From Inflammation to Fibrosis: Novel Insights into the Roles of High Mobility Group Protein Box 1 in Schistosome-Induced Liver Damage

Schistosomiasis is a chronic helminthic disease of both humans and animals and the second most prevalent parasitic disease after malaria. Through a complex migration process, schistosome eggs trapped in the liver can lead to the formation of granulomas and subsequent schistosome-induced liver damage...

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Bibliographic Details
Published in:Pathogens (Basel) 2022-02, Vol.11 (3), p.289
Main Authors: Zhong, Haoran, Gui, Xiang, Hou, Ling, Lv, Rongxue, Jin, Yamei
Format: Article
Language:English
Subjects:
Advanced glycosylation end products
Animal diseases
Animal models
Binding sites
Cell surface
Complications
Cytokines
Damage
Drug development
Eggs
Fibrosis
Glycosylation
Granuloma
granulomas
hepatic fibrosis
high mobility group protein box 1
High mobility group proteins
HMGB1 protein
Hypertension
Immune response
Immune system
Immunosuppressive agents
Infections
Inflammation
Kinases
Liver
Liver diseases
Malaria
Mammals
Mobility
Morbidity
Parasitic diseases
Phenotypes
Praziquantel
Proteins
Receptors
Review
Schistosomiasis
Signal transduction
Stellate cells
Therapeutic targets
Toll-like receptors
Tropical diseases
Vector-borne diseases
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Summary:Schistosomiasis is a chronic helminthic disease of both humans and animals and the second most prevalent parasitic disease after malaria. Through a complex migration process, schistosome eggs trapped in the liver can lead to the formation of granulomas and subsequent schistosome-induced liver damage, which results in high mortality and morbidity. Although praziquantel can eliminate mature worms and prevent egg deposition, effective drugs to reverse schistosome-induced liver damage are scarce. High mobility group box 1 (HMGB1) is a multifunctional cytokine contributing to liver injury, inflammation, and immune responses in schistosomiasis by binding to cell-surface Toll-like receptors and receptors for advanced glycation end products. HMGB1 is increased in the serum of patients with schistosomiasis and enables hepatic stellate cells to adopt a proliferative myofibroblast-like phenotype, which is crucial to schistosome-induced granuloma formation. Inhibition of HMGB1 was found to generate protective responses against fibrotic diseases in animal models. Clinically, HMGB1 presents a potential target for treatment of the chronic sequelae of schistosomiasis. Here, the pivotal role of HMGB1 in granuloma formation and schistosome-induced liver damage, as well the potential of HMGB1 as a therapeutic target, are discussed.
ISSN:2076-0817
2076-0817
DOI:10.3390/pathogens11030289