Resolution of systemic complications in Schistosoma mansoni-infected mice by concomitant treatment with praziquantel and Schisandrin B

2021 ◽

Vol 15 (6) ◽

pp. e0009554

Author(s):

Ho Yin Pekkle Lam ◽

Ting-Ruei Liang ◽

Shih-Yi Peng

Keyword(s):

Liver Fibrosis ◽

Schistosoma Mansoni ◽

Egg Production ◽

Treatment Options ◽

Parasite Burden ◽

Inflammasome Activation ◽

Schisandrin B ◽

Male Adult

Schistosomiasis is second only to malaria as the most devastating parasitic disease in the world. It is caused by the helminths Schistosoma mansoni (S. mansoni), S. haematobium, or S. japonicum. Typically, patients with schistosomiasis suffer from symptoms of liver fibrosis and hepatosplenomegaly. Currently, patients were treated with praziquantel. Although praziquantel effectively kills the worm, it cannot prevent re-infection or resolve liver fibrosis. Also, current treatment options are not ample to completely cure liver fibrosis and splenic damages. Moreover, resistance of praziquantel has been reported in vivo and in vitro studies. Therefore, finding new effective treatment agents is urgently needed. Schisandrin B (Sch B) of Schisandra chinensis has been shown to protect against different liver injuries including fatty liver disease, hepatotoxicity, fibrosis, and hepatoma. We herein investigate the potential of using Sch B to treat S. mansoni-induced liver fibrosis. Results from the present study demonstrate that Sch B is beneficial in treating S. mansoni-induced liver fibrosis and splenic damages, through inhibition of inflammasome activation and apoptosis; and aside from that regulates host immune responses. Besides, Sch B treatment damages male adult worm in the mice, consequently helps to reduce egg production and lessen the parasite burden.

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Ultrastructural analysis of “Sensory” surface nerve endings and “putative” neurotransmitter sites in Schistosoma mansoni Miracidia

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100156791 ◽

1989 ◽

Vol 47 ◽

pp. 962-963

Author(s):

Betty Ruth Jones ◽

Steve Chi-Tang Pan

Keyword(s):

Nervous System ◽

Life Cycle ◽

Schistosoma Mansoni ◽

Snail Host ◽

Complex Life Cycle ◽

Rational Approach ◽

Effective Control ◽

The Social ◽

Social And Economic Development ◽

Basic Biology

INTRODUCTION: Schistosomiasis has been described as “one of the most devastating diseases of mankind, second only to malaria in its deleterious effects on the social and economic development of populations in many warm areas of the world.” The disease is worldwide and is probably spreading faster and becoming more intense than the overall research efforts designed to provide the basis for countering it. Moreover, there are indications that the development of water resources and the demands for increasing cultivation and food in developing countries may prevent adequate control of the disease and thus the number of infections are increasing.Our knowledge of the basic biology of the parasites causing the disease is far from adequate. Such knowledge is essential if we are to develop a rational approach to the effective control of human schistosomiasis. The miracidium is the first infective stage in the complex life cycle of schistosomes. The future of the entire life cycle depends on the capacity and ability of this organism to locate and enter a suitable snail host for further development, Little is known about the nervous system of the miracidium of Schistosoma mansoni and of other trematodes. Studies indicate that miracidia contain a well developed and complex nervous system that may aid the larvae in locating and entering a susceptible snail host (Wilson, 1970; Brooker, 1972; Chernin, 1974; Pan, 1980; Mehlhorn, 1988; and Jones, 1987-1988).

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Beeinflussung der chronisch-entzündlichen Darmerkrankungen durch Schistosoma mansoni und Schistosomen-Strukturen im DSS-Kolitis-Modell der Maus

Zeitschrift für Gastroenterologie ◽

10.1055/s-0028-1089567 ◽

2008 ◽

Vol 46 (09) ◽

Author(s):

P Bodammer ◽

G Waitz ◽

M Löbermann ◽

EC Reisinger ◽

J Emmrich

Keyword(s):

Schistosoma Mansoni

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In vitro schistosomicidal activity of Usnea steineri extract and its major constituent (+)-usnic acid against Schistosoma mansoni

Planta Medica ◽

10.1055/s-0032-1320991 ◽

2012 ◽

Vol 78 (11) ◽

Cited By ~ 5

Author(s):

AIO Salloum ◽

R Lucarini ◽

MG Tozatti ◽

J Medeiros ◽

MLA Silva ◽

...

Keyword(s):

Schistosoma Mansoni ◽

Usnic Acid ◽

Major Constituent

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Inhibitor treatment by rituximabin congenital haemophilia A

Hämostaseologie ◽

10.1055/s-0037-1617028 ◽

2009 ◽

Vol 29 (02) ◽

pp. 151-154 ◽

Cited By ~ 13

Author(s):

Escuriola Ettingshausen ◽

R. Linde ◽

G. Kropshofer ◽

L.-B. Zimmerhackl ◽

W. Kreuz ◽

...

Keyword(s):

B Cell ◽

Immune Tolerance ◽

High Titre ◽

Clotting Factor ◽

Severe Bleeding ◽

High Morbidity ◽

Haemophilia A ◽

Concomitant Treatment ◽

Bleeding Tendency ◽

Severe Haemophilia

SummaryThe development of neutralizing alloanti-bodies (inhibitors) to factor VIII (FVIII) is one of the most serious complications in the treatment of haemophiliacs. Inhibitors occur in approximately 20 to 30% of previously untreated patients (PUPs), predominantly children, with severe haemophilia A within the first 50 exposure days (ED). Immune tolerance induction (ITI) leads to complete elimination of the inhibitor in up to 80% of the patients and offers the possibility to restore regular FVIII prophylaxis. However, patients with high titre inhibitors, in whom standard ITI fails, usually impose with high morbidity and mortality and therefore prompting physicians to alternate therapy regimens. Rituximab, an anti-CD 20 monoclonal antibody has been successfully used in children and adults for the management of B-cell mediated disorders. We report on the use of a new protocol including rituximab in two adolescents with severe haemophilia A and high titre inhibitors, severe bleeding tendency and high clotting factor consumption after failing standard ITI. Both patients received a concomitant treatment with FVIII according to the Bonn protocol, cyclosporine A and immunoglobulin. Treatment with rituximab resulted in a temporary B-cell depletion leading to the disappearance of the inhibitor. FVIII recovery and half-life turned towards normal ranges. In patient 1 the inhibitor reappeared 14 months after the last rituximab administration. In patient 2 complete immune tolerance could be achieved for 60 months. Bleeding frequency diminished significantly and clinical joint status improved in both patients. In patient 1 the treatment course was complicated by aspergillosis and hepatitis B infection. Conclusion: Rituximab may be favourable for patients with congenital haemophilia, high-titre inhibitors and a severe clinical course in whom standard ITI has failed. Prospective studies are required to determine safety, efficacy and predictors of success.

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