A review of the proposed role of neutrophils in rodent amebic liver abscess models

Rafael Campos-Rodríguez, Manuel Gutiérrez-Meza, Rosa Adriana Jarillo-Luna, María Elisa Drago-Serrano, Edgar Abarca-Rojano, Javier Ventura-Juárez, Luz María Cárdenas-Jaramillo, Judith Pacheco-Yepez

Research output: Contribution to journalScientific review

5 Citations (Scopus)

Abstract

© 2016 R.Campos-Rodríguez et al. published by EDP Sciences. 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 (O 2 - , H 2 O 2 , 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.
Original languageAmerican English
JournalParasite
DOIs
StatePublished - 1 Jan 2016

Fingerprint

liver abscess
Amoebic Liver Abscess
neutrophils
Rodentia
Neutrophils
rodents
Amoeba
Animal Models
inflammation
animal models
amebiasis
immune response
Entamoeba histolytica
Host-Parasite Interactions
Amebiasis
myeloperoxidase
Peroxynitrous Acid
gerbils
Gerbillinae
NADPH Oxidase

Cite this

Campos-Rodríguez, Rafael ; Gutiérrez-Meza, Manuel ; Jarillo-Luna, Rosa Adriana ; Drago-Serrano, María Elisa ; Abarca-Rojano, Edgar ; Ventura-Juárez, Javier ; Cárdenas-Jaramillo, Luz María ; Pacheco-Yepez, Judith. / A review of the proposed role of neutrophils in rodent amebic liver abscess models. In: Parasite. 2016.
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title = "A review of the proposed role of neutrophils in rodent amebic liver abscess models",
abstract = "{\circledC} 2016 R.Campos-Rodr{\'i}guez et al. published by EDP Sciences. 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 (O 2 - , H 2 O 2 , 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.",
author = "Rafael Campos-Rodr{\'i}guez and Manuel Guti{\'e}rrez-Meza and Jarillo-Luna, {Rosa Adriana} and Drago-Serrano, {Mar{\'i}a Elisa} and Edgar Abarca-Rojano and Javier Ventura-Ju{\'a}rez and C{\'a}rdenas-Jaramillo, {Luz Mar{\'i}a} and Judith Pacheco-Yepez",
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A review of the proposed role of neutrophils in rodent amebic liver abscess models. / Campos-Rodríguez, Rafael; Gutiérrez-Meza, Manuel; Jarillo-Luna, Rosa Adriana; Drago-Serrano, María Elisa; Abarca-Rojano, Edgar; Ventura-Juárez, Javier; Cárdenas-Jaramillo, Luz María; Pacheco-Yepez, Judith.

In: Parasite, 01.01.2016.

Research output: Contribution to journalScientific review

TY - JOUR

T1 - A review of the proposed role of neutrophils in rodent amebic liver abscess models

AU - Campos-Rodríguez, Rafael

AU - Gutiérrez-Meza, Manuel

AU - Jarillo-Luna, Rosa Adriana

AU - Drago-Serrano, María Elisa

AU - Abarca-Rojano, Edgar

AU - Ventura-Juárez, Javier

AU - Cárdenas-Jaramillo, Luz María

AU - Pacheco-Yepez, Judith

PY - 2016/1/1

Y1 - 2016/1/1

N2 - © 2016 R.Campos-Rodríguez et al. published by EDP Sciences. 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 (O 2 - , H 2 O 2 , 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.

AB - © 2016 R.Campos-Rodríguez et al. published by EDP Sciences. 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 (O 2 - , H 2 O 2 , 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.

U2 - 10.1051/parasite/2016006

DO - 10.1051/parasite/2016006

M3 - Scientific review

C2 - 26880421

JO - Parasite

JF - Parasite

SN - 1252-607X

ER -