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Immunology of Infectious Disease Commons™

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2006

Articles 1 - 6 of 6

Full-Text Articles in Immunology of Infectious Disease

Characterization Of Host Cell Death Induced By Chlamydia Trachomatis, Songmin Ying, Silke F. Fischer, Matthew A. Pettengill, Debye Conte, Stefan A. Paschen, David M. Ojcius, Georg Hacker Nov 2006

Characterization Of Host Cell Death Induced By Chlamydia Trachomatis, Songmin Ying, Silke F. Fischer, Matthew A. Pettengill, Debye Conte, Stefan A. Paschen, David M. Ojcius, Georg Hacker

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Chlamydia are obligate intracellular bacteria that modulate apoptosis of the host cell. Strikingly, chlamydial infection has been reported both to inhibit and to induce apoptosis. Although the ability to inhibit apoptosis has been corroborated by the identification of cellular targets, confirmation of cell death induction has been complicated by a mixture of apoptotic features and atypical cell death during infection, as well as by differences in the experimental techniques used to measure cell death. Here we use a panel of well-established approaches in the study of apoptosis to define the form of cell death induced by Chlamydia trachomatis infection. Infected …

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Fisheries Research Contract Report No. 15 - Aquatic Animal Health Subprogram: Pilchard Herpesvirus Infection In Wild Pilchards (Frdc Project No. 2002/044) Final Report, Brian Jones, Melanie Crockford, Richard Whittington, Mark Crane, Graham Wilcox Oct 2006

Fisheries Research Contract Report No. 15 - Aquatic Animal Health Subprogram: Pilchard Herpesvirus Infection In Wild Pilchards (Frdc Project No. 2002/044) Final Report, Brian Jones, Melanie Crockford, Richard Whittington, Mark Crane, Graham Wilcox

Fisheries Research Contract Reports

In 1995 and again in 1998/9, millions of pilchards (Sardinops sagax neopilchardus) were found dead or dying off the coast of Australia. Some pilchards in New Zealand were also affected during the 1995 epizootic. The epizootics moved progressively in a "bushfire-like" manner against the prevailing currents at a rapid speed. An uncharacterised herpesvirus, pilchard herpesvirus (PHV), was associated with both mortality events and, based on its occurrence in affected fish and the disease pathogenesis, generally accepted as the causative agent, although experimental evidence of its role was not established. Until recently, rapid and sensitive methods to detect PHV were not …

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In Vivo Mature Immunological Synapses Forming Smacs Mediate Clearance Of Virally Infected Astrocytes From The Brain, Carlos Barcia, Clare Thomas, James Curtin, Gwendalyn King, Kolja Wawrowsky, Marianela Candolfi, Weidong Xiong, Chunyan Liu, Kurt Kroeger, Olivier Boyer, Jerzy Kupiec-Weglinski, David Klatzmann, Maria Castro, Pedro Lowenstein Sep 2006

In Vivo Mature Immunological Synapses Forming Smacs Mediate Clearance Of Virally Infected Astrocytes From The Brain, Carlos Barcia, Clare Thomas, James Curtin, Gwendalyn King, Kolja Wawrowsky, Marianela Candolfi, Weidong Xiong, Chunyan Liu, Kurt Kroeger, Olivier Boyer, Jerzy Kupiec-Weglinski, David Klatzmann, Maria Castro, Pedro Lowenstein

Articles

The microanatomy of immune clearance of infected brain cells remains poorly understood. Immunological synapses are essential anatomical structures that channel information exchanges between T cell–antigen-presenting cells (APC) during the priming and effector phases of T cells' function, and during natural killer–target cell interactions. The hallmark of immunological synapses established by T cells is the formation of the supramolecular activation clusters (SMACs), in which adhesion molecules such as leukocyte function-associated antigen 1 segregate to the peripheral domain of the immunological synapse (p-SMAC), which surrounds the T cell receptor–rich or central SMAC (c-SMAC). The inability so far to detect SMAC formation in …

