Project description:The host central nervous system (CNS) response to infection with Trypanosoma brucei (T. b.) gambiense or T. b. rhodesiense parasites, the causing agent of human African trypanosomiasis (HAT), is a poorly explored area. The two parasites are responsible for respectively a chronic and an acute form of HAT. In both cases, however, the disease progresses from a haemolymphatic first stage (S1) to a meningo-encephalitic second stage (S2) due to the penetration of parasites into the CNS. In the present study, we investigated and compared the cerebrospinal fluid (CSF) from S2 patients affected by either T. b. gambiense or T. b. rhodesiense HAT, using a mass spectrometry quantitative proteomics approach. Gene ontology and pathway analyses on the 222 quantified proteins, revealed a predominant activation of the innate immune and the acute phase responses in rhodesiense HAT. These results were further confirmed through the verification of the over-expression of two proteins involved in these mechanisms, C-reactive protein (CRP) and orosomucoid 1 (ORM1), in 126 S2 HAT patients suffering from either the chronic or the acute form of HAT. Both proteins were significantly increased (p<0.0001) in the CSF of rhodesiense HAT patients. These findings contribute in better understanding the pathophysiological mechanisms of late stage HAT caused by T. b. gambiense or T. b. rhodesiense and pave the way for further investigations on the clinical significance of CRP and ORM1. See article: <a href="http://www.sciencedirect.com/science/article/pii/S2212963414000126">Increased acute immune response during the meningo-encephalitic stage of Trypanosoma brucei rhodesiense sleeping sickness compared to Trypanosoma brucei gambiense</a>
Project description:Transcriptome analysis of Sodalis glossinidius derived from Trypanosoma brucei gambiense infection self cleared and infected Glossina palpalis gambiensis. At 3 time points (3, 10 and 20 days) after infectived blood meal, flies were analysed by PCR to isolate the infected and infection self cleared flies. Then, infected and infection self cleared flies midgut were dissected for RNA extraction.
Project description:Transcriptome analysis of Sodalis glossinidius derived from uninfected (controls) and Trypanosoma brucei gambiense infection self cleared Glossina palpalis gambiensis. 10 days after infectived blood meal, flies anal drop were analysed by PCR to isolate the infected self cleared flies. Then, uninfected (controls) and infection self cleared 10 days-flies midgut were dissected for RNA extraction.
Project description:Trypanosoma brucei gambiense is the causative agent of the fatal human disease African sleeping sickness. Using Digital Gene Expression we have compared the transcriptome of two T.b.brucei (STIB 247)xT.b.gambiense (STIB386) hybrids.
Project description:Trypanosoma brucei gambiense is the causative agent of the fatal human disease African sleeping sickness. Using Digital Gene Expression we have compared the transcriptome of a group 1 T.b.gambiense (Eliane) and a T.b.brucei (STIB 247).
Project description:Transcriptome analysis of Sodalis glossinidius derived from Trypanosoma brucei gambiense infection self cleared and infected Glossina palpalis gambiensis. At 3 time points (3, 10 and 20 days) after infectived blood meal, flies were analysed by PCR to isolate the infected and infection self cleared flies. Then, infected and infection self cleared flies midgut were dissected for RNA extraction. Total RNAs were extracted at 3 time points (3, 10 and 20 days) from 24 samples including, for each time, 4 infected and 4 infection self-cleared flies.
Project description:The host range of African trypanosomes is influenced by innate protective molecules in the blood of primates. A subfraction of human high-density lipoprotein (HDL) containing apolipoprotein A-I, apolipoprotein L-I, and haptoglobin-related protein is toxic to Trypanosoma brucei brucei but not the human sleeping sickness parasite Trypanosoma brucei rhodesiense. It is thought that T. b. rhodesiense evolved from a T. b. brucei-like ancestor and expresses a defense protein that ablates the antitrypanosomal activity of human HDL. To directly investigate this possibility, we developed an in vitro selection to generate human HDL-resistant T. b. brucei. Here we show that conversion of T. b. brucei from human HDL sensitive to resistant correlates with changes in the expression of the variant surface glycoprotein (VSG) and abolished uptake of the cytotoxic human HDLs. Complete transcriptome analysis of the HDL-susceptible and -resistant trypanosomes confirmed that VSG switching had occurred but failed to reveal the expression of other genes specifically associated with human HDL resistance, including the serum resistance-associated gene (SRA) of T. b. rhodesiense. In addition, we found that while the original active expression site was still utilized, expression of three expression site-associated genes (ESAG) was altered in the HDL-resistant trypanosomes. These findings demonstrate that resistance to human HDLs can be acquired by T. b. brucei. Keywords: Trypanosoma, VSG, antigenic switching, HDL-resistance
Project description:Trypanosoma brucei gambiense is the causative agent of the fatal human disease African sleeping sickness. Using Digital Gene Expression we have compared the transcriptome of two isogenic T.b.gambiense lines that are either sensitive or resistant to human serum.
Project description:Transcriptome analysis of Sodalis glossinidius derived from uninfected (controls) and Trypanosoma brucei gambiense infection self cleared Glossina palpalis gambiensis. 10 days after infectived blood meal, flies anal drop were analysed by PCR to isolate the infected self cleared flies. Then, uninfected (controls) and infection self cleared 10 days-flies midgut were dissected for RNA extraction. Total RNAs were extracted from 8 samples including: 4 control and 4 infection self-cleared flies.
