica antibody can protect against amebic infection in this system. The SCID mouse may provide a powerful model for studying the components of protective immunity to invasive amebiasis.

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Section: Resultsmentioning

confidence: 66%

A severe combined immunodeficient (SCID) mouse model for infection with Entamoeba histolytica.

Cieslak

Virgin

Stanley

1992

The Journal of Experimental Medicine

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“…Similar events in the liver indicate that the host inflammatory response in that site is initiated also by the interaction between trophozoites and host cells (29)(30)(31). In contrast to the acute E. histolytica infection, chronic amebic abscesses in the liver contain few acute inflammatory cells (32).…”

Section: Introductionmentioning

confidence: 99%

Entamoeba histolytica trophozoites induce an inflammatory cytokine response by cultured human cells through the paracrine action of cytolytically released interleukin-1 alpha.

Eckmann¹,

Reed²,

Smith³

et al. 1995

J. Clin. Invest.

133

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Infection with the protozoan parasite Entamoeba histolytica results in a high mortality worldwide. To initiate infection, E. histolytica trophozoites in the bowel lumen penetrate the epithelium, and cause extensive lysis of host cells. The acute amebic lesions in animal models are characterized by infiltration with inflammatory cells, particularly neutrophils. The acute host response is likely important for determining whether the infection will spread systemically, but little is known regarding the signals which initiate an acute inflammatory response to E. histolytica. In the studies reported herein, we used an in vitro model system to define the proinflammatory signals produced by epithelial and other host cells in response to infection with E. histolytica trophozoites. Coculture of human epithelial and stromal cells and cell lines with trophozoites is shown to increase expression and secretion of an array of chemoattractant and proinflammatory cytokines, including IL-8, GROa, GM-CSF, IL-la, and IL-6. Moreover, high-level secretion of those cytokines is regulated by the paracrine action of cytolytically released IL-la. A second mechanism for trophozoite-induced IL-8 production involves trophozoite-target cell contact via a galactose-inhibitable amebic adherence protein, and appears to be mediated through increased intracellular calcium levels. These studies define novel mechanisms through which acute inflammation can be initiated in the host in response to a cytolytic pathogen, such as E. histolytica. (J. Clin. Invest.

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“…Dysentery occurs following invasion of the colonic epithelium by E. histolytica trophozoites. Prominent pathological features of invasive disease include tissue destruction, acute inflammation, and amebic phagocytosis of human erythrocytes and immune cells (14,26,31,46).…”

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confidence: 99%

Entamoeba histolytica Cell Surface Calreticulin Binds Human C1q and Functions in Amebic Phagocytosis of Host Cells

et al. 2012

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ABSTRACTPhagocytosis of host cells is characteristic of tissue invasion by the intestinal amebaEntamoeba histolytica, which causes amebic dysentery and liver abscesses.Entamoeba histolyticainduces host cell apoptosis and uses ligands, including C1q, on apoptotic cells to engulf them. Two mass spectrometry analyses identified calreticulin in amebic phagosome preparations, and, in addition to its function as an endoplasmic reticulum chaperone, calreticulin is believed to be the macrophage receptor for C1q. The purpose of this study was to determine if calreticulin functions as anE. histolyticaC1q receptor during phagocytosis of host cells. Calreticulin was localized to the surface ofE. histolyticaduring interaction with both Jurkat lymphocytes and erythrocytes and was present in over 75% of phagocytic cups during amebic erythrophagocytosis. Presence of calreticulin on the cell surface was further demonstrated using a method that selectively biotinylated cell surface proteins and by flow cytometry using trophozoites overexpressing epitope-tagged calreticulin. Regulated overexpression of calreticulin increasedE. histolytica's ability to phagocytose apoptotic lymphocytes and calcium ionophore-treated erythrocytes but had no effect on amebic adherence to or destruction of cell monolayers or surface expression of the GalNAc lectin and serine-richE. histolyticaprotein (SREHP) receptors. Finally,E. histolyticacalreticulin bound specifically to apoptotic lymphocytes and to human C1q. Collectively, these data implicate cell surface calreticulin as a receptor for C1q duringE. histolyticaphagocytosis of host cells.

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Pathology of human amebiasis

Cited by 149 publications

References 136 publications

A severe combined immunodeficient (SCID) mouse model for infection with Entamoeba histolytica.

A severe combined immunodeficient (SCID) mouse model for infection with Entamoeba histolytica.

Entamoeba histolytica trophozoites induce an inflammatory cytokine response by cultured human cells through the paracrine action of cytolytically released interleukin-1 alpha.

Entamoeba histolytica Cell Surface Calreticulin Binds Human C1q and Functions in Amebic Phagocytosis of Host Cells

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