Histopathological characterization of Toxocara canis- and T. cati-induced neurotoxocarosis in the mouse model

Springer, Andrea; Heuer, Lea; Janecek-Erfurth, Elisabeth; Beineke, Andreas; Strübe, Christina

doi:10.1007/s00436-019-06395-7

Cited by 18 publications

(14 citation statements)

References 38 publications

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“…Some studies describe the presence of granulomas in liver lesions, with the participation of Th1 immune response and innate immunity cells, mainly eosinophils and macrophages [ 12 , 13 ]. In the brain, it is common to have hemorrhagic areas with recruitment of neutrophils, eosinophils and activation of microglia/macrophages [ 6 , 14 ]. The excretory-secretory T .…”

Section: Introductionmentioning

confidence: 99%

Detrimental role of IL-33/ST2 pathway sustaining a chronic eosinophil-dependent Th2 inflammatory response, tissue damage and parasite burden during Toxocara canis infection in mice

et al. 2021

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Toxocariasis is a neglected disease that affects people around the world. Humans become infected by accidental ingestion of eggs containing Toxocara canis infective larvae, which upon reaching the intestine, hatch, penetrate the mucosa and migrate to various tissues such as liver, lungs and brain. Studies have indicated that Th2 response is the main immune defense mechanism against toxocariasis, however, there are still few studies related to this response, mainly the IL-33/ST2 pathway. Some studies have reported an increase in IL-33 during helminth infections, including T. canis. By binding to its ST2 receptor, IL-33 stimulating the Th2 polarized immune cell and cytokine responses. Thus, we aimed to investigate the role of the IL-33/ST2 pathway in the context of T. canis larval migration and the immunological and pathophysiological aspects of the infection in the liver, lungs and brain from Wild-Type (WT) BALB/c background and genetically deficient mice for the ST2 receptor (ST2-/-). The most important findings revealed that the IL-33/ST2 pathway is involved in eosinophilia, hepatic and cerebral parasitic burden, and induces the formation of granulomas related to tissue damage and pulmonary dysfunction. However, ST2-/- mice, the immune response was skewed to Th1/Th17 type than Th2, that enhanced the control of parasite burden related to IgG2a levels, tissue macrophages infiltration and reduced lung dysfunction. Collectively, our results demonstrate that the Th2 immune response triggered by IL-33/ST2 pathway mediates susceptibility to T. canis, related to parasitic burden, eosinophilia and granuloma formation in which consequently contributes to tissue inflammation and injury.

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Section: Introductionmentioning

confidence: 99%

Detrimental role of IL-33/ST2 pathway sustaining a chronic eosinophil-dependent Th2 inflammatory response, tissue damage and parasite burden during Toxocara canis infection in mice

et al. 2021

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“…Nevertheless, neuroinvasive larvae of Toxocara spp. are able to accumulate and persist in cerebral tissues [43] and even though the infection is characterised by neuroinflammatory hallmarks like hemorrhagic lesions, myelinophages, spheroids and activated microglia [10, 44, 45], larvae are not trapped by inflammatory reactions in cerebral tissues [44, 46]. Knowledge regarding the cerebral immune response during NT is scarce.…”

Section: Discussionmentioning

confidence: 99%

“…However, neutrophil infiltration may play only a subordinate role in the pathogenesis of NT as the pathological picture is dominated by eosinophilic meningitis, microglia activation and neurodegeneration, the latter especially in T . canis -infected mice [45].…”

Section: Discussionmentioning

confidence: 99%

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Multiplex profiling of inflammation-related bioactive lipid mediators in Toxocara canis- and Toxocara cati-induced neurotoxocarosis

Waindok¹,

Janecek-Erfurth²,

Lindenwald³

et al. 2019

PLoS Negl Trop Dis

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BackgroundSomatic migration of Toxocara canis- and T. cati-larvae in humans may cause neurotoxocarosis (NT) when larvae accumulate and persist in the central nervous system (CNS). Host- or parasite-induced immunoregulatory processes contribute to the pathogenesis; however, detailed data on involvement of bioactive lipid mediators, e.g. oxylipins or eico-/docosanoids, which are involved in the complex molecular signalling network during infection and inflammation, are lacking.Methodology/Principal findingsTo elucidate if T. canis- and T. cati-induced NT affects the homeostasis of oxylipins during the course of infection, a comprehensive lipidomic profiling in brains (cerebra and cerebella) of experimentally infected C57BL/6J mice was conducted at six different time points post infection (pi) by liquid-chromatography coupled to electrospray tandem mass spectrometry (LC-ESI-MS/MS). Only minor changes were detected regarding pro-inflammatory prostaglandins (cyclooxygenase pathway). In contrast, a significant increase of metabolites resulting from lipoxygenase pathways was observed for both infection groups and brain regions, implicating a predominantly anti-inflammatory driven immune response. This observation was supported by a significantly increased 13-hydroxyoctadecadienoic acid (HODE)/9-HODE ratio during the subacute phase of infection, indicating an anti-inflammatory response to neuroinfection. Except for the specialised pro-resolving mediator (SPM) neuroprotectin D1 (NPD1), which was detected in mice infected with both pathogens during the subacute phase of infection, no other SPMs were detected.Conclusions/SignificanceThe obtained results demonstrate the influence of Toxocara spp. on oxylipins as part of the immune response of the paratenic hosts. Furthermore, this study shows differences in the alteration of the oxylipin composition between T. canis- and T. cati-brain infection. Results contribute to a further understanding of the largely unknown pathogenesis and mechanisms of host-parasite interactions during NT.

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“…(2017) on T. canis-infected outbred mouse strains. But, Springer et al (2019) detected perivascular cuffs with eosinophils and neutrophils in C57Bl/6 mice infected with T. canis. This could be explained by the difference between the immune response of inbred and outbred mice to T. canis infection.…”

Section: Introductionmentioning

confidence: 90%

Assessment of Neuroinflammatory and Neurodegenerative Alterations in the Brain in a Mouse Model of Visceral Larva Migrans

Elgendy

Othman

Saied

et al. 2020

Journal of the Egyptian Society of Parasitology

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Histopathological characterization of Toxocara canis- and T. cati-induced neurotoxocarosis in the mouse model

Cited by 18 publications

References 38 publications

Detrimental role of IL-33/ST2 pathway sustaining a chronic eosinophil-dependent Th2 inflammatory response, tissue damage and parasite burden during Toxocara canis infection in mice

Detrimental role of IL-33/ST2 pathway sustaining a chronic eosinophil-dependent Th2 inflammatory response, tissue damage and parasite burden during Toxocara canis infection in mice

Multiplex profiling of inflammation-related bioactive lipid mediators in Toxocara canis- and Toxocara cati-induced neurotoxocarosis

Assessment of Neuroinflammatory and Neurodegenerative Alterations in the Brain in a Mouse Model of Visceral Larva Migrans

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