Rafael Campos‐Rodríguez

Host invasion by Entamoeba histolytica, the pathogenic agent of amebiasis, can lead to the development of amebic liver abscess (ALA). Due to the difficulty of exploring host and amebic factors involved in the pathogenesis of ALA in humans, most studies have been conducted with animal models (e.g., mice, gerbils, and hamsters). Histopathological findings reveal that the chronic phase of ALA in humans corresponds to lytic or liquefactive necrosis, whereas in rodent models there is granulomatous inflammation. However, the use of animal models has provided important information on molecules and mechanisms of the host/parasite interaction. Hence, the present review discusses the possible role of neutrophils in the effector immune response in ALA in rodents. Properly activated neutrophils are probably successful in eliminating amebas through oxidative and non-oxidative mechanisms, including neutrophil degranulation, the generation of free radicals (O2(-), H2O2, HOCl) and peroxynitrite, the activation of NADPH-oxidase and myeloperoxidase (MPO) enzymes, and the formation of neutrophil extracellular traps (NETs). On the other hand, if amebas are not eliminated in the early stages of infection, they trigger a prolonged and exaggerated inflammatory response that apparently causes ALAs. Genetic differences in animals and humans are likely to be key to a successful host immune response.

Neutrophil Extracellular Traps

Pathogenesis

10.1051/parasite/2016006

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Citations (23)

Anterior subdiaphragmatic vagotomy decreases the IgA antibody response in the small intestines of BALB/c mice

Journal of Neuroimmunology (2019)

Ivonne Maciel Arciniega-Martínez María Elisa Drago-Serrano M. Salas-Pimentel Javier Ventura‐Juárez Aldo Arturo Reséndiz‐Albor

Lamina propria

BALB/c

Immunoglobulin A

10.1016/j.jneuroim.2019.577072

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Citations (5)

Expression of immune modulator cytokines in human fulminant amoebic colitis

Parasite Immunology (2009)

R. E. SIERRA‐PUENTE Rafael Campos‐Rodríguez Rosa Adriana Jarillo‐Luna Luis Muñoz-Fernández Martín Gerardo Rodriguez

Human fulminant amoebic colitis (FAC) is characterized by ulceration and inflammation of the colon. The specific mixture of pro-inflammatory and anti-inflammatory cytokines may participate in either the host defense or in the pathogenesis of amoebic colitis. Therefore, we studied the expression of IL-8, IL-10, IL-4, TGF-beta and IFN-gamma in human FAC patients and controls through immunohistochemistry analysis. The number of cells expressing IL-8, IL-4 and IL-10 was significantly enhanced in all FAC samples compared to the control samples. However, the expression of TGF- beta in patients was low in the colonic mucosa and high in the lamina propria compared with the control. No expression of IFN-gamma was found in the controls or FAC samples. The production of IL-8 by intestinal epithelial cells may play a role in the pathogenesis of amoebic infection, because this cytokine attracts neutrophils, which lead to an inflammatory reaction that results in tissue damage. The predominant expression of the macrophage down-regulating cytokines, IL-4, IL-10 and TGF-beta, or the Th2-type immune response could inhibit a cell-mediated immune response, which in turn would facilitate parasite invasion in these tissues.

Pathogenesis

Lamina propria

Fulminant

10.1111/j.1365-3024.2009.01118.x

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Citations (18)

List of Contributors

Elsevier eBooks (2016)

István Berczi Rafael Campos‐Rodríguez Roberto Chavira‐Ramírez Kálmán Kovács Dora Lippai

10.1016/b978-0-12-801770-8.00016-1

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