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Pathogenic Microbiology Commons

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Articles 1 - 6 of 6

Full-Text Articles in Pathogenic Microbiology

Utilizing Cmp-Sialic Acid Analogs To Unravel Neisseria Gonorrhoeae Lipooligosaccharide-Mediated Complement Resistance And Design Novel Therapeutics, Sunita Gulati, Ian C. Schoenhofen, Dennis M. Whitfield, Andrew D. Cox, Jianjun Li, Frank St Michael, Evgeny V. Vinogradov, Jacek Stupak, Bo Zheng, Makoto Ohnishi, Magnus Unemo, Lisa A. Lewis, Rachel E. Taylor, Corinna S. Landig, Sandra Diaz, George W. Reed, Ajit Varki, Peter A. Rice, Sanjay Ram Dec 2015

Utilizing Cmp-Sialic Acid Analogs To Unravel Neisseria Gonorrhoeae Lipooligosaccharide-Mediated Complement Resistance And Design Novel Therapeutics, Sunita Gulati, Ian C. Schoenhofen, Dennis M. Whitfield, Andrew D. Cox, Jianjun Li, Frank St Michael, Evgeny V. Vinogradov, Jacek Stupak, Bo Zheng, Makoto Ohnishi, Magnus Unemo, Lisa A. Lewis, Rachel E. Taylor, Corinna S. Landig, Sandra Diaz, George W. Reed, Ajit Varki, Peter A. Rice, Sanjay Ram

Open Access Articles

Neisseria gonorrhoeae deploys a novel immune evasion strategy wherein the lacto-N-neotetraose (LNnT) structure of lipooligosaccharide (LOS) is capped by the bacterial sialyltransferase, using host cytidine-5'-monophosphate (CMP)-activated forms of the nine-carbon nonulosonate (NulO) sugar N-acetyl-neuraminic acid (Neu5Ac), a sialic acid (Sia) abundant in humans. This allows evasion of complement-mediated killing by recruiting factor H (FH), an inhibitor of the alternative complement pathway, and by limiting classical pathway activation ("serum-resistance"). We utilized CMP salts of six additional natural or synthetic NulOs, Neu5Gc, Neu5Gc8Me, Neu5Ac9Ac, Neu5Ac9Az, legionaminic acid (Leg5Ac7Ac) and pseudaminic acid (Pse5Ac7Ac), to define structural requirements of Sia-mediated serum-resistance. While ...


Dna-Containing Immunocomplexes Promote Inflammasome Assembly And Release Of Pyrogenic Cytokines By Cd14+ Cd16+ Cd64high Cd32low Inflammatory Monocytes From Malaria Patients, Isabella C. Hirako, Carolina Gallego-Marin, Marco A. Ataide Oswalso Cruz Founda, Warrison A. Andrade, Humberto Gravina, Bruno C. Rocha, Rosane B. De Oliveira, Dhelio B. Pereira, Joseph Vinetz, Betty Diamond, Sanjay Ram, Douglas T. Golenbock, Ricardo T. Gazzinelli Nov 2015

Dna-Containing Immunocomplexes Promote Inflammasome Assembly And Release Of Pyrogenic Cytokines By Cd14+ Cd16+ Cd64high Cd32low Inflammatory Monocytes From Malaria Patients, Isabella C. Hirako, Carolina Gallego-Marin, Marco A. Ataide Oswalso Cruz Founda, Warrison A. Andrade, Humberto Gravina, Bruno C. Rocha, Rosane B. De Oliveira, Dhelio B. Pereira, Joseph Vinetz, Betty Diamond, Sanjay Ram, Douglas T. Golenbock, Ricardo T. Gazzinelli

Open Access Articles

High levels of circulating immunocomplexes (ICs) are found in patients with either infectious or sterile inflammation. We report that patients with either Plasmodium falciparum or Plasmodium vivax malaria have increased levels of circulating anti-DNA antibodies and ICs containing parasite DNA. Upon stimulation with malaria-induced ICs, monocytes express an NF-kappaB transcriptional signature. The main source of IC-induced proinflammatory cytokines (i.e., tumor necrosis factor alpha [TNF-alpha] and interleukin-1beta [IL-1beta])in peripheral blood mononuclear cells from acute malaria patients was found to be a CD14(+) CD16 (FcgammaRIIIA)(+) CD64 (FcgammaRI)(high) CD32 (FcgammaRIIB)(low) monocyte subset. Monocytes from convalescent patients were predominantly of ...


Rnasek Is A V-Atpase-Associated Factor Required For Endocytosis And The Replication Of Rhinovirus, Influenza A Virus, And Dengue Virus, Jill Perreira, Aaron Aker, George Savidis, Christopher R. Chin, William M. Mcdougall, Jocelyn M. Portmann, Paul Meraner, Miles Smith, Motiur Rahman, Richard E. Baker, Annick Gauthier, Michael Franti, Abraham L. Brass Aug 2015

Rnasek Is A V-Atpase-Associated Factor Required For Endocytosis And The Replication Of Rhinovirus, Influenza A Virus, And Dengue Virus, Jill Perreira, Aaron Aker, George Savidis, Christopher R. Chin, William M. Mcdougall, Jocelyn M. Portmann, Paul Meraner, Miles Smith, Motiur Rahman, Richard E. Baker, Annick Gauthier, Michael Franti, Abraham L. Brass

