Georgios Hajishengallis
University Of Pennsylvania
Project start date: 2012-02-01
Project end date: 2016-12-31
Sponsored Links Excellgen http://Excellgen.com
Grants awarded to Georgios Hajishengallis
Pattern Recognition Of P. Gingivalis Virulence Factors
Georgios Hajishengallis, Associate Professor
Periodontics, Endodontics And Dental Hygieneuniversity Of Louisville
office Of Grants Management
louisville, Ky 40292
Grant 5R01DE015254-05 from National Institute Of Dental & Craniofacial Research IRG: ODCS
Abstract: Toll-like receptors (TLRs) and other pattern-recognition receptors (PRRs) form functional receptor complexes that recognize pathogen-associated molecular patterns (PAMPs). Activation of the TLR signaling pathway by PAMPs leads to induction of immune and inflammatory responses. Porphyromonas gingivalis is an important pathogen in human periodontitis. A major cell surface component of this oral pathogen is the fimbriae, which function as an adhesin. Strikingly, fimbriae activate transcription factor NF-KappaB and induce production of proinflammatory cytokines through interactions with several PRRs. Understanding the molecular basis of how the host recognizes and responds to P. gingivalis fimbriae is essential for developing molecular approaches to control periodontal inflammation. Therefore, the objective of this grant is to elucidate the proinflammatory interactions of fimbriae with PRRs. The application proposes that fimbriae function as a PAMP and interact in a regulated mode, and through discrete epitopes, with different binding PRRs resulting in the activation of proinflammatory TLR signaling. Fimbrial epitopes involved in cellular binding and/or activation will be identified using fimbrial peptides and mutant fimbriae. Importantly, epitopes involved in binding but not activation may find application as antagonists of fimbria-induced inflammation. Experiments in our laboratory have shown that TLR2 and TLR4 mediate fimbria-induced signaling, but initial recognition of fimbriae is mediated by a cooperation between CD14 and CD11 b/CD18, which thus appear to serve as TLR co-receptors. It is posited that fimbriae initially bind to CD14, and the fimbriae/CD14 complex induces TLR2-mediated "inside-out" signaling that leads to activation of the ligand-binding capacity of CD11b/CD18. PRR-fimbriae interactions will be examined in human monocytes and mouse macrophages derived from normal and PRR-deficient mice. Elucidation of the mechanisms whereby PRRs recognize and respond to fimbriae and identification of fimbrial antagonists may facilitate the design of novel approaches to therapeutic intervention in both periodontitis and atherosclerosis, where P. gingivalis has also been implicated
Keywords: Bacteroides gingivalis, bacterial protein, cell adhesion molecule, host organism interaction, molecular shape, pilus, virulence CD antigen, CD14 molecule, bacteria infection mechanism, biological signal transduction, periodontitis, receptor binding, toll like receptor SDS polyacrylamide gel electrophoresis, clinical research, flow cytometry, human subject, ion exchange chromatography, laboratory mouse, tissue /cell culture
Project start date: 2004-07-01
Project end date: 2008-07-31
5R01DE015254-05 (2007): $210496
5R01DE015254-04 (2006): $216783
1R01DE015254-01A2 (2004): $206490
LSU DENTAL COBRE: INTERACTIONS OF P. GINGIVALIS FIMBRAE WITH RECEPTORS
Georgios Hajishengallis, Associate Professor
Louisiana State Univ Hsc New Orleans 433 Bolivar St New Orleans, La 70112
Grant 1P20RR020160-010002 from National Center For Research Resources IRG: ZRR1
Abstract: Toll-like receptors (TLRs) and other pattern-recognition receptors (PRRs) form functional receptor complexes that recognize pathogen-associated molecular patterns (PAMPs). Activation of the TLR signaling pathway by PAMPs leads to induction of immune and inflammatory responses. Porphyromonas gingivalis is an important pathogen in human periodontitis, the pathogenesis of which derives mainly from untoward host inflammatory reactions to subgingival bacterial challenge. Periodontitis is a significant health problem in adults and may precipitate systemic complications such as atherosclerosis. A major cell surface component of P. gingivalis is the fimbriae, which function as an adhesin. Strikingly, fimbriae activate transcription factor NF-kappaB and induce production of proinflammatory cytokines through interactions with several PRRs. Understanding the molecular basis of how the host recognizes and responds to P. gingivalis fimbriae is essential for developing molecular approaches to control periodontal inflammation. Therefore, the objective of this proposal is to elucidate the proinflammatory interactions of fimbriae with PRRs. We hypothesize that fimbriae function as a PAMP and interact in a regulated mode, and through discrete epitopes, with different binding PRRs resulting in the activation of TLR signaling and induction of proinflammatory cytokines. Fimbrial epitopes involved in cellular binding and/or activation will be identified using fimbrial peptides and mutant fimbriae. Importantly, epitopes involved in binding but not activation may find application as antagonists of fimbria-induced inflammation. Our preliminary experiments have shown that TLR2 and TLR4 mediate fimbria-induced signaling, but initial recognition of fimbriae is mediated by cooperation between CD14 and CD11b/CD18, which thus appear to serve as TLR co-receptors. It is postulated that fimbriae initially bind to CD14, and the fimbriae/CD14 complex induces TLR2-mediated "inside-out" signaling that leads to activation of the ligand-binding capacity of CD11b/CD18. PRR-fimbriae interactions will be examined in human monocytes and mouse macrophages derived from normal and PRR-deficient mice. Elucidation of the mechanisms whereby PRRs recognize and respond to fimbriae and identification of flmbrial antagonists may facilitate the design of novel approaches to therapeutic intervention in both periodontitis and atherosclerosis, where P. gingivalis has also been implicated.
