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Heres an interesting one. Seems some autoAbs induced reversibly by

malaria infection in mice were very polyspecific.

====================================

Int Immunol. 1991 Jan;3(1):29-37. Related Articles, Links

Induction of high levels of IgG autoantibodies in mice infected with

Plasmodium chabaudi.

Ternynck T, Falanga PB, Unterkirscher C, Gregoire J, da Silva LP,

Avrameas S.

Unite d'Immunocytochimie, CNRS URA 359, Paris, France.

This study analyzed the effect of infection of mice with a virulent

strain of Plasmodium chabaudi on natural autoantibodies. Mice

received appropriate treatments in order to survive and the serum

autoantibodies were characterized either by enzyme immunoassays

against a panel of self and non-self antigens or by Western

immunoblots using fibroblast or red blood cell (RBC) extracts. IgM

and mainly IgG antibodies directed against actin, myoglobin, myosin,

spectrin, tubulin, and trinitrophenylated-ovalbumin were found a few

days after the parasitemia peak, persisted for several weeks after

parasite clearance, and returned to almost normal levels after 2

months. Following a challenge with parasitized RBCs, a similar

increase in all antibodies was observed, their levels remaining high

20 days post-injection and still remaining at twice the normal level

1 month later. Western blotting detected autoantibodies to many

membrane RBC proteins, e.g. spectrin, and band 3 and its related

polypeptides, as well as against fibroblast constituents, such as

tubulin, actin, and the 70 kd heat shock protein. Autoantibodies

seemed to be polyspecific, since those eluted from infected mouse

RBCs and the IgG antibodies from infected mouse sera affinity-

purified on a mouse tubulin immunoadsorbent reacted with all antigens

of the panel, including parasite extracts. Surprisingly, in mice

which had recovered from infection, autoantibody levels, particularly

anti-spectrin and anti-band 3, rose after the injection of a high

dose of normal instead of parasitized RBCs.(ABSTRACT TRUNCATED AT 250

WORDS)

PMID: 2049335 [PubMed - indexed for MEDLINE]

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:

Good articles you're posting.

In my mind - there's no doubt that various pathogen create havoc with

the immune system, and I concede that autoantibodies are produced

during the course of the infection (can't dispute some of these

papers).

I disagree with their conclusions though, that autoantibodies

continue to do damage AFTER the pathogen is erradicated... they

always make the assumption that the pathogen IS erradicated if they

can't find evidence of it through available teating. I think it's

there, but just can't be found.

I actually made some headway with a Dr. recently talking

about " theory " specifically post- Blah blah syndrome - with resulting

autoimmunity.. AI is really only a theory that's why all these

maladies are called SYNDROMES and not disease.

Barb

>

> Heres an interesting one. Seems some autoAbs induced reversibly by

> malaria infection in mice were very polyspecific.

>

>

> ====================================

>

> Int Immunol. 1991 Jan;3(1):29-37. Related Articles, Links

>

>

> Induction of high levels of IgG autoantibodies in mice infected

with

> Plasmodium chabaudi.

>

> Ternynck T, Falanga PB, Unterkirscher C, Gregoire J, da Silva LP,

> Avrameas S.

>

> Unite d'Immunocytochimie, CNRS URA 359, Paris, France.

>

> This study analyzed the effect of infection of mice with a virulent

> strain of Plasmodium chabaudi on natural autoantibodies. Mice

> received appropriate treatments in order to survive and the serum

> autoantibodies were characterized either by enzyme immunoassays

> against a panel of self and non-self antigens or by Western

> immunoblots using fibroblast or red blood cell (RBC) extracts. IgM

> and mainly IgG antibodies directed against actin, myoglobin,

myosin,

> spectrin, tubulin, and trinitrophenylated-ovalbumin were found a

few

> days after the parasitemia peak, persisted for several weeks after

> parasite clearance, and returned to almost normal levels after 2

> months. Following a challenge with parasitized RBCs, a similar

> increase in all antibodies was observed, their levels remaining

high

> 20 days post-injection and still remaining at twice the normal

level

> 1 month later. Western blotting detected autoantibodies to many

> membrane RBC proteins, e.g. spectrin, and band 3 and its related

> polypeptides, as well as against fibroblast constituents, such as

> tubulin, actin, and the 70 kd heat shock protein. Autoantibodies

> seemed to be polyspecific, since those eluted from infected mouse

> RBCs and the IgG antibodies from infected mouse sera affinity-

> purified on a mouse tubulin immunoadsorbent reacted with all

antigens

> of the panel, including parasite extracts. Surprisingly, in mice

> which had recovered from infection, autoantibody levels,

particularly

> anti-spectrin and anti-band 3, rose after the injection of a high

> dose of normal instead of parasitized RBCs.(ABSTRACT TRUNCATED AT

250

> WORDS)

>

> PMID: 2049335 [PubMed - indexed for MEDLINE]

>

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Its very sad as I ranted in a recent post about the very nice woman

who now has rhuematoid arthritis but they say the lyme has come and

gone. I don't even know if they ever tested for babesia or bartonella.

