Neutrophil extracellular traps and MPO in models of susceptibility and resistance against <i>Entamoeba histolytica</i>

de, Arturo Contis-Montes; Baquero, Andrea Cruz; Rodríguez, Rafael Campos; Jaramillo, Luz María Cárdenas; Flores, José Eduardo Aguayo; Rojas-Hernández, Saúl; García, Alfonso Olivos; Pacheco-Yépez, Judith

doi:10.1111/pim.12714

Cited by 11 publications

(14 citation statements)

References 38 publications

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“…Pathological examinations of patients who died of COVID-19 indicate that vascular impairment and neutrophil extracellular trap (NET) formation seem to play a crucial role in fatal cases, in addition or in combination with various other host factors such as age, gender, immune status and comorbidities (1,(4)(5)(6)(7). NETs are extracellular DNA fibers released by activated neutrophils during the innate immune response in animals and humans (8)(9)(10). They are described as an innate immune defense mechanism against bacteria, viruses, fungi and parasites (10)(11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

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Vasculitis and Neutrophil Extracellular Traps in Lungs of Golden Syrian Hamsters With SARS-CoV-2

Becker¹,

Beythien²,

Buhr

et al. 2021

Front. Immunol.

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Neutrophil extracellular traps (NETs) have been identified as one pathogenetic trigger in severe COVID-19 cases and therefore well-described animal models to understand the influence of NETs in COVID-19 pathogenesis are needed. SARS-CoV-2 infection causes infection and interstitial pneumonia of varying severity in humans and COVID-19 models. Pulmonary as well as peripheral vascular lesions represent a severe, sometimes fatal, disease complication of unknown pathogenesis in COVID-19 patients. Furthermore, neutrophil extracellular traps (NETs), which are known to contribute to vessel inflammation or endothelial damage, have also been shown as potential driver of COVID-19 in humans. Though most studies in animal models describe the pulmonary lesions characterized by interstitial inflammation, type II pneumocyte hyperplasia, edema, fibrin formation and infiltration of macrophages and neutrophils, detailed pathological description of vascular lesions or NETs in COVID-19 animal models are lacking so far. Here we report different types of pulmonary vascular lesions in the golden Syrian hamster model of COVID-19. Vascular lesions included endothelialitis and vasculitis at 3 and 6 days post infection (dpi), and were almost nearly resolved at 14 dpi. Importantly, virus antigen was present in pulmonary lesions, but lacking in vascular alterations. In good correlation to these data, NETs were detected in the lungs of infected animals at 3 and 6 dpi. Hence, the Syrian hamster seems to represent a useful model to further investigate the role of vascular lesions and NETs in COVID-19 pathogenesis.

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Section: Introductionmentioning

confidence: 99%

“…The golden Syrian hamster is described as one potential animal model for SARS-CoV-2 infections (41,42). Furthermore, a study with Entamoeba histolytica identified NET formation in hamsters (9). Therefore, we hypothesized that the hamster is an animal model to investigate the immunepathology of SARS-CoV-2 infections.…”

Section: Introductionmentioning

confidence: 99%

Vasculitis and Neutrophil Extracellular Traps in Lungs of Golden Syrian Hamsters With SARS-CoV-2

Becker¹,

Beythien²,

Buhr

et al. 2021

Front. Immunol.

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“…Díaz-Godínez ( 21 ) suggested that NADPH oxidase, which induces oxidative metabolism, was involved in the release of NETs. Later studies showed that calcium ionophores could induce the production of NETs; that is, the activity of PAD4 was also involved in the release of NETs ( 20 , 57 ). However, these factors are not the key to the production of NETs stimulated by amoebae.…”

Section: Phylum Sarcomastigophora Class Loboseamentioning

confidence: 99%

“…Although both mice and hamsters could be used for these experiments, differences in their NET and MPO levels were observed ( 20 ). In vitro experiments showed that mice produced more NETs and MPO than hamsters, whereas the elastase activity in both groups was very high.…”

Section: Phylum Sarcomastigophora Class Loboseamentioning

confidence: 99%

The State of Art of Extracellular Traps in Protozoan Infections (Review)

2021

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Protozoan parasite infection causes severe diseases in humans and animals, leading to tremendous economic and medical pressure. Natural immunity is the first line of defence against parasitic infection. Currently, the role of natural host immunity in combatting parasitic infection is unclear, so further research on natural host immunity against parasites will provide a theoretical basis for the prevention and treatment of related parasitic diseases. Extracellular traps (ETs) are an important natural mechanism of immunity involving resistance to pathogens. When immune cells such as neutrophils and macrophages are stimulated by external pathogens, they release a fibrous network structure, consisting mainly of DNA and protein, that can capture and kill a variety of extracellular pathogenic microorganisms. In this review, we discuss the relevant recently reported data on ET formation induced by protozoan parasite infection, including the molecular mechanisms involved, and discuss the role of ETs in the occurrence and development of parasitic diseases.

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“…In two animal models of amoebic liver abscess, one with hamsters (susceptible) and another with Balb/c mice (resistant), it was found that inhibition of MPO with 4‐aminobenzoic acid hydrazide, resulted in mice with larger abscesses and fewer damaged amoebas 111 . In addition, in vitro experiments showed that mouse neutrophils produced greater amounts of NET and MPO than hamster neutrophils did, and inhibition of MPO promoted an increase in amoeba viability 112,113 . Histones, proteins also found on NET, show microbicidal activity and may similarly participate in amoeba killing.…”

Section: Innate Immune Responsesmentioning

confidence: 99%

Neutrophils vs. amoebas: Immunity against the protozoan parasiteEntamoeba histolytica

Rosales

2021

Journal of Leukocyte Biology

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Entamoeba histolytica is a protozoan parasite with high prevalence in developing countries, and causes amoebiasis. This disease affects the intestine and the liver, and is the third leading cause of human deaths among parasite infections. E. histolytica infection of the intestine or liver is associated with a strong inflammation characterized by a large number of infiltrating neutrophils. Consequently, several reports suggest that neutrophils play a protective role in amoebiasis. However, other reports indicate that amoebas making direct contact with neutrophils provoke lysis of these leukocytes, resulting in the release of their lytic enzymes, which in turn provoke tissue damage. Therefore, the role of neutrophils in this parasitic infection remains controversial. Neutrophils migrate from the circulation to sites of infection, where they display several antimicrobial functions, including phagocytosis, degranulation, and formation of neutrophil extracellular traps (NET). Recently, it was found that E. histolytica trophozoites are capable of inducing NET formation. Neutrophils in touch with amoebas launched NET in an explosive manner around the amoebas and completely covered them in nebulous DNA and cell aggregates where parasites got immobilized and killed. In addition, the phenotype of neutrophils can be modified by the microbiome resulting in protection against amoebas. This review describes the mechanisms of E. histolytica infection and discusses the novel view of how neutrophils are involved in innate immunity defense against amoebiasis. Also, the mechanisms on how the microbiome modulates neutrophil function are described.

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Neutrophil extracellular traps and MPO in models of susceptibility and resistance against Entamoeba histolytica

Cited by 11 publications

References 38 publications

Vasculitis and Neutrophil Extracellular Traps in Lungs of Golden Syrian Hamsters With SARS-CoV-2

Vasculitis and Neutrophil Extracellular Traps in Lungs of Golden Syrian Hamsters With SARS-CoV-2

The State of Art of Extracellular Traps in Protozoan Infections (Review)

Neutrophils vs. amoebas: Immunity against the protozoan parasiteEntamoeba histolytica

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