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.
Cold-responsive (COR) genes participate in the response of plants to low-temperature stress. In this study, we isolated and characterized a cold-responsive and light-inducible gene COR15B from Arabidopsis thaliana. Chloroplast damage caused by mutations (albino mutants seca1, secy1, and tic20) or by a norflurazon (NF) treatment resulted in a reduction of COR15B transcription. A semi-quantitative RT-PCR analysis shows that COR15B was induced by the salt stress in an abscisic acid-dependent manner. An over-expression of COR15B in Arabidopsis resulted in transgenic lines more sensitive to the NaCl treatment than the wild type. However, COR15B knockdown did not significantly affect the sensitivity of the cor15b mutant to the salt stress. Furthermore, we found that the expression of COR15A, a homologous gene of COR15B, was significantly elevated in cor15b mutant plants. All these results suggest that plants acquire the ability to fully express COR15B only after development of functional chloroplasts. The expressional reprogramming and functional backup may exist between COR15 homologues in Arabidopsis.
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