Re: it appears that OSP A really IS expressed in mammalian hosts

[Guest guest]

I think where the confusion lies, is that at the actual time

of infection (Tick feeding) OspA not up regulated from the ticks

gut...

But ecentually, it certainly is expressed in the Human host - as

humans and animals will make antibodies against the molecular weights

of 31 and 34 kDa - and I've posted about it several times. Oasp A

and B are rarely talked about separately - And B is rarely talked

about at all.

Barb

> As I recall, more than one member here has asserted flatly that the

> Bb spirochete's OSP A is not expressed in mammals. This finding

> seems to state otherwise.

>

> Any thoughts?

>

>

>

> Infect Immun. 2003 Jul;71(7):4003-10. Related Articles, Links

>

>

> Host-adapted Borrelia burgdorferi in mice expresses OspA during

> inflammation.

>

> Crowley H, Huber BT.

>

> Department of Pathology, Tufts University School of Medicine,

> Boston, Massachusetts 02111, USA.

>

> Antibody responses to outer surface protein A (OspA) of Borrelia

> burgdorferi may occur during periods of arthritis late in the

> clinical course of untreated Lyme disease. These antibody responses

> are paradoxical, given the conclusive evidence demonstrating that

B.

> burgdorferi transmitted to the mammalian host expresses little or

no

> OspA. The parallel occurrence of OspA antibodies and arthritic

> episodes suggests that OspA expression is upregulated during

> infection with B. burgdorferi. We hypothesized that this was due to

> the inflammatory environment caused by the immune response to the

> spirochete. To test our hypothesis, we adapted an in vivo model

that

> mimics the host-pathogen interaction. Dialysis chambers containing

> B. burgdorferi were implanted into the peritoneal cavities of mice

> in the presence or absence of zymosan, a yeast cell wall extract

> that induces inflammation. Spirochetes were harvested 2 days later,

> and OspA expression was assessed at the protein and transcription

> level by Western blotting and real-time reverse transcription-PCR,

> respectively. Flow cytometry was also utilized to evaluate OspA

> protein expression on individual spirochetes. B. burgdorferi

> maintained in an inflammatory in vivo environment show an increased

> OspA expression relative to B. burgdorferi kept under normal in

vivo

> conditions. Furthermore, host-adapted B. burgdorferi with a low

OspA

> phenotype upregulates OspA expression when transferred to an

> inflammatory in vivo environment. The results obtained by these

> techniques uniformly identify inflammation as a mediator of in vivo

> OspA expression in host-adapted B. burgdorferi, providing insights

> into the behavior of live spirochetes in the mammalian host.

>

> PMID: 12819088 [PubMed - indexed for MEDLINE]

[Guest guest]

Who said that? OspA is the one known surface unchanging antigen which

is why Steere et al tried to make a vaccine from it even though its

highly immunogenic and ruined some peoples health as a result.

Its true its highly expressed in the tickgut and much less so in the

human from what i understand ospC takes over and changes all the time.

Dastardly bug.

> As I recall, more than one member here has asserted flatly that the

> Bb spirochete's OSP A is not expressed in mammals. This finding

> seems to state otherwise.

>

> Any thoughts?

>

>

>

> Infect Immun. 2003 Jul;71(7):4003-10. Related Articles, Links

>

>

> Host-adapted Borrelia burgdorferi in mice expresses OspA during

> inflammation.

>

> Crowley H, Huber BT.

>

> Department of Pathology, Tufts University School of Medicine,

> Boston, Massachusetts 02111, USA.

>

> Antibody responses to outer surface protein A (OspA) of Borrelia

> burgdorferi may occur during periods of arthritis late in the

> clinical course of untreated Lyme disease. These antibody responses

> are paradoxical, given the conclusive evidence demonstrating that

B.

> burgdorferi transmitted to the mammalian host expresses little or

no

> OspA. The parallel occurrence of OspA antibodies and arthritic

> episodes suggests that OspA expression is upregulated during

> infection with B. burgdorferi. We hypothesized that this was due to

> the inflammatory environment caused by the immune response to the

> spirochete. To test our hypothesis, we adapted an in vivo model

that

> mimics the host-pathogen interaction. Dialysis chambers containing

> B. burgdorferi were implanted into the peritoneal cavities of mice

> in the presence or absence of zymosan, a yeast cell wall extract

> that induces inflammation. Spirochetes were harvested 2 days later,

> and OspA expression was assessed at the protein and transcription

> level by Western blotting and real-time reverse transcription-PCR,

> respectively. Flow cytometry was also utilized to evaluate OspA

> protein expression on individual spirochetes. B. burgdorferi

> maintained in an inflammatory in vivo environment show an increased

> OspA expression relative to B. burgdorferi kept under normal in

vivo

> conditions. Furthermore, host-adapted B. burgdorferi with a low

OspA

> phenotype upregulates OspA expression when transferred to an

> inflammatory in vivo environment. The results obtained by these

> techniques uniformly identify inflammation as a mediator of in vivo

> OspA expression in host-adapted B. burgdorferi, providing insights

> into the behavior of live spirochetes in the mammalian host.

>

> PMID: 12819088 [PubMed - indexed for MEDLINE]

[Guest guest]

Is " B " as immunogenic as ospA?

Does it change like OspC? Anybody know?

I NEED ONE UNCHANGING ANTIBODY THAT IS NOT OSP " A " .

PLEASE FIND ME ONE.

Seriously.

> > As I recall, more than one member here has asserted flatly that

the

> > Bb spirochete's OSP A is not expressed in mammals. This finding

> > seems to state otherwise.

