Topic: Bacterial secrets of secretion: EuroConference on the biology of type IV secretion pr
treepatrol
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Baron C, OCallaghan D, Lanka E. Ludwig-Maximilians-Universit�t, Department Biologie I, Bereich Genetik und Mikrobiologie, Maria-Ward-Str. 1a, D-80638 M�nchen, Germany. [email protected]
Type IV secretion systems (TFSS) mediate secretion or direct cell-to-cell transfer of virulence factors (proteins or protein-DNA complexes) from many Gram-negative animal, human and plant pathogens,
such as Agrobacterium tumefaciens, Bartonella tribocorum, Bordetella pertussis, Brucella suis, Helicobacter pylori, Legionella pneumophila and Rickettsia prowazekii, into eukaryotic cells.
Bacterial conjugation is also classified as a TFSS-like process mediating the spread of broad-host-range plasmids between Gram-negative bacteria such as RP4 and R388, which carry antibiotic resistance genes. Genetic, biochemical, cell biological and structural biology experiments led to significant progress in the understanding of several aspects of TFSS processes.
X-ray crystallography revealed that homologues of the A. tumefaciens inner membrane-associated proteins VirB11 and VirD4 from H. pylori and R388, respectively, may form channels for substrate translocation or assembly of the transmembrane TFSS machinery.
Biochemical and cell biological experiments revealed interactions between components of the periplasmic core components VirB8, VirB9 and VirB10, which may form the translocation channel.
Analysis of A. tumefaciens virulence proteins VirE2 and VirF suggested that the periplasmic translocation route of the pertussis toxin from B. pertussis may be more generally valid than previously anticipated.
Secretion and modification of toxins from H. pylori and L. pneumophila profoundly affect host cell metabolism, thus entering the discipline of cellular microbiology. [[just like lyme]]
Finally, results from genome sequencing projects revealed the presence of up to three TFSS in a single organism, and the analysis of their interplay and adaptation to different functions will be a future challenge.
TFSS-carrying plasmids were discovered in different ecosystems, suggesting that genetic exchange may speed up their evolution and adaptation to different cell-cell interactions.
PMID: 11918819 [PubMed - indexed for MEDLINE]
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
Baron C, OCallaghan D, Lanka E. Ludwig-Maximilians-Universit�t, Department Biologie I, Bereich Genetik und Mikrobiologie, Maria-Ward-Str. 1a, D-80638 M�nchen, Germany. [email protected]
Type IV secretion systems (TFSS) mediate secretion or direct cell-to-cell transfer of virulence factors (proteins or protein-DNA complexes) from many Gram-negative animal, human and plant pathogens,
such as Agrobacterium tumefaciens, Bartonella tribocorum, Bordetella pertussis, Brucella suis, Helicobacter pylori, Legionella pneumophila and Rickettsia prowazekii, into eukaryotic cells.
Bacterial conjugation is also classified as a TFSS-like process mediating the spread of broad-host-range plasmids between Gram-negative bacteria such as RP4 and R388, which carry antibiotic resistance genes.
Genetic, biochemical, cell biological and structural biology experiments led to significant progress in the understanding of several aspects of TFSS processes.
X-ray crystallography revealed that homologues of the A. tumefaciens inner membrane-associated proteins VirB11 and VirD4 from H. pylori and R388, respectively, may form channels for substrate translocation or assembly of the transmembrane TFSS machinery.
Biochemical and cell biological experiments revealed interactions between components of the periplasmic core components VirB8, VirB9 and VirB10, which may form the translocation channel.
Analysis of A. tumefaciens virulence proteins VirE2 and VirF suggested that the periplasmic translocation route of the pertussis toxin from B. pertussis may be more generally valid than previously anticipated.
Secretion and modification of toxins from H. pylori and L. pneumophila profoundly affect host cell metabolism, thus entering the discipline of cellular microbiology. [[just like lyme]]
Finally, results from genome sequencing projects revealed the presence of up to three TFSS in a single organism, and the analysis of their interplay and adaptation to different functions will be a future challenge.
TFSS-carrying plasmids were discovered in different ecosystems, suggesting that genetic exchange may speed up their evolution and adaptation to different cell-cell interactions.
PMID: 11918819 [PubMed - indexed for MEDLINE]
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Bartonella tribocorum
Frontal and stealth attack strategies in microbial pathogenesis D. Scott Merrell1 & Stanley Falkow Abstract Interactions between microbes and human hosts can range from a benign, even symbiotic collaboration to a competition that may turn fatal -- resulting in death of the host, the microbe or both.
Despite advances that have been made over the past decades in understanding microbial pathogens, more people worldwide still die every year from infectious disease than from any other cause.
This highlights the relevance of continuing to probe the mechanisms used by microorganisms to cause disease, and emphasizes the need for new model systems to advance our understanding of host-pathogen interactions.
1: Nat Genet. 2007 Dec;39(12):1469-76. Epub 2007 Nov 25.
Genomic analysis of Bartonella identifies type IV secretion systems as host adaptability factors.
Saenz HL, Engel P, Stoeckli MC, Lanz C, Raddatz G, Vayssier-Taussat M, Birtles R, Schuster SC, Dehio C.
Focal Area Infection Biology, Biozentrum, University of Basel, CH-4056 Basel, Switzerland.
