Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."
 


9 July 2017

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1988 Steere says Lyme is like a B cell leukemia

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CDC "SPIDER"

Fungal Exosomes Inhibit Apoptosis

IDSA: "Vaccines serve the mfgs, not their victims"

RICO_filed_USDOJ

BlumenthalAntiTrust Lawsuit

Exosomes, Blebs

Spirochetal_Dementia


PDFs
CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994
BarbourFishpdf.pdf
 

Pathogenic Fungi

Bush's warcrimes, Oct 2000

Trainer

170708

 

 


Exosomology is very big in industry right now so just GoogleNews it.



Gram negative bacteria, TLR2/1 agonist bearers etc, and shed exosomes.  This is all *** BIG *** with the NIH. "Exosomes" or "Vesicles" shed by these bacteria.
 

OspA-and similar fungal lipoprotein-containing Blebs or Vesicles (see arrows in the below micrograph by Alan Barbour) are shed lipoproteins, so everyone with "Lyme disease," also has LYMErix Disease, because that is actually the disease - the chronic exposure to Borrelial OspA-like blebs resulting in immunosuppression, tolerance to mycoplasma in the blood (causes fatigue), results in no antibodies being produced, and the activation of Epstein-Barr/Similars.
 


http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=7103461

 

Cadavid and the NIH say these shed vesicles or blebs go to the brain and inflame it:

 

 

 

 

 

 

 

 

 

 

An NIH patent, explaining how Lyme causes LYMErix-disease:

"The invention relates to novel antigens associated with Borrelia burgdorferi which are exported (or shed) in vivo and whose detection is a means of diagnosing Lyme disease. The antigens are extracellular membrane vesicles and other bioproducts including the major extracellular protein antigen. Another object of the invention is to provide antibodies, monoclonal and/or polyclonal, labeled and/or unlabeled, that are raised against the antigens. A further object of the invention is to provide a method of diagnosing Lyme disease by detecting the antigens in a biological sample taken from a host using the antibodies in conventional immunoassay formats. Another object of the invention is to provide kits, for the diagnosis of Lyme disease, comprising the antibodies and ancillary reagents. The advantage of the antibodies used in the invention is that they react with the antigens from geographically diverse strains of Borrelia burgdorferi, but do not react with antigens from related Borrelia spirochetes."
http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=5,217,872.PN.&OS=PN/5,217,872&RS=PN/5,217,872



2011, THE BLEBS ARE COVERED IN SLYMERIX>>> "Although we uncovered the existence of at least 10 distinct OM complexes harboring several unique subunits, the complexome is dominated by the frequent occurrence of a limited diversity of membrane proteins, most notably P13, outer surface protein (Osp) A, -B, -C, and -D and Lp6.6." 

Characterization of multiprotein complexes of the Borrelia burgdorferi outer membrane vesicles.
http://www.ncbi.nlm.nih.gov/pubmed/21875077



See where NIH's Martin and Marques say these OspA-ish molecules are responsible for humoral immunosuppression with chronic brain inflammation:
http://www.actionlyme.org/151026_OCCAMS-RAZOR.htm


 


30+ reports:

http://www.ncbi.nlm.nih.gov/pubmed/?term=Borrelia+and+vesicles

 

 


This one is by Dave Dorward (Rocky Mountain Bioweapons Labs, NIH), that is what started it all and Willy Burgdorfer mentioned it in several conferences. Particularly important, he says this only occurs in gram negative bacteria (once again the Primers Shell Game report is important):

1990, DNA Is Packaged within Membrane-Derived Vesicles of GramNegativebut Not Gram-Positive Bacteria

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC184538/pdf/aem00087-0464.pdf

 

 

1993, BINGO >>> 

Specific adherence of Borrelia burgdorferi extracellular vesicles to human endothelial cells in culture.

Borrelia burgdorferi produces extracellular vesicles which contain some of the outer surface proteins of the bacterium (e.g., OspA and OspB). Borrelial vesicles, isolated by differential centrifugation and filtration, were tested for the ability to bind to cultured human umbilical vein endothelial (HUVE) cells in culture. The recently described lipoprotein OspD was expressed on vesicles. Vesicles exhibited differential expression of OspB and OspD in a relationship with passage number and medium serum supplement type, respectively. Qualitative immunoblotting analyses demonstrated dose-dependent, passage number-dependent adsorption of vesicles by HUVE cells. This adsorption was demonstrated to be dependent upon a borrelial component of the vesicle and not due to the presence of minor contamination with intact spirochetes. Quantitative experiments examining inhibition of B. burgdorferi-HUVE association as a function of prior vesicle-HUVE association demonstrated dependence upon (i) a borrelial component(s) in the vesicle, (ii) low passage number, and (iii) vesicle protein concentration. However, vesicle pretreatment of the HUVE cell monolayer was not requisite for this inhibition. Vesicles from highly passaged borrelias were noninhibitory for B. burgdorferi-HUVE cell association, regardless of the serum used to supplement the medium. The use of vesicles as a tool for studying B. burgdorferi pathogenesis and/or physiology is proposed.

