近日,，比利時研究人員通過研究表示，借助改造宿主自身攜帶的有益細(xì)菌,，可以抑制昏睡癥罪魁禍?zhǔn)族F體蟲的生長,，從而達(dá)到遏制昏睡癥傳播的目的。
昏睡癥,，學(xué)名為非洲錐蟲病,，是一種致命性疾病，在非洲一些地區(qū)相當(dāng)流行,。錐體蟲寄生于采采蠅,，經(jīng)由后者叮咬進(jìn)入人體，導(dǎo)致發(fā)病,?；疾〕跗冢梭w會出現(xiàn)發(fā)燒,、頭疼,、關(guān)節(jié)疼痛和發(fā)癢的癥狀,；這一病癥進(jìn)入第二階段、錐體蟲侵入人體神經(jīng)系統(tǒng)后,，人體會出現(xiàn)反應(yīng)遲鈍,、嗜睡的癥狀。如果不經(jīng)治療,，患者有生命危險,。
針對昏睡癥的傳統(tǒng)治療方案出現(xiàn)于50多年前?；颊呓邮苤委煏r極其痛苦,，同時需要承擔(dān)其他副作用，大約5%至20%接受治療的患者因注射藥物后導(dǎo)致的并發(fā)癥死亡,。
因此,，醫(yī)學(xué)界一直在尋找治療這一病癥的其他可選方案。比利時安特衛(wèi)普熱帶醫(yī)學(xué)研究所一個團(tuán)隊把研究焦點集中在如何防止人體染病,，而非如何治療,。相關(guān)成果論文刊登于期刊《微生物細(xì)胞工廠》Microbial Cell Factories上 。
英國廣播公司2月15日援引成果論文報道,，采采蠅與人類類似,，會攜帶一些有益細(xì)菌。研究人員發(fā)現(xiàn),，一種采采蠅攜帶的共生菌或許有能力向錐體蟲發(fā)起攻擊,。
借助改變這種共生菌的基因，研究人員得以使它釋放出一種納米抗體,，殺死錐體蟲或者阻止這種寄生蟲的生長,。
倫敦大學(xué)衛(wèi)生與熱帶醫(yī)學(xué)院學(xué)者戴維·霍恩評價：“這是一項具有發(fā)展前景的觀念。”（生物谷Bioon.com）
doi:10.1186/1475-2859-11-23
PMC:
PMID:
Expression and extracellular release of a functional anti-trypanosome Nanobody(R) in Sodalis glossinidius, a bacterial symbiont of the tsetse fly
Linda De Vooght, Guy Caljon, Benoit Stijlemans, Patrick De Beatselier, Marc Coosemans and Jan Van Den Abbeele
Background Sodalis glossinidius, a gram-negative bacterial endosymbiont of the tsetse fly, has been proposed as a potential in vivo drug delivery vehicle to control trypanosome parasite development in the fly, an approach known as paratransgenesis. Despite this interest of S. glossinidius as a paratransgenic platform organism in tsetse flies, few potential effector molecules have been identified so far and to date none of these molecules have been successfully expressed in this bacterium. Results In this study, S. glossinidius was transformed to express a single domain antibody, (Nanobody(R)) Nb_An33, that efficiently targets conserved cryptic epitopes of the variant surface glycoprotein (VSG) of the parasite Trypanosoma brucei. Next, we analyzed the capability of two predicted secretion signals to direct the extracellular delivery of significant levels of active Nb_An33. We show that the pelB leader peptide was successful in directing the export of fully functional Nb_An33 to the periplasm of S. glossinidius resulting in significant levels of extracellular release. Finally, S. glossinidius expressing pelBNb_An33 exhibited no significant reduction in terms of fitness, determined by in vitro growth kinetics, compared to the wild-type strain. Conclusions These data are the first demonstration of the expression and extracellular release of functional trypanosome-interfering Nanobodies(R) in S. glossinidius. Furthermore, Sodalis strains that efficiently released the effector protein were not affected in their growth, suggesting that they may be competitive with endogenous microbiota in the midgut environment of the tsetse fly. Collectively, these data reinforce the notion for the potential of S. glossinidius to be developed into a paratransgenic platform organism.