Keywords: Bacteroides gingivalis, host organism interaction, inflammation, microorganism interaction, oral health, pilus, toll like receptor, CD14 molecule, biological signal transduction, cytokine, dental research, macrophage, monocyte, oral bacteria, clinical research, flow cytometry, human subject, laboratory mouse
Project start date: 2004-09-03
Project end date: 2005-07-31
ORAL IMMUNITY AND ADJUVANT RECEPTORS
Georgios Hajishengallis
University Of Louisville, Office Of Grants Management, Louisville, Ky 40292
Grant 2R01DE017138-06 from National Institute Of Dental & Craniofacial Research
Abstract: This application addresses the compelling need to develop new and improved vaccine adjuvants for stimulating protective immunity at mucosal surfaces. The proposal involves a consortium arrangement between the University of Louisville, the University at Buffalo, and the Hauptman-Woodward Institute, and brings together complementary and integrated expertise in vaccine adjuvant research, structural and molecular biology, and induction of mucosal immunity. Studies by this group have succeeded to dissociate useful adjuvant properties from the toxicity of LT-IIb, an AB5-type heat-labile enterotoxin of Escherichia coli. Specifically, the recombinantly expressed B pentameric subunit of LT-IIb (LT-IIb-B5) not only lacks enterotoxicity but, strikingly, can activate the Toll-like receptor (TLR)-2/TLR1 signaling complex and stimulate antibody responses to co-administered vaccine proteins. Proof-of-concept preliminary studies have shown that certain engineered point-substitution mutations in the active region of LT-IIb-B5 enhance its ability to interact with TLR2 and TLR1. The overall objective of this application is to better characterize the physical and functional interaction of LT-IIb-B5 with the TLR2/TLR1 heterodimer, engineer improved versions of LT-IIb-B5 in terms of TLR2/TLR1-mediated adjuvanticity, and develop potential adjuvants through studies in preclinical models of vaccination against oral infection. This will be accomplished through appropriate and innovative molecular biological, structural, and immunological studies outlined in the following four specific aims 1) To rationally engineer enhanced TLR2-interactive versions of LT-IIb-B5. 2) To structurally characterize the LT-IIb- B5-TLR2/TLR1 interaction using small-angle X-ray scattering (SAXS). 3) To evaluate the engineered LT-IIb-B5 mutants for in vitro TLR2/TLR1-dependent immunostimulatory activities. 4) To determine the ability of LT-IIb-B5 and improved engineered versions thereof to induce protective immunity in vivo. The generated data will form the basis for the long-term goal which is to establish LT-IIb-B5 and improved engineered derivatives as effective adjuvants in vaccine formulations against pathogens which colonize or invade via oral, respiratory, or urogenital mucosal surfaces. The objective of this application is to rationally engineer novel Toll-like receptor-dependent mucosal adjuvants. These constructs will be evaluated for their capacity to stimulate protective immunity using appropriate preclinical mouse models. The focus of this proposal is on a novel vaccine against periodontitis, an oral inflammatory disease with an impact on systemic health, although the developed mucosal adjuvants can also be used in vaccine formulations against pathogens which colonize or invade via oral, respiratory, or urogenital mucosal surfaces. This work is timely and important given the paucity of safe and effective vaccine adjuvants and the tremendous health impact of infectious diseases
Keywords: Address; Adjuvant; Adjuvanticity; Antibody Formation; Antibody Production; Antibody Response; Area; Bacteroides gingivalis; Binding; Binding (Molecular Function); Biological; Blood Serum; Bone Marrow; Buffaloes; CD4 Positive T Lymphocytes; CD4 T cells; CD4 lymphocyte; CD4+ T cell; CD4+ T-Lymphocyte; CD4-Positive Lymphocytes; Cell Communication and Signaling; Cell Signaling; Cells, CD4; Chronic Periodontitis; Collaborations; Communicable Diseases; Complex; Crystallographies; Crystallography; DKFZp547I0610; DKFZp564I0682; DNA Molecular Biology; Data; Dendritic Cells; Dependence; Disease; Disorder; Drug Formulations; E coli; Engineering; Engineerings; Enterotoxins; Escherichia coli; Exhibits; Figs; Figs - dietary; Formulation; Formulations, Drug; Funding; Gangliosides; Genetic