The bacterial genus Bartonella comprises 21 pathogens causing characteristic intraerythrocytic infections. Bartonella bacilliformis is a severe pathogen representing an ancestral lineage, whereas the other species are benign pathogens that evolved by radial speciation.
Here, we have used comparative and functional genomics to infer pathogenicity genes specific to the radiating lineage, and we suggest that these genes may have facilitated adaptation to the host environment.
We determined the complete genome sequence of Bartonella tribocorum by shotgun sequencing and functionally identified 97 pathogenicity genes by signature-tagged mutagenesis.
Eighty-one pathogenicity genes belong to the core genome (1,097 genes) of the radiating lineage inferred from genome comparison of B. tribocorum, Bartonella henselae and Bartonella quintana. Sixty-six pathogenicity genes are present in B. bacilliformis, and one has been lost by deletion.
The 14 pathogenicity genes specific for the radiating lineage encode two laterally acquired type IV secretion systems, suggesting that these systems have a role in host adaptability.
PMID: 18037886 [PubMed - indexed for MEDLINE]
Related Links
16S/23S rRNA intergenic spacer regions for phylogenetic analysis, identification, and subtyping of Bartonella species. [J Clin Microbiol. 2001] PMID:11473990
The VirB/VirD4 type IV secretion system of Bartonella is essential for establishing intraerythrocytic infection. [Mol Microbiol. 2002] PMID:12421311
The louse-borne human pathogen Bartonella quintana is a genomic derivative of the zoonotic agent Bartonella henselae. [Proc Natl Acad Sci U S A. 2004] PMID:15210978
Phylogenetic classification of Bartonella species by comparing groEL sequences. [Int J Syst Evol Microbiol. 2002] PMID:11837299
Molecular phylogeny of the genus Bartonella: what is the current knowledge? [FEMS Microbiol Lett. 2001] PMID:11410341
Species B. alsatica B. bacilliformis B. birtlesii B. bovis B. capreoli B. clarridgeiae B. doshiae B. elizabethae B. grahamii B. henselae B. koehlerae B.muris B. peromysci B. quintana B. rochalimae B. schoenbuchii B. talpae B. taylorii B. tribocorum B. vinsonii spp. arupensis B. vinsonii spp. berkhoffii B. vinsonii spp. vinsonii B. washoensis etc.
Bartonella (formerly known as Rochalimaea) is a genus of Gram-negative bacteria. Facultative intracellular parasites, Bartonella species can infect healthy people but are considered especially important as opportunistic pathogens.
Bartonella are transmitted by insect vectors such as ticks, fleas, sand flies and mosquitoes. At least eight Bartonella species or subspecies are known to infect humans.
In June 2007, a new species under the genus, called Bartonella rochalimae, was discovered. This is the sixth species known to infect humans ((Could this be Dr B's ?)), and the ninth species and subspecies, overall, known to infect humans.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
Bartonella has the ability to gather dna from Host us, or from other bacteria spirochetes? Maybe These two are swapping stuff and thats why we cant shake it ? Also it is a intracellular parisite. Like Dr B said the ones who are treated long time may also have this BLO ?
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
AliG
Frequent Contributor (1K+ posts)
Member # 9734
posted
quote:Facultative intracellular parasites, Bartonella species can infect healthy people but are considered especially important as opportunistic pathogens.
Bartonella are transmitted by insect vectors such as ticks, fleas, sand flies and mosquitoes.
So someone infected with Bb but not Bartonella, at an earlier point in testing, could contract any of these opportunists from mosquitoes et al.
I wonder if this could be why I could have developed Barty Sx, and LLMD said (figuratively scratching head) "Hmmmm, you had tested negative for Bartonella".
Great find! Thanks for this really awful & incredibly depressing post, Tree. I'll have to print this out for him, he may want to re-test.
-------------------- Note: I'm NOT a medical professional. The information I share is from my own personal research and experience. Please do not construe anything I share as medical advice, which should only be obtained from a licensed medical practitioner. Posts: 4881 | From Middlesex County, NJ | Registered: Jul 2006
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treepatrol
Honored Contributor (10K+ posts)
Member # 4117
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Theres a big connection here with B12 also . aint this getting crazy mosquiters heprin link Guess what b12 helps the fight fibrin problem.
Homocysteinemia (hyperhomocysteinemia). This amino acid abnormality is an independent and major risk factor for coronary artery disease, stroke and osteonecrosis, and a somewhat lesser risk factor for deep vein thrombosis and arterial thrombosis.
Usual it is inherited as an autosomal dominant trait but it can be acquired by a deficiency of vitamin B12 or folate, or renal insufficiency. It is suggested that plasma levels be measured, along with a fasting lipid profile and lipoprotein (a) levels, in all patients assesses for atherosclerosis risk
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
up
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
GretaM
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Up please.
Why bart is such a beast argh.
Don't have the brain power tonight. Will wade through the pubbmed tomorrow.
Posts: 4358 | From British Columbia, Canada | Registered: Jun 2013
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![[Eek!]](eek.gif)
![[Frown]](frown.gif)
post, Tree. ![[kiss]](graemlins/kissing.gif)
I'll have to print this out for him, he may want to re-test.![[Big Grin]](biggrin.gif)
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