Clinical Spectrum of Schistosomiasis: An Update

Carbonell, Cristina; Rodríguez‐Alonso, Beatriz; López-Bernús, Amparo; Almeida, Hugo; Galindo‐Pérez, Inmaculada; Velasco‐Tirado, Virginia; Marcos, Miguel; Pardo‐Lledías, Javier; Belhassen‐García, Moncef

doi:10.3390/jcm10235521

Cited by 43 publications

(32 citation statements)

References 59 publications

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“…Schistosomiasis is a globally distributed neglected tropical disease, which primarily occurs in tropical and subtropical regions [ 16 ]. Worldwide, approximately 236 million people are infected with schistosomes, 90% of which are located in sub-Saharan Africa, and results in approximately 300,000 deaths per year [ 17 , 18 ]. In China, according to the national schistosomiasis epidemic bulletin in 2020, although schistosomiasis has a low prevalence, there remains a large number of patients with schistosomiasis liver fibrosis [ 2 ].…”

Section: Discussionmentioning

confidence: 99%

Pathological Changes in Hepatic Sinusoidal Endothelial Cells in Schistosoma japonicum-Infected Mice

Jiang

Zhou

et al. 2023

TropicalMed

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Schistosomiasis japonica is a zoonotic parasitic disease causing liver fibrosis. Liver sinusoidal endothelial cells (LSECs) exhibit fenestrations, which promote hepatocyte regeneration and reverses the process of liver fibrosis. To investigate the pathological changes of LSECs in schistosomiasis, we established a Schistosomiasis model. The population, phenotype, and secretory function of LSECs were detected by flow cytometry at 20, 28, and 42 days post infection. The changes in LSEC fenestration and basement membrane were observed through scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Quantitative real-time PCR and Western blotting were used to detect the expression of molecules associated with epithelial–mesenchymal transition (EMT) and fibrosis of LSECs and the liver. The flow cytometry results showed that the total LSEC proportions, differentiated LSEC proportions, and nitric oxide (NO) secretion of LSECs were decreased, and the proportion of dedifferentiated LSECs increased significantly post infection. The electron microscopy results showed that the number of fenestrate was decreased and there was complete basement membrane formation in LSECs following infection. The qPCR and Western blot results showed that EMT, and fibrosis-related indicators of LSECs and the liver changed significantly during the early stages of infection and were aggravated in the middle and late stages. The pathological changes in LSECs may promote EMT and liver fibrosis induced by Schistosoma japonicum infection.

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Section: Discussionmentioning

confidence: 99%

Pathological Changes in Hepatic Sinusoidal Endothelial Cells in Schistosoma japonicum-Infected Mice

Jiang

Zhou

et al. 2023

TropicalMed

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“…The clinical severity of each of these stages depends on both parasite and host factors, including worm burden and the ability of the human host to mount an effective immune response 3 . During or immediately after skin penetration by infective cercariae, hypersensitive reactions triggered by antigens released by migrating larvae may lead to ‘cercarial dermatitis’, characterized by a maculopapular pruritic reaction 24,25 . Acute schistosomiasis (or Katayama fever) occurs during the pre‐patent phase of the infection, and is characterized by fever, cough, and myalgia, and is mainly observed in individuals exposed to the parasite for the first time.…”

Section: The Pathophysiology Of Schistosomiasismentioning

confidence: 99%

“…3 During or immediately after skin penetration by infective cercariae, hypersensitive reactions triggered by antigens released by migrating larvae may lead to 'cercarial dermatitis', characterized by a maculopapular pruritic reaction. 24,25 Acute schistosomiasis (or Katayama fever) occurs during the prepatent phase of the infection, and is characterized by fever, cough, and myalgia, and is mainly observed in individuals exposed to the parasite for the first time. This symptomatology is believed to be related to parasite antigens released by the migrating schistosomula that can lead to the formation of immune complexes and systemic hypersensitivity.…”