Alteration; Genetic Change; Genetic defect; Genitourinary; Genitourinary system; Goals; Health; Heating; Immunity; Immunization; Immunologic Stimulation; Immunological Stimulation; Immunostimulation; In Vitro; Infection; Infectious Disease Pathway; Infectious Diseases; Infectious Diseases and Manifestations; Infectious Disorder; Inflammatory; Institutes; Intracellular Communication and Signaling; Invaded; Investigators; KIAA0012; Ligands; Lipid Binding; Lipid Rafts, Cell Membrane; Mammals, Mice; Masks; Mediating; Membrane Microdomains; Mice; Modeling; Molecular; Molecular Biology; Molecular Interaction; Mucosal Immunity; Murine; Mus; Mutation; Oral; P. gingivalis; P.gingivalis; Paper; Parents; Periodontitis; Porphyromonas gingivalis; Pre-Clinical Model; Preclinical Models; Property; Property, LOINC Axis 2; Proteins; Qualifying; Radiation, X-Rays; Radiation, X-Rays, Gamma-Rays; Receptor Protein; Relative; Relative (related person); Research; Research Personnel; Researchers; Reticuloendothelial System, Bone Marrow; Roentgen Rays; Sensitization, Immunologic; Sensitization, Immunological; Serum; Sialoglycosphingolipids; Signal Transduction; Signal Transduction Systems; Signaling; Site; Solutions; Solvents; Sphingolipid Microdomains; Sphingolipid-Cholesterol Rafts; Structure; Surface; T4 Cells; T4 Lymphocytes; TIL4; TLR protein; TLR1; TLR1 gene; TLR2; TLR2 receptor; Technology; Testing; Time; Toll-Like Receptor 2; Toll-like receptors; Toll/Interleukin 1 Receptor-Like 4; Toll/Interleukin 1 Receptor-Like Protein 4; Toxic effect; Toxicities; Universities; Urogenital; Urogenital System; Vaccination; Vaccine Adjuvant; Vaccines; Veiled Cells; Work; X-Radiation; X-Rays; Xrays; antibody biosynthesis; base; biological signal transduction; disease/disorder; gene product; genome mutation; helper T cell; immunoglobulin biosynthesis; improved; in vivo; infection mouth; innovate; innovation; innovative; interdisciplinary collaboration; lipid raft; mouse model; mutant; new vaccines; next generation vaccines; novel; novel vaccines; oral immunity; oral infection; oral infectious; pathogen; pre-clinical; preclinical; receptor; respiratory; rsc786; structural biology; urogenital system (urinary part)
Relevance: The objective of this application is to rationally engineer novel Toll-like receptor-dependent mucosal adjuvants. These constructs will be evaluated for their capacity to stimulate protective immunity using appropriate preclinical mouse models. The focus of this proposal is on a novel vaccine against periodontitis, an oral inflammatory disease with an impact on systemic health, although the developed mucosal adjuvants can also be used in vaccine formulations against pathogens which colonize or invade via oral, respiratory, or urogenital mucosal surfaces. This work is timely and important given the paucity of safe and effective vaccine adjuvants and the tremendous health impact of infectious diseases
Project start date: 2006-02-01
Project end date: 2015-08-31
Budget start date: 15-SEP-2010
Budget end date: 31-AUG-2011
PFA/PA: PA-10-067
2R01DE017138-06 (2010): $424189
5R01DE017138-02 (2007): $352575
1R01DE017138-01 (2006): $373659
PATTERN RECOGNITION OF P. GINGIVALIS VIRULENCE FACTORS
Georgios Hajishengallis, Associate Professor
University Of Louisville, Office Of Grants Management, Louisville, Ky 40292
Grant 5R01DE015254-08 from National Institute Of Dental & Craniofacial Research
Abstract: Innate immunity plays a central role in infection-driven inflammatory conditions, including periodontitis which is one of the most common chronic disorders of infectious origin in humans. However, successful microbial pathogens, such as the periodontopathogen Porphyromonas gingivalis, have evolved mechanisms which proactively manipulate the innate immune response. Subversion of innate immunity may additionally undermine the overall host defense, since the innate immune response plays an instructive role in adaptive immunity. This research proposal has been designed to investigate and elucidate molecular mechanisms whereby P. gingivalis modifies innate immune signaling pathways leading to increased virulence and persistence within the host. Although innate recognition and signaling in response to P. gingivalis is primarily mediated by the Toll-like receptor 2 (TLR2)-centered pattern recognition apparatus, preliminary