Larval Ascariasis

Holland, Celia V.; Behnke, Jerzy M.; Dold, Christina

doi:10.1016/b978-0-12-396978-1.00005-7

Cited by 15 publications

(16 citation statements)

References 88 publications

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“…The larvae migrate from the alveolar capillaries through the pulmonary parenchyma, causing disruption of the alveolar walls. At this stage, larvae L3 change to L4 and ascend the bronchial tree, where they can be expectorated or swallowed; at this last stage, the larvae returns to the gastrointestinal tract, and reach sexual maturity to become male and female adult worms [21,22,23]. Related to this damage is the immune response induced by A .…”

Section: Introductionmentioning

confidence: 99%

Comorbidity associated to Ascaris suum infection during pulmonary fibrosis exacerbates chronic lung and liver inflammation and dysfunction but not affect the parasite cycle in mice

et al. 2019

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Ascariasis is considered the most neglected tropical disease, and is a major problem for the public health system. However, idiopathic pulmonary fibrosis (IPF) is a result of chronic extracellular deposition of matrix in the pulmonary parenchyma, and thickening of the alveolar septa, which reduces alveolar gas exchange. Considering the high rates of ascariasis and pulmonary fibrosis, we believe that these two diseases may co-exist and possibly lead to comorbidities. We therefore investigated the mechanisms involved in comorbidity of Ascaris suum (A. suum) infection, which could interfere with the progression of pulmonary fibrosis. In addition, we evaluated whether a previous lung fibrosis could interfere with the pulmonary cycle of A. suum in mice. The most important findings related to comorbidity in which A. suum infection exacerbated pulmonary and liver injury, inflammation and dysfunction, but did not promote excessive fibrosis in mice during the investigated comorbidity period. Interestingly, we found that pulmonary fibrosis did not alter the parasite cycle that transmigrated preferentially through preserved but not fibrotic areas of the lungs. Collectively, our results demonstrate that A. suum infection leads to comorbidity, and contributes to the aggravation of pulmonary dysfunction during pulmonary fibrosis, which also leads to significant liver injury and inflammation, without changing the A. suum cycle in the lungs.

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Section: Introductionmentioning

confidence: 99%

Comorbidity associated to Ascaris suum infection during pulmonary fibrosis exacerbates chronic lung and liver inflammation and dysfunction but not affect the parasite cycle in mice

et al. 2019

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“…Despite being abnormal hosts, and, therefore, having a truncated migratory path, mice have proven to be excellent model systems for Ascaris research (Holland et al ., 2013). Mice have some advantages with respect to the natural porcine host, because of size, husbandry and ethical constraints and a lack of inbred strains.…”

Section: Introductionmentioning

confidence: 99%

Ascaris lumbricoidesandAscaris suumvary in their larval burden in a mouse model

et al. 2020

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Ascariasis is a neglected tropical disease, caused by Ascaris lumbricoides, affecting 800 million people worldwide. Studies focused on the early stage of parasite infection, occurring in the gut, liver and lungs, require the use of a mouse model. In these models, the porcine ascarid, Ascaris suum, is often used. The results obtained from these studies are then used to draw conclusions about A. lumbricoides infections in humans. In the present study, we sought to compare larval migration of A. suum and A. lumbricoides in mouse models. We used a previously developed mouse model of ascariasis, which consists of two mouse strains, where one mouse strain – C57BL/6J – is a model for relative susceptibility and the other – CBA/Ca – for relative resistance. Mice of both strains were infected with either A. suum or A. lumbricoides. The larval burden was assessed in two key organs, the liver and lungs, starting at 6 h post infection (p.i.) and ending on day 8 p.i. Additionally, we measured the larval size of each species (μm) at days 6, 7 and 8 p.i. in the lungs. We found that larval burden in the liver is significantly higher for A. lumbricoides than for A. suum. However, the inverse is true in the lungs. Additionally, our results showed a reduced larval size for A. lumbricoides compared to A. suum.