Section: Introductionmentioning

confidence: 99%

The role of the host gut microbiome in the pathophysiology of schistosomiasis

Stark

Rinaldi

Cortés

et al. 2023

Parasite Immunology

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The pathophysiology of schistosomiasis is linked to the formation of fibrous granulomas around eggs that become trapped in host tissues, particularly the intestines and liver, during their migration to reach the lumen of the vertebrate gut. While the development of Schistosoma egg-induced granulomas is the result of finely regulated crosstalk between egg-secreted antigens and host immunity, evidence has started to emerge of the likely contribution of an additional player-the host gut microbiota-to pathological processes that culminate with the formation of these tissue lesions. Uncovering the role(s) of schistosome-mediated changes in gut microbiome composition and function in granuloma formation and, more broadly, in the pathophysiology of schistosomiasis, will shed light on the mechanisms underlying this three-way parasite-host-microbiome interplay.Such knowledge may, in turn, pave the way towards the discovery of novel therapeutic targets and control strategies.

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“…Adult worms eventually settle in blood vessels, where the female worms produce hundreds to thousands of eggs per day [ 4 ]. Some eggs are passed out in the host’s feces or urine to continue the next life-cycle, and others are deposited in body tissues such as the liver, small intestine (for S. mansoni , S. japonicum , and S. mekongi ), and bladder (for S. haematobium ), causing an imbalance in immunoregulation and progressive organ lesions [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Activation of primary hepatic stellate cells and liver fibrosis induced by targeting TGF-β1/Smad signaling in schistosomiasis in mice

Huang

Cao

et al. 2022

Parasites Vectors

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Background In mice, liver fibrosis is the most serious pathologic change during Schistosoma japonicum (S. japonicum) infection. Schistosomiasis is mainly characterized by schistosome egg-induced granulomatous fibrosis. Hepatic stellate cells (HSCs) are mainly responsible for the net accumulation of collagens and fibrosis formation in the liver. Activated HSCs regulated by transforming growth factor-β1 (TGF-β1)/Smad signaling have emerged as the critical regulatory pathway in hepatitis virus or carbon tetrachloride-induced liver fibrosis. However, the detailed mechanism of HSC activation in schistosome-induced liver fibrosis is poorly understood. Methods Schistosoma japonicum-induced murine models and a control group were generated by abdominal infection with 15 (± 1) cercariae. The purity of cultured primary HSCs was evaluated by immunocytochemistry. The histopathological changes in the livers of infected mice were estimated by hematoxylin–eosin and Masson staining. Dynamic expression of pro-fibrotic molecules and microRNAs was detected by real-time quantitative PCR (RT-qPCR). Mainly members involved in the TGF-β1/Smad signaling pathway were examined via RT-qPCR and Western blot. Results The egg-induced granulomatous inflammation formed at 4 weeks post-infection (wpi) and developed progressively. Alpha-smooth muscle actin (α-SMA), collagen I, collagen III, TGF-β1, Smad2, Smad3, and Smad4 showed a significant increase in mitochondrial RNA (mRNA) and protein expression compared with the control group at 7 and 9 weeks post-infection (wpi), while an opposite effect on Smad7 was observed. In addition, the mRNA expression of microRNA-21 (miRNA-21) was significantly increased at 7 wpi, and the mRNA expression of miRNA-454 was decreased starting from 4 wpi. Conclusion Our present findings revealed that HSCs regulated by the TGF-β1/Smad signaling pathway play an important role in liver fibrosis in S. japonicum-infected mice, which may provide proof of concept for liver fibrosis in schistosomiasis. Graphical Abstract

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Clinical Spectrum of Schistosomiasis: An Update

Cited by 43 publications

References 59 publications

Pathological Changes in Hepatic Sinusoidal Endothelial Cells in Schistosoma japonicum-Infected Mice

Pathological Changes in Hepatic Sinusoidal Endothelial Cells in Schistosoma japonicum-Infected Mice

The role of the host gut microbiome in the pathophysiology of schistosomiasis

Activation of primary hepatic stellate cells and liver fibrosis induced by targeting TGF-β1/Smad signaling in schistosomiasis in mice

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