生物谷援引：據(jù)英國《每日電訊報》網(wǎng)站近日報道，科學家研究發(fā)現(xiàn),，導致食物變質的細菌進入太空后會更加致命,。
研究人員認為，其他類型的細菌在太空中也會有類似的變化,，因此前往月球或火星的載人項目可能會滋生一些在某些情況下更致命的細菌,，盡管它們并不會成為有更強耐藥性的所謂超級細菌。然而,，好消息是,，研究人員弄懂了細菌變得更加致命的原因，從而為抗菌素的開發(fā)指明了新的方向,。
亞利桑那州立大學進行的一項最新研究顯示,，進入太空的細菌在太空失重環(huán)境中也會像人體一樣受到重大的影響。該大學的謝里爾·尼克森和詹姆斯·威爾遜首次研究了太空飛行對于鼠傷寒沙門氏菌的基因反應和致病力的影響,。鼠傷寒沙門氏菌是引起食物中毒的主要致病菌,。
他們發(fā)表在《國家科學院學報》上的報告描述了這種細菌在１２天的太空飛行后怎樣變得更具毒性。這些細菌是在２００６年９月由航天飛機帶上太空的,，宇航員海德馬里·Ｍ·斯蒂芬尼辛－派珀負責細菌的培養(yǎng)試驗,。與地球上的細菌相比，到過太空的沙門氏菌出現(xiàn)了１６７個基因的表達變化,，其對老鼠的致命殺傷力是地球上細菌的近３倍,。
研究顯示,，長途的太空旅行主要對調節(jié)基因表達的Ｈｆｑ蛋白產生影響，從而引發(fā)基因變化,，使沙門氏菌的毒性增強,。研究還顯示，Ｈｆｑ將是今后藥物對抗胃腸道細菌時的主要目標,，因為目前還沒有針對沙門氏菌食物中毒的人類疫苗,。此外，這一成果可能還為沙門氏菌抗藥性增強的研究帶來了新的曙光,。
研究人員目前認為,，與微重力有關的液體條件是導致細菌毒性增強的原因。不過,，要得出進一步的研究結論,，他們還打算明年再進行一次細菌太空之旅。（新華網(wǎng)）
原始出處:
Published online before print September 27, 2007
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0707155104
Microbiology
Space flight alters bacterial gene expression and virulence and reveals a role for global regulator Hfq
( microgravity | Space Shuttle | low shear modeled microgravity | rotating wall vessel | Salmonella )
J. W. Wilson a,b, C. M. Ott c, K. Höner zu Bentrup b, R. Ramamurthy b, L. Quick a, S. Porwollik d, P. Cheng d, M. McClelland d, G. Tsaprailis e, T. Radabaugh e, A. Hunt e, D. Fernandez a, E. Richter a, M. Shah f, M. Kilcoyne f, L. Joshi f, M. Nelman-Gonzalez g, S. Hing h, M. Parra h, P. Dumars h, K. Norwood i, R. Bober i, J. Devich i, A. Ruggles i, C. Goulart j, M. Rupert j, L. Stodieck j, P. Stafford k, L. Catella i, M. J. Schurr b,l, K. Buchanan b,m, L. Morici b, J. McCracken b,n, P. Allen b,o, C. Baker-Coleman b,o, T. Hammond b,o, J. Vogel p, R. Nelson q, D. L. Pierson c, H. M. Stefanyshyn-Piper r, and C. A. Nickerson a,b,s
aCenter for Infectious Diseases and Vaccinology, fCenter for Glycoscience Technology, kCenter for Innovations in Medicine, and qCenter for Combinatorial Sciences, The Biodesign Institute, Arizona State University, Tempe, AZ 85287; bTulane University Health Sciences Center, New Orleans, LA 70112; cHabitability and Environmental Factors Division and rAstronaut Office, Johnson Space Center, National Aeronautics and Space Administration, Houston, TX 77058; dSidney Kimmel Cancer Center, San Diego, CA 92121; eCenter for Toxicology, University of Arizona, Tucson, AZ 85721; gWyle Laboratories, Houston, TX 77058; hAmes Research Center, National Aeronautics and Space Administration, Moffett Field, CA 94035; iSpace Life Sciences Laboratory, Kennedy Space Center, Cape Canaveral, FL 32920; jBioServe, University of Colorado, Boulder, CO 80309; lUniversity of Colorado at Denver and Health Sciences Center, Denver, CO 80262; mOklahoma City University, Oklahoma City, OK 73106; nSection of General Surgery, University of Chicago, Chicago, IL 60637; oSoutheast Louisiana Veterans Health Care System, New Orleans, LA 70112; and pRNA Biology Group, Max Planck Institute for Infection Biology, 10117 Berlin, Germany
Edited by Arnold L. Demain, Drew University, Madison, NJ, and approved August 27, 2007 (received for review July 30, 2007)
A comprehensive analysis of both the molecular genetic and phenotypic responses of any organism to the space flight environment has never been accomplished because of significant technological and logistical hurdles. Moreover, the effects of space flight on microbial pathogenicity and associated infectious disease risks have not been studied. The bacterial pathogen Salmonella typhimurium was grown aboard Space Shuttle mission STS-115 and compared with identical ground control cultures. Global microarray and proteomic analyses revealed that 167 transcripts and 73 proteins changed expression with the conserved RNA-binding protein Hfq identified as a likely global regulator involved in the response to this environment. Hfq involvement was confirmed with a ground-based microgravity culture model. Space flight samples exhibited enhanced virulence in a murine infection model and extracellular matrix accumulation consistent with a biofilm. Strategies to target Hfq and related regulators could potentially decrease infectious disease risks during space flight missions and provide novel therapeutic options on Earth.
sTo whom correspondence should be addressed at: The Biodesign Institute, Center for Infectious Diseases and Vaccinology, Arizona State University, 1001 South McAllister Avenue, Tempe, AZ 85287.
C. A. Nickerson, E-mail: [email protected]
