生物谷援引：据英国《每日电讯报》网站近日报道，科学家研究发现，导致食物变质的细菌进入太空后会更加致命。
研究人员认为，其他类型的细菌在太空中也会有类似的变化，因此前往月球或火星的载人项目可能会滋生一些在某些情况下更致命的细菌，尽管它们并不会成为有更强耐药性的所谓超级细菌。然而，好消息是，研究人员弄懂了细菌变得更加致命的原因，从而为抗菌素的开发指明了新的方向。
亚利桑那州立大学进行的一项最新研究显示，进入太空的细菌在太空失重环境中也会像人体一样受到重大的影响。该大学的谢里尔·尼克森和詹姆斯·威尔逊首次研究了太空飞行对于鼠伤寒沙门氏菌的基因反应和致病力的影响。鼠伤寒沙门氏菌是引起食物中毒的主要致病菌。
他们发表在《国家科学院学报》上的报告描述了这种细菌在１２天的太空飞行后怎样变得更具毒性。这些细菌是在２００６年９月由航天飞机带上太空的，宇航员海德马里·Ｍ·斯蒂芬尼辛－派珀负责细菌的培养试验。与地球上的细菌相比，到过太空的沙门氏菌出现了１６７个基因的表达变化，其对老鼠的致命杀伤力是地球上细菌的近３倍。
研究显示，长途的太空旅行主要对调节基因表达的Ｈｆｑ蛋白产生影响，从而引发基因变化，使沙门氏菌的毒性增强。研究还显示，Ｈｆｑ将是今后药物对抗胃肠道细菌时的主要目标，因为目前还没有针对沙门氏菌食物中毒的人类疫苗。此外，这一成果可能还为沙门氏菌抗药性增强的研究带来了新的曙光。
研究人员目前认为，与微重力有关的液体条件是导致细菌毒性增强的原因。不过，要得出进一步的研究结论，他们还打算明年再进行一次细菌太空之旅。（新华网）
原始出处:
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: cheryl.nickerson@asu.edu