 

http://www.ncbi.nlm.nih.gov/pubmed/8359911





1993, NIH RML, Garon

HERE IS THE NIH TALKING ABOUT IT SOME MORE IN 1993:

Specific and nonspecific responses of murine B cells to membrane blebs of Borrelia burgdorferi.

Lymphocyte blastogenesis assays and immunoblotting were used to investigate and compare murine B-cell responses to preparations of extracellular membrane blebs (BAg) and spirochetes (Ag) of Borrelia burgdorferi. Immunoblotting BAg, Ag, and medium control preparations with serum from naive and infected C57BL/10 mice revealed that BAg and Ag had similar specific reactivity profiles except that major antigens of 83, 60, and 41 kDa were detected in Ag but not in BAg. It was determined that 1 microgram (dry weight) of Ag contained 0.0051 and 0.0063 microgram of outer surface proteins A (OspA) and OspB, respectively, whereas 1 microgram (dry weight) of BAg contained 0.0024 microgram of OspA and 0.0015 microgram of OspB. *** Both BAg and Ag caused blastogenesis in cultures of spleen cells from both groups of mice, but BAg-stimulated lymphocytes exhibited significantly greater (P < or = 0.05) blastogenesis after 2 or 6 days of culture than did lymphocytes stimulated by Ag or medium control.*** Flow cytometry and antibody capture enzyme-linked immunosorbent assays identified responding lymphocytes as B cells which secreted polyclonal immunoglobulin M (IgM) but not IgG or IgA. Treatment of BAg and lipopolysaccharide controls with polymyxin B resulted in as much as 20.7 and 54.3% mean decreases in blastogenesis, respectively. *** Fractionation of BAg or Ag by ultracentrifugation before culture with spleen cells from naive mice indicated that B-cell blastogenesis was probably associated with spirochetal membranes.*** The results of this study demonstrate that specific humoral responses are directed towards extracellular membrane blebs which lack the 83-, 60-, and 41-kDa antigens of intact spirochetes and that blebs also possess significant nonspecific mitogenic activity for murine B cells. This activity was not due entirely to typical lipopolysaccharide or OspA and OspB lipoproteins.
http://www.ncbi.nlm.nih.gov/pubmed/8454350

The following reports are citing the article above ^^^ by the NIH about how the blebs / vesicles / exosomes cause disease:

http://www.ncbi.nlm.nih.gov/pubmed?linkname=pubmed_pubmed_citedin&from_uid=8454350
 

 

2010, Duke

Virulence and immunomodulatory roles of bacterial outer membrane vesicles.

Outer membrane (OM) vesicles are ubiquitously produced by Gram-negative bacteria during all stages of bacterial growth. OM vesicles are naturally secreted by both pathogenic and nonpathogenic bacteria. Strong experimental evidence exists to categorize OM vesicle production as a type of Gram-negative bacterial virulence factor. A growing body of data demonstrates an association of active virulence factors and toxins with vesicles, suggesting that they play a role in pathogenesis. One of the most popular and best-studied pathogenic functions for membrane vesicles is to serve as natural vehicles for the intercellular transport of virulence factors and other materials directly into host cells. The production of OM vesicles has been identified as an independent bacterial stress response pathway that is activated when bacteria encounter environmental stress, such as what might be experienced during the colonization of host tissues. Their detection in infected human tissues reinforces this theory. Various other virulence factors are also associated with OM vesicles, including adhesins and degradative enzymes. As a result, OM vesicles are heavily laden with pathogen-associated molecular patterns (PAMPs), virulence factors, and other OM components that can impact the course of infection by having toxigenic effects or by the activation of the innate immune response. However, infected hosts can also benefit from OM vesicle production by stimulating their ability to mount an effective defense. Vesicles display antigens and can elicit potent inflammatory and immune responses. In sum, OM vesicles are likely to play a significant role in the virulence of Gram-negative bacterial pathogens.
http://www.ncbi.nlm.nih.gov/pubmed/20197500



2011, Bartold,  SPIROCHETES, LIVING IN YOUR LYMPH NODES (WITH THEIR PARTNERs, EBV ET AL) WRECKING YOUR IMMUNE SYSTEM. Once again, location being the Force Multiplier . And whoever is not paying attention will be in jail for a week; I WILL BE WATCHING YOU....

Lymphoadenopathy during lyme borreliosis is caused by spirochete migration-induced specific B cell activation.

