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Post by LymeEnigma on Sept 6, 2008 17:29:52 GMT -8
Neurobiol Aging. 2006 Feb;27(2):228-36. Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes. Miklossy J, Kis A, Radenovic A, Miller L, Forro L, Martins R, Reiss K, Darbinian N, Darekar P, Mihaly L, Khalili K. Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3. judmik@telus.net The pathological hallmarks of Alzheimer's disease (AD) consist of beta-amyloid plaques and neurofibrillary tangles in affected brain areas. The processes, which drive this host reaction are unknown. To determine whether an analogous host reaction to that occurring in AD could be induced by infectious agents, we exposed mammalian glial and neuronal cells in vitro to Borrelia burgdorferi spirochetes and to the inflammatory bacterial lipopolysaccharide (LPS). Morphological changes analogous to the amyloid deposits of AD brain were observed following 2-8 weeks of exposure to the spirochetes. Increased levels of beta-amyloid precursor protein (AbetaPP) and hyperphosphorylated tau were also detected by Western blots of extracts of cultured cells that had been treated with spirochetes or LPS. These observations indicate that, by exposure to bacteria or to their toxic products, host responses similar in nature to those observed in AD may be induced. PMID: 15894409 [PubMed - indexed for MEDLINE] www.ncbi.nlm.nih.gov/pubmed/15894409?ordinalpos=12&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSumEmphasis mine. |
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Post by LymeEnigma on Sept 6, 2008 17:32:38 GMT -8
Glycoconjugates: Roles in Neural Diseases Caused by Exogenous Pathogens pp.381-389 (9) Author: Cara-Lynne Schengrund Abstract Numerous reports indicate that lipid or protein associated carbohydrates are essential for infection of cells by various viruses, bacteria, or bacterial toxins, some of which affect the nervous system. Examples of such pathogens include tetanus and botulinum neurotoxin, Shiga and Shiga-like toxins, Borrelia burgdorferi, Mycobacterium leprae, and human immunodeficiency virus. This review discusses evidence indicating that carbohydrates are essential for these pathogens to induce their deleterious effects, the putative function of the carbohydrates, and how this knowledge might be used to combat the effects of the pathogen. Keywords: Botulinum toxin, tetanus toxin, Lyme disease, leprosy, HIV, glycosphingolipids, multivalent carbohydrate ligands, carbohydrate antigens Affiliation: Department of Biochemistry and Molecular Biology, The Pennsylvania State University College of Medicine, 500 University Dr., Hershey, PA 17033, USA. www.bentham-direct.org/pages/content.php?CNSNDDT/2006/00000005/00000004/0003Z.SGM
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Post by LymeEnigma on Sept 6, 2008 17:34:18 GMT -8
Folia Microbiol (Praha). 2004;49(5):625-9. Immunochemical analysis of lipopolysaccharide-like component extracted from Borrelia burgdorferi sensu lato. Schwarzová K, Ciznár I. Institute of Preventive and Clinical Medicine, Slovak Health University, Bratislava, Slovakia. virukats@savba.sk Immunoelectrophoresis and its modifications were applied to analysis of a lipopolysaccharide-like component (LPS-LC) extracted from Borrelia garinii strains K24 and K48 isolated from Ixodes ricinus and Borrelia burgdorferi sensu stricto strain B31. A modification of the hot phenol-water method was used for isolation of LPS. Immunoelectrophoresis (IE) and crossed immunoelectrophoresis (CIE) of LPS-LC with polyclonal rabbit antisera revealed a pattern and properties partially similar to LPS from other Gram-negative bacteria. B. garinii LPS-LC formed in CIE a diffuse band extending from the start to the anode. Similarly, the shape and position of the band in IE did not show major differences from LPS of other Gram-negative bacteria. The LPS-LC extracted from the three genomic groups of B. burgdorferi sensu lato were found to have similar immunochemical properties irrespective of their genotype origin. PMID: 15702557 [PubMed - indexed for MEDLINE] www.ncbi.nlm.nih.gov/pubmed/15702557?ordinalpos=13&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum |
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Post by LymeEnigma on Sept 6, 2008 17:39:39 GMT -8