Open Access Articles

Human rhinovirus (HRV) causes upper respiratory infections and asthma exacerbations. We screened multiple orthologous RNAi reagents and identified host proteins that modulate HRV replication. Here, we show that RNASEK, a transmembrane protein, was needed for the replication of HRV, influenza A virus, and dengue virus. RNASEK localizes to the cell surface and endosomal pathway and closely associates with the vacuolar ATPase (V-ATPase) proton pump. RNASEK is required for endocytosis, and its depletion produces enlarged clathrin-coated pits (CCPs) at the cell surface. These enlarged CCPs contain endocytic cargo and are bound by the scissioning GTPase, DNM2. Loss of RNASEK alters the ...


Eif2alpha Confers Cellular Tolerance To S. Aureus Alpha-Toxin, Gisela Von Hoven, Claudia Neukirch, Martina Meyenburg, Sabine Fuser, Maria Bidna Petrivna, Amable J. Rivas, Alexey Ryazanov, Randal J. Kaufman, Raffi V. Aroian, Matthias Husmann Jul 2015

Eif2alpha Confers Cellular Tolerance To S. Aureus Alpha-Toxin, Gisela Von Hoven, Claudia Neukirch, Martina Meyenburg, Sabine Fuser, Maria Bidna Petrivna, Amable J. Rivas, Alexey Ryazanov, Randal J. Kaufman, Raffi V. Aroian, Matthias Husmann

Open Access Articles

We report on the role of conserved stress-response pathways for cellular tolerance to a pore forming toxin. First, we observed that small molecular weight inhibitors including of eIF2alpha-phosphatase, jun-N-terminal kinase (JNK), and PI3-kinase sensitized normal mouse embryonal fibroblasts (MEFs) to the small pore forming S. aureus alpha-toxin. Sensitization depended on expression of mADAM10, the murine ortholog of a proposed high-affinity receptor for alpha-toxin in human cells. Similarly, eIF2alpha (S51A/S51A) MEFs, which harbor an Ala knock-in mutation at the regulated Ser51 phosphorylation site of eukaryotic translation initiation factor 2alpha, were hyper-sensitive to alpha-toxin. Inhibition of translation with cycloheximide did not ...


Virulence Of Group A Streptococci Is Enhanced By Human Complement Inhibitors, David Ermert, Jutamas Shaughnessy, Thorsten Joeris, Jakub Kaplan, Catherine J. Pang, Evelyn A. Kurt-Jones, Peter A. Rice, Sanjay Ram, Anna M. Blom Jul 2015

Virulence Of Group A Streptococci Is Enhanced By Human Complement Inhibitors, David Ermert, Jutamas Shaughnessy, Thorsten Joeris, Jakub Kaplan, Catherine J. Pang, Evelyn A. Kurt-Jones, Peter A. Rice, Sanjay Ram, Anna M. Blom

Open Access Articles

Streptococcus pyogenes, also known as Group A Streptococcus (GAS), is an important human bacterial pathogen that can cause invasive infections. Once it colonizes its exclusively human host, GAS needs to surmount numerous innate immune defense mechanisms, including opsonization by complement and consequent phagocytosis. Several strains of GAS bind to human-specific complement inhibitors, C4b-binding protein (C4BP) and/or Factor H (FH), to curtail complement C3 (a critical opsonin) deposition. This results in diminished activation of phagocytes and clearance of GAS that may lead to the host being unable to limit the infection. Herein we describe the course of GAS infection in ...


Chitin Recognition Via Chitotriosidase Promotes Pathologic Type-2 Helper T Cell Responses To Cryptococcal Infection, Darin L. Wiesner, Charles A. Specht, Chrono K. Lee, Kyle D. Smith, Liliane Mukaremera, S. Thera Lee, Chun G. Lee, Jack A. Elias, Judith N. Nielsen, David R. Boulware, Paul R. Bohjanen, Marc K. Jenkins, Stuart M. Levitz, Kirsten Nielsen Mar 2015

Chitin Recognition Via Chitotriosidase Promotes Pathologic Type-2 Helper T Cell Responses To Cryptococcal Infection, Darin L. Wiesner, Charles A. Specht, Chrono K. Lee, Kyle D. Smith, Liliane Mukaremera, S. Thera Lee, Chun G. Lee, Jack A. Elias, Judith N. Nielsen, David R. Boulware, Paul R. Bohjanen, Marc K. Jenkins, Stuart M. Levitz, Kirsten Nielsen

Open Access Articles

Pulmonary mycoses are often associated with type-2 helper T (Th2) cell responses. However, mechanisms of Th2 cell accumulation are multifactorial and incompletely known. To investigate Th2 cell responses to pulmonary fungal infection, we developed a peptide-MHCII tetramer to track antigen-specific CD4+ T cells produced in response to infection with the fungal pathogen Cryptococcus neoformans. We noted massive accruement of pathologic cryptococcal antigen-specific Th2 cells in the lungs following infection that was coordinated by lung-resident CD11b+ IRF4-dependent conventional dendritic cells. Other researchers have demonstrated that this dendritic cell subset is also capable of priming protective Th17 cell responses to another pulmonary ...