> >

> > Any thoughts?

> >

> >

> >

> > Infect Immun. 2003 Jul;71(7):4003-10. Related Articles, Links

> >

> >

> > Host-adapted Borrelia burgdorferi in mice expresses OspA during

> > inflammation.

> >

> > Crowley H, Huber BT.

> >

> > Department of Pathology, Tufts University School of Medicine,

> > Boston, Massachusetts 02111, USA.

> >

> > Antibody responses to outer surface protein A (OspA) of Borrelia

> > burgdorferi may occur during periods of arthritis late in the

> > clinical course of untreated Lyme disease. These antibody

responses

> > are paradoxical, given the conclusive evidence demonstrating that

> B.

> > burgdorferi transmitted to the mammalian host expresses little or

> no

> > OspA. The parallel occurrence of OspA antibodies and arthritic

> > episodes suggests that OspA expression is upregulated during

> > infection with B. burgdorferi. We hypothesized that this was due

to

> > the inflammatory environment caused by the immune response to the

> > spirochete. To test our hypothesis, we adapted an in vivo model

> that

> > mimics the host-pathogen interaction. Dialysis chambers

containing

> > B. burgdorferi were implanted into the peritoneal cavities of

mice

> > in the presence or absence of zymosan, a yeast cell wall extract

> > that induces inflammation. Spirochetes were harvested 2 days

later,

> > and OspA expression was assessed at the protein and transcription

> > level by Western blotting and real-time reverse transcription-

PCR,

> > respectively. Flow cytometry was also utilized to evaluate OspA

> > protein expression on individual spirochetes. B. burgdorferi

> > maintained in an inflammatory in vivo environment show an

increased

> > OspA expression relative to B. burgdorferi kept under normal in

> vivo

> > conditions. Furthermore, host-adapted B. burgdorferi with a low

> OspA

> > phenotype upregulates OspA expression when transferred to an

> > inflammatory in vivo environment. The results obtained by these

> > techniques uniformly identify inflammation as a mediator of in

vivo

> > OspA expression in host-adapted B. burgdorferi, providing

insights

> > into the behavior of live spirochetes in the mammalian host.

> >

> > PMID: 12819088 [PubMed - indexed for MEDLINE]

[Guest guest]

Thanks Scha this is most enlightening, and appears to

clarify/supercede the disconnect between the existence of anti-OspA

seroreactivity in humans on one hand, and on the other hand the

observation that mice can be experimentally infected by skin graft

from other mice even after OspA vaccination has protected them from

infection via tick.

The knowledge from this paper is of use in interpreting one of the

key descriptive studies of borreliosis, the 1996 Nanagara et al IEM

study of needle-biopsied synovial fluid and membrane. They used gold-

nanoparticle-conjugated anti-OspA mAb to locate Bb using electron

microscopy, presumably selecting that target because they knew OspA

to be invariant. They state that the labelling was somewhat

inconsistent. Perhaps some Bb individuals in this situation express

much more OspA than others.

Not that this has to do directly with your post, but what is MOST

interesting about the Nanagara paper is their discovery of OspA

antigens upon forms they were unable to identify without the use of

the mAb. This could be the " dark matter " ie the missing borrelial

biomass, and there could be more of it which was missed by this

technique on account of lacking OspA. This material was primarily in

macrophage cytoplasm.

> As I recall, more than one member here has asserted flatly that the

> Bb spirochete's OSP A is not expressed in mammals. This finding

> seems to state otherwise.

>

> Any thoughts?

>

>

>

> Infect Immun. 2003 Jul;71(7):4003-10. Related Articles, Links

>

>

> Host-adapted Borrelia burgdorferi in mice expresses OspA during

> inflammation.

>

> Crowley H, Huber BT.

>

> Department of Pathology, Tufts University School of Medicine,

> Boston, Massachusetts 02111, USA.

>

> Antibody responses to outer surface protein A (OspA) of Borrelia

> burgdorferi may occur during periods of arthritis late in the

> clinical course of untreated Lyme disease. These antibody responses

> are paradoxical, given the conclusive evidence demonstrating that

B.

> burgdorferi transmitted to the mammalian host expresses little or

no

> OspA. The parallel occurrence of OspA antibodies and arthritic

> episodes suggests that OspA expression is upregulated during

> infection with B. burgdorferi. We hypothesized that this was due to

> the inflammatory environment caused by the immune response to the

> spirochete. To test our hypothesis, we adapted an in vivo model

that

> mimics the host-pathogen interaction. Dialysis chambers containing

> B. burgdorferi were implanted into the peritoneal cavities of mice

> in the presence or absence of zymosan, a yeast cell wall extract

> that induces inflammation. Spirochetes were harvested 2 days later,

> and OspA expression was assessed at the protein and transcription

> level by Western blotting and real-time reverse transcription-PCR,

> respectively. Flow cytometry was also utilized to evaluate OspA

> protein expression on individual spirochetes. B. burgdorferi

> maintained in an inflammatory in vivo environment show an increased

> OspA expression relative to B. burgdorferi kept under normal in

vivo

> conditions. Furthermore, host-adapted B. burgdorferi with a low

OspA

> phenotype upregulates OspA expression when transferred to an

> inflammatory in vivo environment. The results obtained by these

> techniques uniformly identify inflammation as a mediator of in vivo

> OspA expression in host-adapted B. burgdorferi, providing insights

> into the behavior of live spirochetes in the mammalian host.

>

> PMID: 12819088 [PubMed - indexed for MEDLINE]