Lymphadenopathy is a hallmark of acute infection with Borrelia burgdorferi, a tick-borne spirochete and causative agent of Lyme borreliosis, but the underlying causes and the functional consequences of this lymph node enlargement have not been revealed. The present study demonstrates that extracellular, live spirochetes accumulate in the cortical areas of lymph nodes following infection of mice with either host-adapted, or tick-borne B. burgdorferi and that they, but not inactivated spirochetes, drive the lymphadenopathy. The ensuing lymph node response is characterized by strong, rapid extrafollicular B cell proliferation and differentiation to plasma cells, as assessed by immunohistochemistry, flow cytometry and ELISPOT analysis, while germinal center reactions were not consistently observed. The extrafollicular nature of this B cell response and its strongly IgM-skewed isotype profile bear the hallmarks of a T-independent response. The induced B cell response does appear, however, to be largely antigen-specific. Use of a cocktail of recombinant, in vivo-expressed B. burgdorferi-antigens revealed the robust induction of borrelia-specific antibody-secreting cells by ELISPOT. Furthermore, nearly a quarter of hybridomas generated from regional lymph nodes during acute infection showed reactivity against a small number of recombinant Borrelia-antigens. Finally, neither the quality nor the magnitude of the B cell responses was altered in mice lacking the Toll-like receptor adaptor molecule MyD88. Together, these findings suggest a novel evasion strategy for B. burgdorferi: subversion of the quality of a strongly induced, potentially protective borrelia-specific antibody response via B. burdorferi's accumulation in lymph nodes.
http://www.ncbi.nlm.nih.gov/pubmed/21637808




NIH SAYS...

1991, Dorward, Garon:

Immune capture and detection of Borrelia burgdorferi antigens in urine, blood, or tissues from infected ticks, mice, dogs, and humans.

"The results indicated that B. burgdorferi appears to shed surface antigens which are readily detectable in urine, blood, and several organs from infected hosts."

http://www.ncbi.nlm.nih.gov/pubmed/1864935



2010, - sounds like Barbour's explanation in 1996, re the role blebbing (which we now know of as exosomes or outer membrane vesicles shed by these bugs):

B cell activation by outer membrane vesicles--a novel virulence mechanism.

 "DNA associated with OMV [LIKE SPIROCHETAL BLEBS/VESICLES] induced full B cell activation by signaling through TLR9 [HANDLES EBV, DNA]. Importantly, this concept was verified in vivo, as OMV equipped with MID and DNA were found in a 9-year old patient suffering from Moraxella sinusitis. In conclusion, Moraxella avoid direct interaction with host B cells by redirecting the adaptive humoral immune response using its superantigen-bearing OMV as decoys."
http://www.ncbi.nlm.nih.gov/pubmed/20090836


 

2012, Seattle Wash,

Membrane Vesicle Release in Bacteria, Eukaryotes, and Archaea: a Conserved yet Underappreciated Aspect of Microbial Life

"The production of spherical, membranous vesicles from microbial cell surfaces is conserved among organisms from all three branches of the tree of life, spanning both prokaryotes and eukaryotes: Gram-negative and Gram-positive bacteria (16, 47, 58, 73), archaea (17, 18), fungi (3, 6567), and parasites (82, 83). For consistency in this review, we will refer to bacterial and archaeal structures as membrane vesicles (MVs) and fungal and parasitic vesicles as either exosomes or shedding microvesicles (two distinct populations referred to collectively as microvesicles [55]). The microscopic observation of microbial MVs spans more than 50 years, and numerous functions have been attributed to these extracellular vesicles by many investigators. The release of vesicles provides flexibility to respond to environmental cues, secrete components destined for the cell surface, virulence factors, and antigens, and interact with the host in the case of pathogens. Because MV release is conserved across many organisms, MV-mediated functions are likely to be critical to microbial life.