J Infect Dis. 1994 May;169(5):1014-22. Borrelia burgdorferi and Escherichia coli lipopolysaccharides induce nitric oxide and interleukin-6 production in cultured rat brain cells. Tatro JB, Romero LI, Beasley D, Steere AC, Reichlin S. Division of Endocrinology, New England Medical Center Hospitals, Boston, MA 02111. Borrelia burgdorferi, the spirochetal agent of Lyme disease, infects the central nervous system (CNS), but the factors that mediate inflammation and neurologic dysfunction are not known. Sonicated B. burgdorferi stimulated in a concentration-dependent manner the production of nitric oxide (NO) in glial-enriched primary cultures of neonatal rat brain cells via induction of NO synthase activity. Lipopolysaccharide (LPS) of Escherichia coli also stimulated nitrite accumulation in a concentration-dependent manner. Stimulation of NO production by B. burgdorferi sonicate and E. coli LPS was associated with increased levels of mRNA coding for the cytokine-inducible form of NO synthase. B. burgdorferi sonicate also stimulated release of interleukin-6, with a concentration-response relationship similar to that for its stimulation of nitrite production, as did E. coli LPS. A competitive antagonist of E. coli LPS, Rhodopseudomonas sphaeroides lipid A, inhibited LPS-induced stimulation of NO synthase activity but markedly potentiated that of B. burgdorferi, indicating that the initial triggering mechanism of B. burgdorferi is distinct from that of E. coli LPS. Induction of NO synthase by bacterial agents within the brain may represent a common pathway of CNS inflammation and neurotoxicity. PMID: 7513330 [PubMed - indexed for MEDLINE] www.ncbi.nlm.nih.gov/pubmed/7513330?ordinalpos=52&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum |
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Post by LymeEnigma on Sept 6, 2008 17:46:41 GMT -8
Microbiologica. 1986 Apr;9(2):249-52. Endotoxicity associated with the Lyme disease Borrelia: recent findings. Fumarola D, Munno I, Marcuccio C, Miragliotta G. The endotoxicity of Borrelia burgdorferi, the causative agent of Lyme Disease, a tick-borne spirochetosis, was studied using Limulus assay and pyrogen test in rabbit. Some suspensions of Ixodes ricinus and Ixodes dammini associated Borrelia were able to gelify Limulus lysate and demonstrated a febrile response in rabbit. These findings and other recent data demonstrating an endotoxin-like activity of the Lyme Disease agent are discussed in the context of the pathogenic mechanisms of the illness. PMID: 3713546 [PubMed - indexed for MEDLINE] www.ncbi.nlm.nih.gov/pubmed/3713546?ordinalpos=74&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum |
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Post by LymeEnigma on Sept 6, 2008 17:48:30 GMT -8
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Post by LymeEnigma on Sept 6, 2008 17:51:28 GMT -8
J Neurol. 1993 May;240(5):278-83. Borrelia burgdorferi myositis: report of eight patients. Reimers CD, de Koning J, Neubert U, Preac-Mursic V, Koster JG, Müller-Felber W, Pongratz DE, Duray PH. Friedrich-Baur-Institute, Clinic for Internal Medicine Innenstadt, Munich, Germany. Myositis is a rare manifestation of Lyme disease of unknown pathogenesis. This study describes the course of disease in eight patients with Lyme disease, aged 37-70 years, all of whom were suffering from histologically proven myositis. The clinical, electrophysiological, and myopathological findings are reported. One patient showed signs and symptoms of myositis of all limbs. In six patients myositis was localized in the vicinity of skin lesions, arthritis or neuropathy caused by Borrelia burgdorferi. In another patient suffering from pronounced muscle weakness of the legs and cardiac arrest, inflammation of the myocardium, the conducting system and skeletal muscles was revealed at autopsy. Muscle biopsy revealed lymphoplasmocellular infiltrates combined with few fibre degenerations in three patients. The lymphoplasmocellular infiltrates were found predominantly in the vicinity of small vessels. Several spirochetes were stained in six of seven muscle biopsy samples by means of the immunogold-silver technique. Culturing of B. Burgdorferi from the muscle biopsy samples was, however, unsuccessful. Antibiotic treatment succeeded in curing the myositis in four of six patients. In one patients signs and symptoms improved. One patient died from cardiac arrest caused by myocarditis and Guillain-Barré syndrome. The outcome is unknown in one patient. Clinical and myopathological findings indicate that Lyme myositis can be caused either by local spreading of B. burgdorferi or an unknown antigen or toxin from adjacent tissues or haematogenously. PMID: 8326331 [PubMed - indexed for MEDLINE] www.ncbi.nlm.nih.gov/pubmed/8326331?ordinalpos=54&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum |
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Post by nyxie63 on Sept 7, 2008 6:45:30 GMT -8
