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Full-Text Articles in Bacterial Infections and Mycoses
Chlamydia Pneumoniae Infection Of Neuronal Cells Induces Changes In Calcium-Associated Gene Expression Consistent With Alzheimer’S Disease, Christopher Andrew Cappellini, Ahmad B. Cader, Keith G. Williams, Juliana Zoga, Susan T. Hingley
Chlamydia Pneumoniae Infection Of Neuronal Cells Induces Changes In Calcium-Associated Gene Expression Consistent With Alzheimer’S Disease, Christopher Andrew Cappellini, Ahmad B. Cader, Keith G. Williams, Juliana Zoga, Susan T. Hingley
Scholarly Posters
Background and Significance: Previous studies have shown that cells infected with Chlamydia pneumoniae (Cpn) exhibit altered gene expression consistent with that observed in Alzheimer’s disease (AD). Furthermore, AD neurodegeneration has been linked to dysregulation of intracellular calcium and calcium-related processes. Therefore, we hypothesize that one mechanism by which pathogenesis evolves in AD is through infection-induced changes in expression of calcium-related genes. Objectives: To determine if infection of neuronal cells with Cpn alters expression of calciumrelated genes associated with neurodegeneration. Methods: SK-N-MC neuronal cells were infected with Cpn (AR39 strain; MOI=1) for 3 to 72 hours, then calcium-related genes were screened …
Autophagy And Apoptotic Genes Implicated In Alzheimer’S Disease Are Modulated Following Infection Of Neuronal Cells With Chlamydia Pneumoniae, Denah M. Appelt, Ian Kohler, Annette K. Slutter, Juliana Zoga, Susan T. Hingley, Brian J. Balin
Autophagy And Apoptotic Genes Implicated In Alzheimer’S Disease Are Modulated Following Infection Of Neuronal Cells With Chlamydia Pneumoniae, Denah M. Appelt, Ian Kohler, Annette K. Slutter, Juliana Zoga, Susan T. Hingley, Brian J. Balin
Scholarly Posters
Background: The focus of the current studies was to determine the relationship between the molecular mechanisms interconnecting autophagy and apoptosis following Chlamydia pneumoniae infection in neuronal cells. Dysfunctions in apoptosis and autophagy have been implicated in the neurodegeneration associated with Alzheimer’s disease (AD). Autophagy in AD pathogenesis has been shown to play a role in amyloid processing through the endosomal-lysosomal system. Apoptosis may contribute to the neuronal cell loss observed in AD; however, there is limited evidence of the apoptotic process proceeding to terminal completion. Although Aβ1-42 has been shown to induce apoptosis in neurons and may be an early …
Gestational Diabetes Clinic For Indigent Latinos, Sara Wilson Reece
Gestational Diabetes Clinic For Indigent Latinos, Sara Wilson Reece
Scholarly Posters
Gestational diabetes mellitus (GDM), “carbohydrate intolerance of variable severity with onset or fist recognition during pregnancy,” results from insulin resistance and relative insulin deficiency usually in second trimester.¹ • Gestational diabetes (GDM) impacts between 4% and 9% of all pregnancies. • Gestational diabetes (GDM) results in increased fetal complications of macrosomia, shoulder dystocia and neonatal hyperglycemia as well as maternal risks of preeclampsia and polyhydramnois. • Women who are Hispanic or Asian decent are at highest risk of developing GDM. • Diagnosis ² • Perform 75-gramoral glucose tolerance test (OGTT) at 24 – 28 weeks of gestation in women not …
Analysis Of Chlamydia Pneumoniae And Ad-Like Pathology In The Brains Of Balb/C Mice Following Direct Intra-Cranial Infection, Jessica Rachel Barton, Christine J. Hammond, Amy L. Brady, Denah M. Appelt, Brian J. Balin, Christopher Scott Little
Analysis Of Chlamydia Pneumoniae And Ad-Like Pathology In The Brains Of Balb/C Mice Following Direct Intra-Cranial Infection, Jessica Rachel Barton, Christine J. Hammond, Amy L. Brady, Denah M. Appelt, Brian J. Balin, Christopher Scott Little
Scholarly Posters
