Erythrina abyssinica prevents meningoencephalitis in chronic Trypanosoma brucei brucei mouse model

2014 ◽  
Vol 29 (2) ◽  
pp. 509-519 ◽  
Author(s):  
Johnson Nasimolo ◽  
Stephen Gitahi Kiama ◽  
Peter Karuri Gathumbi ◽  
Andrew Ndegwa Makanya ◽  
John Maina Kagira
2017 ◽  
Vol 16 (10) ◽  
pp. 2373-2378
Author(s):  
Yan-Bing Ding ◽  
Jun Chen ◽  
Li-Xia Huang ◽  
Ye-Li Gong ◽  
Fa-Hu Yuan ◽  
...  

Purpose: To evaluate the antitrypanosomal activity of Malva sylvestris (MS) extract in a Trypanosoma brucei brucei-infected  mouse model of sleeping sickness.Methods: Sleeping sickness was induced by the intraperitoneal injection of Trypanosoma brucei brucei infected blood in mice.  Confirmation of parasitaemia was performed by estimating the parasite count in the plasma on the 12th day after inoculation. All the mice were divided into five groups: control group that received neither infection nor treatment; negative control that was  infected with the parasite but did not receive treatment; MS-treated group that receive MS extract (250 and 500 mg/kg, ip) and standard (STD) group that received levamisole (7.5 mg/kg, ip) for 7 days after the development of parasitaemia. A further parasite count was performed in the blood and cerebrospinal fluid (CSF) after the treatment period. Humoral antibody response,  delayed hypersensitivity reaction, and mobilization of leucocytes were determined after the treatment period in SRBC-sensitized mice.Results: The results indicate that treatment with MS significantly decreased body weight and parasite count in the blood and CSF of mice with Trypanosoma brucei brucei-induced sleeping sickness compared with that in the negative control group. There was a significant increase in paw swelling and decrease in secondary antibody in the MS-treated group compared with that in the  negative control group. However, treatment with MS extract also enhanced the mobilization of the total leucocyte count compared with that in the negative control group.Conclusion: The results demonstrate the anti-trypanosomal activity of Malva sylvestris extract via immunomodulation in a  Trypanosoma brucei brucei-infected mouse model of sleeping sickness.Keywords: Malva sylvestris, Trypanosoma brucei brucei, Sleeping sickness, Immunomodulatory activity, Delayed hypersensitivity reaction


Author(s):  
Folashade Sarah Ojeleye ◽  
Helen Ileigo Inabo ◽  
Clement Myah Zaman Whong ◽  
Bolanle Olufunke Priscilla Musa ◽  
Ochuko Orakpoghenor

2000 ◽  
Vol 8 (1) ◽  
pp. 31-38 ◽  
Author(s):  
Yajuan Liu ◽  
Manal Mustafa ◽  
Hu-Lun Li ◽  
Lauri Nuortio ◽  
Amged Mustafa ◽  
...  

Acta Tropica ◽  
1991 ◽  
Vol 50 (2) ◽  
pp. 169-183 ◽  
Author(s):  
Klaus Bender ◽  
Bruno Betschart ◽  
Johann Schaller ◽  
Urs Kämpfer ◽  
Hermann Hecker

2010 ◽  
Vol 54 (7) ◽  
pp. 2893-2900 ◽  
Author(s):  
Antoaneta Y. Sokolova ◽  
Susan Wyllie ◽  
Stephen Patterson ◽  
Sandra L. Oza ◽  
Kevin D. Read ◽  
...  

ABSTRACT The success of nifurtimox-eflornithine combination therapy (NECT) for the treatment of human African trypanosomiasis (HAT) has renewed interest in the potential of nitro drugs as chemotherapeutics. In order to study the implications of the more widespread use of nitro drugs against these parasites, we examined the in vivo and in vitro resistance potentials of nifurtimox and fexinidazole and its metabolites. Following selection in vitro by exposure to increasing concentrations of nifurtimox, Trypanosoma brucei brucei nifurtimox-resistant clones designated NfxR1 and NfxR2 were generated. Both cell lines were found to be 8-fold less sensitive to nifurtimox than parental cells and demonstrated cross-resistance to a number of other nitro drugs, most notably the clinical trial candidate fexinidazole (∼27-fold more resistant than parental cells). Studies of mice confirmed that the generation of nifurtimox resistance in these parasites did not compromise virulence, and NfxR1 remained resistant to both nifurtimox and fexinidazole in vivo. In the case of fexinidazole, drug metabolism and pharmacokinetic studies indicate that the parent drug is rapidly metabolized to the sulfoxide and sulfone form of this compound. These metabolites retained trypanocidal activity but were less effective in nifurtimox-resistant lines. Significantly, trypanosomes selected for resistance to fexinidazole were 10-fold more resistant to nifurtimox than parental cells. This reciprocal cross-resistance has important implications for the therapeutic use of nifurtimox in a clinical setting and highlights a potential danger in the use of fexinidazole as a monotherapy.


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