www3.interscience.wiley.com/journal/69000399/abstractBorrelia burgdorferi induces matrix metalloproteinases by neural cultures George Perides *, Linda M. Tanner-Brown, Manuel A. Eskildsen, Mark S. Klempner Tupper Research Institute, Department of Medicine, Tufts University School of Medicine, New England Medical Center, Boston, Massachusetts email: George Perides (gperides@caregroup.harvard.edu) *Correspondence to George Perides, Department of Surgery, Dana 807, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02111. Funded by: NIH; Grant Number: AI37241, AI31610, AI 65308 Earle P. Charlton Award Keywords astrocytes; neuroborreliosis; Lyme disease Abstract Matrix metalloproteinases (MMPs) are associated with chronic neurologic diseases such as multiple sclerosis and senile dementia. Lyme disease is a multisystemic infection involving the nervous system, skin, joints, and heart. Neurologic manifestations of chronic Lyme disease include encephalopathy and cranial and peripheral neuropathy. Borrelia burgdorferi, the spirochaete causing Lyme disease, has been cultured from the cerebrospinal fluid (CSF), and B. burgdorferi DNA is frequently detected in the CSF of patients with Lyme neuroborreliosis. We used cerebral and cerebellar primary cultures to determine whether B. burgdorferi induces the production of MMPs by primary neural cultures. B. burgdorferi in a dose- and time-dependent manner induced the expression of MMP-9 by primary neural cultures but had no effect on the expression of MMP-2. Human and rat type I astrocytes expressed MMP-9 when incubated with B. burgdorferi in the same manner as primary neural cultures. This response may play a role in the symptomatology and the pathogenesis of Lyme neuroborreliosis. J. Neurosci. Res. 58:779-790, 1999. © 1999 Wiley-Liss, Inc.
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Post by nyxie63 on Sept 7, 2008 6:49:31 GMT -8
cvi.asm.org/cgi/content/abstract/14/11/1420Anaplasma phagocytophilum-Borrelia burgdorferi Coinfection Enhances Chemokine, Cytokine, and Matrix Metalloprotease Expression by Human Brain Microvascular Endothelial CellsDennis J. Grab,1* Elvis Nyarko,1,# Nicole C. Barat,2 Olga V. Nikolskaia,1 and J. Stephen Dumler2 Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287,1 Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 212052 Received 26 July 2007/ Returned for modification 12 September 2007/ Accepted 19 September 2007 Borrelia burgdorferi and Anaplasma phagocytophilum coinfect and are transmitted by Ixodes species ticks. Clinical indicators suggest that A. phagocytophilum coinfection contributes to the severity, dissemination, and, possibly, sequelae of Lyme disease. Previous in vitro studies showed that spirochete penetration through human brain microvascular endothelial cells of the blood-brain barrier is facilitated by endothelial cell-derived matrix metalloproteases (MMPs). A. phagocytophilum-infected neutrophils continuously release MMPs and other vasoactive biomediators. We examined B. burgdorferi infection of brain microvascular barriers during A. phagocytophilum coinfection and showed that coinfection enhanced reductions in transendothelial electrical resistance and enhanced or synergistically increased production of MMPs (MMP-1, -3, -7, -8, and -9), cytokines (interleukin 6 [IL-6], IL-10, and tumor necrosis factor alpha), and chemokines (IL-8 and macrophage inflammatory protein 1) known to affect vascular permeability and inflammatory responses.
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Post by LymeEnigma on Sept 7, 2008 8:32:30 GMT -8
Great finds, Nyxie!
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Post by nyxie63 on Sept 9, 2008 2:12:11 GMT -8
Looks like they're finally starting to catch on.  Chronic Bacterial and Viral Infections in Neurodegenerative and Neurobehavioral DiseasesPosted 06/23/2008 Garth L. Nicolson, PhD Abstract Often, patients with neurodegenerative or neurobehavioral diseases have chronic, neuropathic infections that could be important in disease inception, disease progression, or increasing the types or severities of signs and symptoms. Although controversial, the majority of patients with various neurodegenerative or neurobehavioral conditions, such as amyotrophic lateral sclerosis, multiple sclerosis, Alzheimer's disease, Parkinson's disease, and autistic spectrum disorders, show evidence of central nervous system or systemic bacterial and viral infections. For example, using serology or polymerase chain reaction evidence of Chlamydia pneumoniae, Borrelia burgdorferi, Mycoplasma species, human herpesvirus-1 and -6, and other bacterial and viral infections revealed high infection rates that were not found in control subjects. Although chronic infections were not found in some studies, and the specific role of chronic infections in neurological disease pathogenesis has not been determined or is inconclusive, the data suggest that chronic bacterial or viral infections could be common features of progressive neurodegenerative and neurobehavioral diseases. The rest of the article is here: www.medscape.com/viewarticle/574944 |
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