Inhibition of apoptosis in neuronal cells infected with Chlamydophila (Chlamydia) pneumoniae

Appelt, Denah M.; Roupas, Maria R; Way, Deana S.; Bell, Marcus G.; Albert, Elizabeth; Hammond, Christine J.; Balin, Brian J.

doi:10.1186/1471-2202-9-13

Cited by 33 publications

(26 citation statements)

References 38 publications

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“…We further showed that astrocytes and microglia were host cells for the organism in the AD brain, and in recent studies we and others have identified neurons as host cells for the organism as well (Balin et al, 1998; Gérard et al, 2006; Appelt et al, 2008). …”

Section: Introductionsupporting

confidence: 69%

Initial characterization of Chlamydophila (Chlamydia) pneumoniae cultured from the late-onset Alzheimer brain

Dreses-Werringloer

Bhuiyan

Zhao

et al. 2009

International Journal of Medical Microbiology

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Previous studies from this laboratory provided evidence that the intracellular bacterial pathogen Chlamydophila (Chlamydia) pneumoniae is present in the late-onset Alzheimer’s disease (AD) brain. Here we report culture of the organism from two AD brain samples, each of which originated from a different geographic region of North America. Culturable organisms were detectable after one and two passages in HEp-2 cells, respectively, for the two samples. Both isolates, designated Tor-1 and Phi-1, were demonstrated to be authentic C. pneumoniae using PCR assays targeting the C. pneumoniae-specific genes Cpn0695, Cpn1046, and tyrP. Assessment of inclusion morphology and quantitation of infectious yields in epithelial (HEp-2), astrocytic (U-87 MG), and microglial (CHME-5) cell lines demonstrated an active, rather than a persistent, growth phenotype for both isolates in all host cell types. Sequencing of the omp1 gene from each isolate, and directly from DNA prepared from several additional AD brain tissue samples PCR-positive for C. pneumoniae, revealed genetically diverse chlamydial populations. Both brain isolates carry several copies of the tyrP gene, a triple copy in Tor-1, and predominantly a triple copy in Phi-1 with a minor population component having a double copy. This observation indicated that the brain isolates are more closely related to respiratory than to vascular/atheroma strains of C. pneumoniae.

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Section: Introductionsupporting

confidence: 69%

Initial characterization of Chlamydophila (Chlamydia) pneumoniae cultured from the late-onset Alzheimer brain

Dreses-Werringloer

Bhuiyan

Zhao

et al. 2009

International Journal of Medical Microbiology

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“…Listeria monocytogenes, Borrelia burgdorferi , Treponema pallidum and Mycobacterim leprae target neurons at the periphery in order to evade the host immune response and gain access to the relatively ‘immune‐privileged’ environment of the CNS. C. pneumoniae , similar to M. tuberculosis , establishes infection within the lung, disseminates and through phagocyte facilitation traverses the blood–brain barrier, where the bacteria are free to infect neurons 86 , 87 , 88 , 89 , 90 . It was recently demonstrated the association and subsequent internalisation of M. tuberculosis by murine and human‐derived neuronal cell lines and primary neurons in culture and in vivo.…”

Section: Glial and Neuronal Cellsmentioning

confidence: 99%

Mycobacterium tuberculosis infection of the ‘non‐classical immune cell’

et al. 2015

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Mycobacterium tuberculosis can infect 'non-classical immune cells', which comprise a significant constituency of cells that reside outside of those defined as 'classical immune cells' from myeloid or lymphoid origin. Here we address the influence of specific 'non-classical immune cells' in host responses and their effects in controlling mycobacterial growth or enabling an environment conducive for bacilli persistence. The interaction of M. tuberculosis with epithelial cells, endothelial cells, fibroblasts, adipocytes, glia and neurons and downstream cellular responses that often dictate immune regulation and disease outcome are discussed. Functional integration and synergy between 'classical' and 'non-classical immune cells' are highlighted as critical for determining optimal immune outcomes that favour the host.

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“…[35] The ability of the intracellular C. pneumoniae to enable the neuron to resist apoptosis and enter a chronic infective/inflammatory state has been more recently described. [36] The suggested consequence of this latency is an upregulation of amyloid production and processing. More recently, it has been demonstrated that the brains of Alzheimer's disease individuals carrying APOE4 have increased C. pneumoniae burden compared with non-APOE4 carriers.…”

Section: Chlamydophila Pneumoniaementioning

confidence: 99%

Role of Infection in the Pathogenesis of Alzheimerʼs Disease

Holmes

Cotterell

2009

CNS Drugs

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While our understanding of the neuropathology of Alzheimer's disease continues to grow, its pathogenesis remains a subject of intense debate. Genetic mutations contribute to a minority of early-onset autosomal dominant cases, but most cases are of either late-onset familial or sporadic form. CNS infections, most notably herpes simplex virus type 1, Chlamydophila pneumoniae and several types of spirochetes, have been previously suggested as possible aetiological agents in the development of sporadic Alzheimer's disease but with little consistent evidence. However, peripheral infections may have a role to play in accelerating neurodegeneration in Alzheimer's disease by activating already primed microglial cells within the CNS. Potential pharmacological interventions could aim at modification of this peripheral inflammatory response through targeting various agents involved in this inflammatory pathway. However, benefit could also be gained clinically through the meticulous detection, treatment and prevention of infections in individuals either alone or in combination with anti-inflammatory therapy.

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Inhibition of apoptosis in neuronal cells infected with Chlamydophila (Chlamydia) pneumoniae

Cited by 33 publications

References 38 publications

Initial characterization of Chlamydophila (Chlamydia) pneumoniae cultured from the late-onset Alzheimer brain

Initial characterization of Chlamydophila (Chlamydia) pneumoniae cultured from the late-onset Alzheimer brain

Mycobacterium tuberculosis infection of the ‘non‐classical immune cell’

Role of Infection in the Pathogenesis of Alzheimerʼs Disease

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