Alzheimer’s disease (AD) is an age-related progressive neurodegenerative disorder and the most common form of dementia. The pathology in the central nervous system (CNS) impairs memory and cognition, hindering the capabilities and the quality of life of the individual. This project continues studying the role of infection and Alzheimer’s disease, as previous studies in this laboratory have done, and contributes to the overall understanding of the possible causes of this disease. In this study, BALB/c mice were infected, via direct intracranial injection, with a respiratory isolate (AR-39) of Chlamydia pneumoniae. Their brains were analyzed at 7 and 14 days post-infection, …
Infection Of Neuronal Cells By Chlamydia Pneumoniae And Herpes Simplex Virus Type 1 Alters Expression Of Genes Associated With Alzheimer’S Disease, Morgan M. Devins, Fiora D. Zoga, Brian J. Balin, Denah M. Appelt, Susan T. Hingley
Infection Of Neuronal Cells By Chlamydia Pneumoniae And Herpes Simplex Virus Type 1 Alters Expression Of Genes Associated With Alzheimer’S Disease, Morgan M. Devins, Fiora D. Zoga, Brian J. Balin, Denah M. Appelt, Susan T. Hingley
Scholarly Posters
Several studies have suggested an infectious etiology for Alzheimer’s disease (AD). We have been investigating a potential role for both Chlamydia pneumoniae and Herpes simplex virus type 1 (HSV1) in the initiation of sporadic late-onset AD. Our current study focuses on investigation of gene expression using Alzheimer-specific Real-Time PCR microarrays on RNA derived from SKNMC human neuronal cells infected with C. pneumoniae and/or HSV1. There are distinct differences in the patterns of gene regulation by the two pathogens. For example, C. pneumoniae induces expression of genes involved in amyloid production and processing, such as β-amyloid precursor protein (APP), β-site APP-cleaving …
Analysis Of Chlamydia Pneumoniae-Infected Monocytes Following Incubation With A Novel Peptide, Acaly18, Implicates The Inflammasome In Clearance Of Infection, Brian J. Balin, James D. Thacker, Charles Lim, Corey M. Caruthers, Susan T. Hingley, Juliana Zoga, Denah M. Appelt
Analysis Of Chlamydia Pneumoniae-Infected Monocytes Following Incubation With A Novel Peptide, Acaly18, Implicates The Inflammasome In Clearance Of Infection, Brian J. Balin, James D. Thacker, Charles Lim, Corey M. Caruthers, Susan T. Hingley, Juliana Zoga, Denah M. Appelt
Scholarly Posters
Chlamydia pneumoniae infection may be a trigger for the pathology observed in sporadic lateonset Alzheimer’s disease as a function of initiating neuroinflammation following entry of the organism into the brain. We have hypothesized that one entry mechanism may be by bloodborne infected monocytes trafficking the infection into the brain. This study focuses on infection of monocytes in vitro followed by analysis using immunofluorescence labeling and RT-PCR-microarray techniques. The microarrays utilized consisted of an Alzheimer’s disease pathway array and an innate and adaptive immunity array from SAbiosciences. Analysis by real time PCR for both gene arrays was performed on uninfected and …
Herpes Simplex Virus 1 And Chlamydophila (Chlamydia) Pneumoniae Promote Ab 1-42 Amyloid Processing In Murine Astrocytes Linking An Infectious Process To Alzheimer's Disease, Laura R. Triplett, Adam L. Dore, Kevin S. Kralik, Brian J. Balin, Susan T. Hingley, Denah M. Appelt
Herpes Simplex Virus 1 And Chlamydophila (Chlamydia) Pneumoniae Promote Ab 1-42 Amyloid Processing In Murine Astrocytes Linking An Infectious Process To Alzheimer's Disease, Laura R. Triplett, Adam L. Dore, Kevin S. Kralik, Brian J. Balin, Susan T. Hingley, Denah M. Appelt
Scholarly Posters
Background: Several studies have suggested an infectious etiology for Alzheimer's disease (AD). Previously, our laboratory identified Chlamydia pneumoniae (Cpn) from autopsied sporadic AD brains, as well as developed a BALB/c mouse model that demonstrated infection-induced amyloid plaques similar to those found in AD. Hypothesis: We propose that an additional pathogen such as herpes simplex virus type 1 (HSV1), also may be a contributing factor in toin the pathology seen in AD. HSV1, in addition to Cpn, may be triggering the abnormal cleavage of the beta amyloid precursor protein (bAPP) into Ab1-42 , thereby contributing to amyloid plaque formation. Our current …