-
Je něco špatně v tomto záznamu ?
Commensal intestinal bacterial strains trigger ankylosing enthesopathy of the ankle in inbred B10.BR (H-2(k)) male mice
Z. Šinkorová, J. Čapková, J. Niederlová, R. Štěpánková, J. Šinkora
Jazyk angličtina Země Spojené státy americké
Typ dokumentu práce podpořená grantem
- MeSH
- ankylózující spondylitida imunologie mikrobiologie MeSH
- DNA bakterií analýza MeSH
- druhová specificita MeSH
- grampozitivní bakteriální infekce imunologie MeSH
- grampozitivní bakterie genetika imunologie izolace a purifikace patogenita MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- organismy bez specifických patogenů MeSH
- polymerázová řetězová reakce MeSH
- rizikové faktory MeSH
- sekvenční analýza DNA MeSH
- slizniční imunita imunologie MeSH
- střevní nádory imunologie mikrobiologie MeSH
- stupeň závažnosti nemoci MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
Joint disease ankylosing enthesopathy (ANKENT) naturally occurs in inbred mice with C57Bl/10 genetic background. ANKENT has many parallels to human ankylosing spondylitis (AS) and represents an animal model for AS. Environmental conditions (i.e., microbial load of the organism) are among the risk factors for ANKENT, similar to AS. The role of microflora in the development of ANKENT was investigated. ANKENT was tested in four experimental groups of germ-free mice associated with different numbers of various intestinal microbes and three control groups: germ-free, specific pathogen-free, and conventional (CV) mice. Mice were colonized either with anaerobic bacteria isolated from the intestine of a CV mouse or with bacterial strains obtained from the collection of microorganisms. Microbes were characterized and checked by microbiological cultivation methods and with the use of polymerase chain reaction amplification and rDNA sequence analysis. Joint disease developed in GF mice colonized with a mixture containing Bacteroides spp. and Enterococcus sp., and/or Veillonella sp. and Staphylococcus sp. No ANKENT appeared in males colonized with probiotic bacterium Lactobacillus sp. In control groups ANKENT occurred in SPF and CV animals; the GF animals remained healthy. The results confirmed that the germ-free conditions protect from joint inflammation, and thus microbes are necessary for ANKENT development. In colonized mice the ANKENT was triggered by luminal anaerobic bacteria, which are common components of intestinal microflora.
Citace poskytuje Crossref.org
- 000
- 03506naa 2200505 a 4500
- 001
- bmc11006224
- 003
- CZ-PrNML
- 005
- 20221005125134.0
- 008
- 110331s2008 xxu e eng||
- 009
- AR
- 024 7_
- $a 10.1016/j.humimm.2008.08.296 $2 doi
- 035 __
- $a (PubMed)18840492
- 040 __
- $a ABA008 $b cze $c ABA008 $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xxu
- 100 1_
- $a Šinkorová, Zuzana, $d 1963- $7 xx0106471
- 245 10
- $a Commensal intestinal bacterial strains trigger ankylosing enthesopathy of the ankle in inbred B10.BR (H-2(k)) male mice / $c Z. Šinkorová, J. Čapková, J. Niederlová, R. Štěpánková, J. Šinkora
- 314 __
- $a University of Defence, Faculty of Military Health Sciences, Hradec Kralove, Czech Republic.
- 520 9_
- $a Joint disease ankylosing enthesopathy (ANKENT) naturally occurs in inbred mice with C57Bl/10 genetic background. ANKENT has many parallels to human ankylosing spondylitis (AS) and represents an animal model for AS. Environmental conditions (i.e., microbial load of the organism) are among the risk factors for ANKENT, similar to AS. The role of microflora in the development of ANKENT was investigated. ANKENT was tested in four experimental groups of germ-free mice associated with different numbers of various intestinal microbes and three control groups: germ-free, specific pathogen-free, and conventional (CV) mice. Mice were colonized either with anaerobic bacteria isolated from the intestine of a CV mouse or with bacterial strains obtained from the collection of microorganisms. Microbes were characterized and checked by microbiological cultivation methods and with the use of polymerase chain reaction amplification and rDNA sequence analysis. Joint disease developed in GF mice colonized with a mixture containing Bacteroides spp. and Enterococcus sp., and/or Veillonella sp. and Staphylococcus sp. No ANKENT appeared in males colonized with probiotic bacterium Lactobacillus sp. In control groups ANKENT occurred in SPF and CV animals; the GF animals remained healthy. The results confirmed that the germ-free conditions protect from joint inflammation, and thus microbes are necessary for ANKENT development. In colonized mice the ANKENT was triggered by luminal anaerobic bacteria, which are common components of intestinal microflora.
- 590 __
- $a bohemika - dle Pubmed
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a DNA bakterií $x analýza $7 D004269
- 650 _2
- $a grampozitivní bakterie $x genetika $x imunologie $x izolace a purifikace $x patogenita $7 D006094
- 650 _2
- $a grampozitivní bakteriální infekce $x imunologie $7 D016908
- 650 _2
- $a slizniční imunita $x imunologie $7 D018928
- 650 _2
- $a střevní nádory $x imunologie $x mikrobiologie $7 D007414
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a myši $7 D051379
- 650 _2
- $a myši inbrední C57BL $7 D008810
- 650 _2
- $a polymerázová řetězová reakce $7 D016133
- 650 _2
- $a rizikové faktory $7 D012307
- 650 _2
- $a sekvenční analýza DNA $7 D017422
- 650 _2
- $a stupeň závažnosti nemoci $7 D012720
- 650 _2
- $a druhová specificita $7 D013045
- 650 _2
- $a organismy bez specifických patogenů $7 D013047
- 650 _2
- $a ankylózující spondylitida $x imunologie $x mikrobiologie $7 D013167
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Čapková, Jana $7 xx0126343
- 700 1_
- $a Niederlová, Jaroslava, $d 1972- $7 xx0074926
- 700 1_
- $a Štěpánková, Renata. $7 xx0246647
- 700 1_
- $a Šinkora, Jiří. $7 xx0222436
- 773 0_
- $t Human Immunology $g Roč. 69, č. 12 (2008), s. 845-850 $x 0198-8859 $w MED00002076
- 910 __
- $a ABA008 $b B 1603 $y 2 $z 0
- 990 __
- $a 20110414100822 $b ABA008
- 991 __
- $a 20221005125129 $b ABA008
- 999 __
- $a ok $b bmc $g 833831 $s 698316
- BAS __
- $a 3
- BMC __
- $a 2008 $b 69 $c 12 $d 845-850 $i 0198-8859 $m Human immunology $n Hum Immunol $x MED00002076
- LZP __
- $a 2011-1B09/dkjp