Post by itsybitsyone on May 27, 2008 12:08:59 GMT -8
Invasion of human neuronal and glial cells by an infectious strain of Borrelia burgdorferi.Livengood JA, Gilmore RD Jr.Centers for Disease Control and Prevention, Division of Vector-borne Infectious Diseases, 3150 Rampart Road, CSU Foothills Campus, Fort Collins, CO 80522, USA
Microbes Infect.
2006 Nov-Dec;8(14-15):2832-40.
Human infection by Borrelia burgdorferi, the etiological agent for Lyme disease, can result in serious acute and late-term disorders including neuroborreliosis, a degenerative condition of the peripheral and central nervous systems. To examine the mechanisms involved in the cellular pathogenesis of neuroborreliosis, we investigated the ability of B. burgdorferi to attach to and/or invade a panel of human neuroglial and cortical neuronal cells. In all neural cells tested, we observed B. burgdorferi in association with the cell by confocal microscopy. Further analysis by differential immunofluorescent staining of external and internal organisms, and a gentamicin protection assay demonstrated an intracellular localization of B. burgdorferi. A non-infectious strain of B. burgdorferi was attenuated in its ability to associate with these neural cells, suggesting that a specific borrelial factor related to cellular infectivity was responsible for the association. Cytopathic effects were not observed following infection of these cell lines with B. burgdorferi, and internalized spirochetes were found to be viable. Invasion of neural cells by B. burgdorferi provides a putative mechanism for the organism to avoid the host's immune response while potentially causing functional damage to neural cells during infection of the CNS.
INFECTION AND IMMUNITY, Dec. 1994, p. 5559-5567 Vol. 62, No. 12
American Society for Microbiology
Diverse Lyme Disease Spirochetes Bind Integrin oLIIbI33 on
Human Platelets
JENIFER COBURN, STEPHEN W. BARTHOLD, AND JOHN M. LEONG
Division of Rheumatology and Immunology, Tufts-New England Medical Center, Boston, Massachusetts and
Section of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-80162
Lyme disease is a chronic, multisystemic infection caused by Borrelia bwgdorferi sensu lato. An infectious strain
of B. burgdorferi was previously shown to bind to human platelets via the integrin "IHAj3. In this study, a diverse
group of Lyme disease spirochetes was tested for platelet- and aOII,3-binding activity. This collection included
representatives of each of the three species that cause Lyme disease, B. bwgdorfe,i (sensu stricto), B. garinji, and B.
afzelii. Strains were characterized for infectivity in mouse models or were low-passage isolates from human patients.
Each of the 11 infectious strains bound to platelets immobilized in microtiter wells and in suspension. Binding to
platelets in suspension was specifically inhibited by a blocking anti-allbP3 antibody, and representatives of each
species bound to purified QIIAj3. The strains that did not bind aIIbB3 or platelets were all noninfectious. No obvious
relationship was observed between binding to platelets and expression of the bacterial outer surface protein OspA,
OspB, or OspC, as assessed by immunoblotting. These results demonstrate that integrin ac 03-binding activity is
widespread among the Bomrlia species that cause Lyme disease and are consistent with a role for %aIIA binding in
the transmission and/or pathogenesis of Lyme disease.
Microbes Infect.
2006 Nov-Dec;8(14-15):2832-40.
Human infection by Borrelia burgdorferi, the etiological agent for Lyme disease, can result in serious acute and late-term disorders including neuroborreliosis, a degenerative condition of the peripheral and central nervous systems. To examine the mechanisms involved in the cellular pathogenesis of neuroborreliosis, we investigated the ability of B. burgdorferi to attach to and/or invade a panel of human neuroglial and cortical neuronal cells. In all neural cells tested, we observed B. burgdorferi in association with the cell by confocal microscopy. Further analysis by differential immunofluorescent staining of external and internal organisms, and a gentamicin protection assay demonstrated an intracellular localization of B. burgdorferi. A non-infectious strain of B. burgdorferi was attenuated in its ability to associate with these neural cells, suggesting that a specific borrelial factor related to cellular infectivity was responsible for the association. Cytopathic effects were not observed following infection of these cell lines with B. burgdorferi, and internalized spirochetes were found to be viable. Invasion of neural cells by B. burgdorferi provides a putative mechanism for the organism to avoid the host's immune response while potentially causing functional damage to neural cells during infection of the CNS.
INFECTION AND IMMUNITY, Dec. 1994, p. 5559-5567 Vol. 62, No. 12
American Society for Microbiology
Diverse Lyme Disease Spirochetes Bind Integrin oLIIbI33 on
Human Platelets
JENIFER COBURN, STEPHEN W. BARTHOLD, AND JOHN M. LEONG
Division of Rheumatology and Immunology, Tufts-New England Medical Center, Boston, Massachusetts and
Section of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-80162
Lyme disease is a chronic, multisystemic infection caused by Borrelia bwgdorferi sensu lato. An infectious strain
of B. burgdorferi was previously shown to bind to human platelets via the integrin "IHAj3. In this study, a diverse
group of Lyme disease spirochetes was tested for platelet- and aOII,3-binding activity. This collection included
representatives of each of the three species that cause Lyme disease, B. bwgdorfe,i (sensu stricto), B. garinji, and B.
afzelii. Strains were characterized for infectivity in mouse models or were low-passage isolates from human patients.
Each of the 11 infectious strains bound to platelets immobilized in microtiter wells and in suspension. Binding to
platelets in suspension was specifically inhibited by a blocking anti-allbP3 antibody, and representatives of each
species bound to purified QIIAj3. The strains that did not bind aIIbB3 or platelets were all noninfectious. No obvious
relationship was observed between binding to platelets and expression of the bacterial outer surface protein OspA,
OspB, or OspC, as assessed by immunoblotting. These results demonstrate that integrin ac 03-binding activity is
widespread among the Bomrlia species that cause Lyme disease and are consistent with a role for %aIIA binding in
the transmission and/or pathogenesis of Lyme disease.