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Recruitment Of Bad By The Chlamydia Trachomatis Vacuole Correlates With Host-Cell Survival, Philippe Verbeke, Lynn Welter-Stahl, S. Ying, J. Hansen, Georg Hacker, Toni Darville, David M. Ojcius May 2006

Recruitment Of Bad By The Chlamydia Trachomatis Vacuole Correlates With Host-Cell Survival, Philippe Verbeke, Lynn Welter-Stahl, S. Ying, J. Hansen, Georg Hacker, Toni Darville, David M. Ojcius

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Chlamydiae replicate intracellularly in a vacuole called an inclusion. Chlamydial-infected host cells are protected from mitochondrion-dependent apoptosis, partly due to degradation of BH3-only proteins. The host-cell adapter protein 14-3-3β can interact with host-cell apoptotic signaling pathways in a phosphorylation-dependent manner. In Chlamydia trachomatis-infected cells, 14-3-3β co-localizes to the inclusion via direct interaction with a C. trachomatis-encoded inclusion membrane protein. We therefore explored the possibility that the phosphatidylinositol-3 kinase (PI3K) pathway may contribute to resistance of infected cells to apoptosis. We found that inhibition of PI3K renders C. trachomatis-infected cells sensitive to staurosporine-induced apoptosis, which is accompanied by mitochondrial cytochrome c …

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Intercellular Spreading Of Porphyromonas Gingivalis Infection In Primary Gingival Epithelial Cells, Özlem Yilmaz, Philippe Verbeke, Richard J. Lamont, David M. Ojcius Jan 2006

Intercellular Spreading Of Porphyromonas Gingivalis Infection In Primary Gingival Epithelial Cells, Özlem Yilmaz, Philippe Verbeke, Richard J. Lamont, David M. Ojcius

All Dugoni School of Dentistry Faculty Articles

Porphyromonas gingivalis, an important periodontal pathogen, is an effective colonizer of oral tissues. The organism successfully invades, multiplies in, and survives for extended periods in primary gingival epithelial cells (GECs). It is unknown whether P. gingivalis resides in the cytoplasm of infected cells throughout the infection or can spread to adjacent cells over time. We developed a technique based on flow cytofluorometry and fluorescence microscopy to study propagation of the organism at different stages of infection of GECs. Results showed that P. gingivalis spreads cell to cell and that the amount of spreading increases gradually over time. There was a …

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Premature Induction Of An Immunosuppressive Regulatory T Cell Response During Acute Simian Immunodeficiency Virus Infection, Jacob D. Estes, Qingsheng Li, Matthew R. Reynolds, Stephen W. Wietgrefe, Lijie Duan, Timothy Schacker, Louis J. Picker, David I. Watkins, Jeffrey D. Lifson, Cavan Reilly, John V. Carlis, Ashley T. Haase Jan 2006

Premature Induction Of An Immunosuppressive Regulatory T Cell Response During Acute Simian Immunodeficiency Virus Infection, Jacob D. Estes, Qingsheng Li, Matthew R. Reynolds, Stephen W. Wietgrefe, Lijie Duan, Timothy Schacker, Louis J. Picker, David I. Watkins, Jeffrey D. Lifson, Cavan Reilly, John V. Carlis, Ashley T. Haase

Qingsheng Li Publications

Here we report the results of an investigation into the possibility that one mechanism responsible for the establishment of persistent human immunodeficiency virus infection is an early regulatory T (Treg) cell response that blunts virus- specific responses. Using the simian immunodeficiency virus (SIV)–infected rhesus macaque model, we show that, indeed, viral replication and immune activation in lymphatic tissue drive a premature immunosuppressive response, with dramatic increases in the frequencies of CD4+CD25+FOXP3+ Treg cells, transforming growth factor–β1+ cells, interleukin–10+ cells, and indoleamine 2,3-dioxygenase+CD3+ cells.When we compared SIV infection with rhesus cytomegalovirus (RhCMV) …

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