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“…Furthermore, the presence of adult worms in the intestine contributes to significant chronic morbidity and, in some cases, more acute complications [ 4 ]. Therefore, investigation of the role of the liver—a key organ in Ascaris larval migration, and likely attrition and consequent establishment of adult worms in the intestine could prove fruitful [ 29 ]. The liver has previously been identified as the organ of interest to investigate susceptibility and resistance to Ascaris infection [ 31 , 32 ].…”

Section: Discussionmentioning

confidence: 99%

“…Despite its global prevalence and sheer numbers of individuals it infects, ascariasis remains a classic neglected disease [ 1 ] and part of the explanation for this neglect, is because pigs as animal models are costly and laborious and we lack the versatility of inbred strains. The majority of model organisms that have been infected with Ascaris are so-called abnormal hosts, whereby the parasite does not complete its life-cycle, but manifests itself as the early migratory phase [ 29 ]. Furthermore, in the vast majority of such experimental systems, the basis of resistance or susceptibility to infection has not been clearly established [ 29 ].…”

Section: Introductionmentioning

confidence: 99%

“…The majority of model organisms that have been infected with Ascaris are so-called abnormal hosts, whereby the parasite does not complete its life-cycle, but manifests itself as the early migratory phase [ 29 ]. Furthermore, in the vast majority of such experimental systems, the basis of resistance or susceptibility to infection has not been clearly established [ 29 ]. In contrast, a convenient and repeatable mouse model for exploring the susceptibility to Ascaris during the early phase of infection has been developed [ 30 – 32 ].…”

Section: Introductionmentioning

confidence: 99%

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A Proteomic Investigation of Hepatic Resistance to Ascaris in a Murine Model

et al. 2016

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The helminth Ascaris causes ascariasis in both humans and pigs. Humans, especially children, experience significant morbidity including respiratory complications, growth deficits and intestinal obstruction. Given that 800 million people worldwide are infected by Ascaris, this represents a significant global public health concern. The severity of the symptoms and associated morbidity are related to the parasite burden and not all hosts are infected equally. While the pathology of the disease has been extensively examined, our understanding of the molecular mechanisms underlying resistance and susceptibility to this nematode infection is poor. In order to investigate host differences associated with heavy and light parasite burden, an experimental murine model was developed utilising Ascaris-susceptible and -resistant mice strains, C57BL/6J and CBA/Ca, respectively, which experience differential burdens of migratory Ascaris larvae in the host lungs. Previous studies identified the liver as the site where this difference in susceptibility occurs. Using a label free quantitative proteomic approach, we analysed the hepatic proteomes of day four post infection C57BL/6J and CBA/Ca mice with and without Ascaris infection to identify proteins changes potentially linked to both resistance and susceptibility amongst the two strains, respectively. Over 3000 proteins were identified in total and clear intrinsic differences were elucidated between the two strains. These included a higher abundance of mitochondrial proteins, particularly those associated with the oxidative phosphorylation pathway and reactive oxygen species (ROS) production in the relatively resistant CBA/Ca mice. We hypothesise that the increased ROS levels associated with higher levels of mitochondrial activity results in a highly oxidative cellular environment that has a dramatic effect on the nematode’s ability to successfully sustain a parasitic association with its resistant host. Under infection, both strains had increased abundances in proteins associated with the oxidative phosphorylation pathway, as well as the tricarboxylic acid cycle, with respect to their controls, indicating a general stress response to Ascaris infection. Despite the early stage of infection, some immune-associated proteins were identified to be differentially abundant, providing a novel insight into the host response to Ascaris. In general, the susceptible C57BL/6J mice displayed higher abundances in immune-associated proteins, most likely signifying a more active nematode cohort with respect to their CBA/Ca counterparts. The complement component C8a and S100 proteins, S100a8 and S100a9, were highly differentially abundant in both infected strains, signifying a potential innate immune response and the importance of the complement pathway in defence against macroparasite infection. In addition, the signatures of an early adaptive immune response were observed through the presence of proteins, such as plastin-2 and dipeptidyl peptidase 1. A marked decrease in proteins associated wi...

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Larval Ascariasis

Cited by 15 publications

References 88 publications

Comorbidity associated to Ascaris suum infection during pulmonary fibrosis exacerbates chronic lung and liver inflammation and dysfunction but not affect the parasite cycle in mice

Comorbidity associated to Ascaris suum infection during pulmonary fibrosis exacerbates chronic lung and liver inflammation and dysfunction but not affect the parasite cycle in mice

Ascaris lumbricoidesandAscaris suumvary in their larval burden in a mouse model

A Proteomic Investigation of Hepatic Resistance to Ascaris in a Murine Model

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