Her immunosuppressive drugs require liver monitoring and bring her

white blood count down to 3 and lower, requiring backing off the

drugs a bit etc.

Its the hit and run model, and that makes no sense I agree. Infection

is " information " and so are antibodies, they're a response to

information. Get rid of the " Information " that the bacteria are

sending the immune system and there is no need to create the auto

antibodies.

One problem though is all our infections are so much more virulent. I

do think lyme is bioweaponized and maybe babesia but even the

naturally occuring lyme is surely much more virulent now than 20

years ago just by antibiotic overusage.

> >

> > Heres an interesting one. Seems some autoAbs induced reversibly

by

> > malaria infection in mice were very polyspecific.

> >

> >

> > ====================================

> >

> > Int Immunol. 1991 Jan;3(1):29-37. Related Articles, Links

> >

> >

> > Induction of high levels of IgG autoantibodies in mice infected

> with

> > Plasmodium chabaudi.

> >

> > Ternynck T, Falanga PB, Unterkirscher C, Gregoire J, da Silva LP,

> > Avrameas S.

> >

> > Unite d'Immunocytochimie, CNRS URA 359, Paris, France.

> >

> > This study analyzed the effect of infection of mice with a

virulent

> > strain of Plasmodium chabaudi on natural autoantibodies. Mice

> > received appropriate treatments in order to survive and the serum

> > autoantibodies were characterized either by enzyme immunoassays

> > against a panel of self and non-self antigens or by Western

> > immunoblots using fibroblast or red blood cell (RBC) extracts.

IgM

> > and mainly IgG antibodies directed against actin, myoglobin,

> myosin,

> > spectrin, tubulin, and trinitrophenylated-ovalbumin were found a

> few

> > days after the parasitemia peak, persisted for several weeks

after

> > parasite clearance, and returned to almost normal levels after 2

> > months. Following a challenge with parasitized RBCs, a similar

> > increase in all antibodies was observed, their levels remaining

> high

> > 20 days post-injection and still remaining at twice the normal

> level

> > 1 month later. Western blotting detected autoantibodies to many

> > membrane RBC proteins, e.g. spectrin, and band 3 and its related

> > polypeptides, as well as against fibroblast constituents, such as

> > tubulin, actin, and the 70 kd heat shock protein. Autoantibodies

> > seemed to be polyspecific, since those eluted from infected mouse

> > RBCs and the IgG antibodies from infected mouse sera affinity-

> > purified on a mouse tubulin immunoadsorbent reacted with all

> antigens

> > of the panel, including parasite extracts. Surprisingly, in mice

> > which had recovered from infection, autoantibody levels,

> particularly

> > anti-spectrin and anti-band 3, rose after the injection of a high

> > dose of normal instead of parasitized RBCs.(ABSTRACT TRUNCATED AT

> 250

> > WORDS)

> >

> > PMID: 2049335 [PubMed - indexed for MEDLINE]

> >

>

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On Friday, November 4, 2005, at 12:52 PM, jill1313 wrote:

> One problem though is all our infections are so much more virulent. I

> do think lyme is bioweaponized and maybe babesia but even the

> naturally occuring lyme is surely much more virulent now than 20

> years ago just by antibiotic overusage.

Would antibiotic overusage really effect Bb bacteria in general? Seems

to me it is pretty much contained within the sick subject. I mean,

hopefully my own Bb bacteria aren't going any further than they have

already gone (to my son, and who knows maybe my husband, who is now

having knee pain and inflammation but won't take the time to get a test

while on tour in the US). I suppose mosquitoes could be biting me and

spreading my blood around and therefore my Bb bacteria that have now

been exposed to a year's worth of various abx....

- Kate

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Of course it would. Most folks live in endemic areas and get multiple

tickbites they don't know about. Mosquitoes prefer a host already

infected with malaria for obvious reasons--allows the parasite to

effectively spread. The microbe protects itself. You aren't the

endstage host. Even your urine sheds bb. You may pass it on to unborn

babies, perhaps, but more likely for most folks is they are bitten

and rebitten and ticks without it, get it. And like any bacterium, bb

can become resistant with antibiotic overusage.

>

> > One problem though is all our infections are so much more

virulent. I

> > do think lyme is bioweaponized and maybe babesia but even the

> > naturally occuring lyme is surely much more virulent now than 20

> > years ago just by antibiotic overusage.

>

> Would antibiotic overusage really effect Bb bacteria in general?

Seems

> to me it is pretty much contained within the sick subject. I mean,

> hopefully my own Bb bacteria aren't going any further than they

have

> already gone (to my son, and who knows maybe my husband, who is now

> having knee pain and inflammation but won't take the time to get a

test

> while on tour in the US). I suppose mosquitoes could be biting me

and

> spreading my blood around and therefore my Bb bacteria that have

now

> been exposed to a year's worth of various abx....

>

> - Kate

>

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