"Both bacterial MVs and archaeal MVs are derived from the cell surface (Fig. 1A and and2A).2A). Early observation of Gram-negative bacterial MVs revealed the release of an antigenic complex of lipopolysaccharide (LPS) and lipoprotein into the surrounding medium following amino acid deprivation of an Escherichia coli lysine auxotroph (40), which was initially proposed to be derived from the LPS-containing outer membrane (OM) of the bacteria (29). Since these early investigations, many groups have developed methodologies to isolate and analyze bacterial MVs. Although reconciling these differences in experimental design often makes it difficult to draw generalized conclusions, it is well accepted that Gram-negative bacterial MVs range from 10 to 300 nm in diameter and contain OM and periplasmic constituents, including proteins, lipoproteins, phospholipids, and LPS (43, 58). The contents of the inner membrane (IM) and cytoplasm were generally thought to be excluded from MVs, although recent analyses of the bacterial MV proteome suggest that some proteins typically annotated as having cytoplasmic localization consistently appear in MVs (15, 45, 92, 94). In addition to bacterial membrane proteins, toxins and signaling molecules can be incorporated into the membrane or lumen of the MV; MV release then serves as a secretion mechanism (42, 54, 95). Although Gram-negative bacterial MVs have been most rigorously studied, recent observation of Gram-positive MV release has demonstrated that this is a function more widely conserved across all bacteria. MVs derived from Gram-positive bacteria, such as Bacillus spp., are similarly sized (50 to 150 nm in diameter [47, 73]) and are rich in membrane lipids as well as toxins (including the anthrax toxin)."
....
"TLR ligands in bacterial MVs (including LPS and ***lipoproteins***) stimulate maturation of and cytokine release by macrophages and dendritic cells (reference 2 and unpublished observations) and likely contribute to the pathogenesis of inflammatory infections such as neisserial sepsis (8, 9). Likewise, MVs carrying peptidoglycan, the ligand for the cytosolic innate immune receptor NOD1, are able to initiate NOD1 signaling and downstream NF-κB-dependent inflammatory responses (35, 36). Furthermore, infected antigen-presenting cells may no longer be capable of properly processing and presenting antigens, potentially inhibiting initiation of adaptive immune responses. MVs released by pathogenic organisms are nonviable and contain antigens recognized by the adaptive immune system (2, 4). These surface organelles may therefore represent an important source of antigen in vivo (Fig. 4E)."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370574



1995,

Borrelia burgdorferi vesicle production occurs via a mechanism independent of immunoglobulin M involvement.

"Borrelia burgdorferi produces extracellular vesicles containing various borrelial protein antigens when propagated in vitro in culture media. *** Commonly observed components of borrelial vesicle preparations are borrelial surface antigens [LIKE OSPA], bovine serum albumin, and the heavy chains of rabbit immunoglobulin G and immunoglobulin M. This study employed ultracentrifugation to harvest borrelial vesicles and analyzed these preparations by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western immunoblotting. We demonstrated that the rabbit mu heavy-chain band observed was devoid of OspA or at most levels below those detectable by immunoblot. We also demonstrated the recovery of borrelial vesicles at relative centrifugal forces as low as 25,000 x g, compared with the force of > 200,000 x g normally employed. Further, the mu heavy-chain band was recovered from uninoculated growth media processed at 25,000 x g, suggesting that it behaves as a particle rather than as a soluble molecule under these conditions. Lastly, vesicles were demonstrated to be present in preparations harvested from growth media supplemented with fetal calf serum, suggesting that vesicle production by B. burgdorferi can occur in the absence of immunoglobulins."

http://www.ncbi.nlm.nih.gov/pubmed/7591146



1995, SUNY, Coyle, Benach, Schutzer,  SUNY'S BLEB-CAPTURE METHOD:

Detection of Borrelia burgdorferi-specific antigen in antibody-negative cerebrospinal fluid in neurologic Lyme disease.

"B burgdorferi antigen can be detected in CSF that is otherwise normal by conventional methodology, and can be present without positive CSF antibody. Since CSF antigen implies intrathecal seeding of the infection, the diagnosis of neurologic infection by B burgdorferi should not be excluded solely on the basis of normal routine CSF or negative CSF antibody analyses."

http://www.ncbi.nlm.nih.gov/pubmed/7501150



IL-10 is an immune-suppressor cytokine released also in the presence of OspA fungo-exosomes or blebs or just plain OspA:


Exosomes released from Mycoplasma infected tumor cells activate inhibitory B cells.

Mycoplasmas cause numerous human diseases and are common opportunistic pathogens in cancer patients and immunocompromised individuals. Mycoplasma infection elicits various host immune responses. Here we demonstrate that mycoplasma-infected tumor cells release exosomes (myco+ exosomes) that specifically activate splenic B cells and induce splenocytes cytokine production. Induction of cytokines, including the proinflammatory IFN-γ and the anti-inflammatory IL-10, was largely dependent on the presence of B cells. B cells were the major IL-10 producers. In splenocytes from B cell deficient μMT mice, induction of IFN-γ+ T cells by myco+ exosomes was greatly increased compared with wild type splenocytes. In addition, anti-CD3-stimulated T cell proliferation was greatly inhibited in the presence of myco+ exosome-treated B cells. Also, anti-CD3-stimulated T cell signaling was impaired by myco+ exosome treatment. Proteomic analysis identified mycoplasma proteins in exosomes that potentially contribute to the effects. Our results demonstrate that mycoplasma-infected tumor cells release exosomes carrying mycoplasma components that preferentially activate B cells, which in turn, are able to inhibit T cell activity. These results suggest that mycoplasmas infecting tumor cells can exploit the exosome pathway to disseminate their own components and modulate the activity of immune cells, in particular, activate B cells with inhibitory activity.

http://www.ncbi.nlm.nih.gov/pubmed/22558358