studies indicate that this periodontal pathogen instigates the association of the chemokine receptor CXCR4 with TLR2 resulting in cross-talk and altered signaling downstream of TLR2. On the basis of additional preliminary evidence, the overall hypothesis is that P. gingivalis, through its cell surface fimbriae, exploits CXCR4 and manipulates TLR2 intracellular signaling in ways that suppress the proinflammatory/antimicrobial pathway but enhance a distinct proadhesive pathway; both of these activities have the potential to increase the survival capacity of the pathogen, thereby prolonging P. gingivalis infection and potentiating its impact on periodontal disease. In vitro immunological approaches using transfected cell lines or primary macrophages will elucidate the mechanistic basis of TLR2/CXCR4 cross-talk, which is hypothesized to involve the cAMP-dependent protein kinase A. Moreover, the biological significance of the putative exploitation of CXCR4 by P. gingivalis will be investigated using a mouse periodontitis model, in which a CXCR4 antagonist (AMD3100) is expected to suppress P. gingivalis virulence. The long-term objective of investigating CXCR4-dependent mechanisms whereby P. gingivalis manipulates TLR2 signaling is to identify effective antagonists for redirecting the innate response to benefit the host. The fight against HIV and AIDS has produced a number of drugs including CXCR4 antagonists, which are available for investigation in other formidable diseases where CXCR4 may play a pathophysiological role. Such CXCR4 antagonists may find therapeutic application in human periodontitis. Periodontitis is one of the most common chronic disorders of infectious origin in humans, and is also associated with systemic diseases such as atherosclerosis. This research proposal presents evidence that the periodontal pathogen P. gingivalis exploits a host receptor, namely CXCR4, for undermining host defense and promoting its virulence. We believe that CXCR4 antagonists may find therapeutic application in human periodontitis and, in this context; we will test a CXCR4 antagonist (AMD3100) for its ability to inhibit P. gingivalis-induced periodontitis in a mouse model
Keywords: 1-Phosphatidylinositol 3-Kinase; AIDS; AIDS Virus; AMD-3100; AMD3100; ATP[{..}]1-phosphatidyl-1D-myo-inositol 3-phosphotransferase; Acquired Immune Deficiency; Acquired Immune Deficiency Syndrome; Acquired Immune Deficiency Syndrome Virus; Acquired Immuno-Deficiency Syndrome; Acquired Immunodeficiency Syndrome; Acquired Immunodeficiency Syndrome Virus; Adenosine Cyclic Monophosphate-Dependent Protein Kinases; Adhesives; Alveolar Bone Loss; Alveolar Resorption; Atheroscleroses; Atherosclerosis; Atherosclerotic Cardiovascular Disease; B2-1 protein; BRM; Bacteroides gingivalis; Biological; Biological Response Modifiers; Biomodulators; Buccal Cavity; CD14; CD14 gene; CXC-R4; CXCR-4; CXCR4; CXCR4 Signaling Pathway; CXCR4 gene; Cavitas Oris; Cell Communication and Signaling; Cell Line; Cell Lines, Strains; Cell Signaling; Cell surface; CellLine; Chronic Disease; Chronic Illness; Chronic Periodontitis; Complex; Cyclic AMP-Dependent Protein Kinases; D2S201E; Data; Development; Disease; Disorder; Drugs; Exhibits; Extracellular Matrix, Integrins; FB22; FRET; Fluorescence Resonance Energy Transfer; Funding; HIV; HM89; HSY3RR; HTLV-III; Head and Neck, Buccal Cavity; Host Defense; Human; Human Immunodeficiency Viruses; Human T-Cell Leukemia Virus Type III; Human T-Cell Lymphotropic Virus Type III; Human T-Lymphotropic Virus Type III; Human, General; INFLM; Immune; Immune Mediators; Immune Mediators/Modulators; Immune Regulators; Immune response; Immunity, Innate; Immunity, Native; Immunity, Natural; Immunity, Non-Specific; Immunologic Deficiency Syndrome, Acquired; In Vitro; Infection; Inflammation; Inflammatory; Integrins; Intracellular Communication and Signaling; Investigation; LAP3; LAV-HTLV-III; LCR1; LESTR; Lymphadenopathy-Associated Virus; Mammals, Mice; Man (Taxonomy); Man, Modern; Mediating; Medication; Mice; Microbe; Modeling; Molecular; Mouth; Murine; Mus; NPY3R; NPYR; NPYRL; NPYY3R; Natural Immunity; Oral cavity; P. gingivalis; P.gingivalis; PI-3 Kinase; PI-3K; PI3-Kinase; PKA; Parodontosis; Pathogenicity Factors; Pathway interactions; Pattern Recognition; Pattern Recognition/Display/Analysis; Pattern recognition receptor; Periodontal Bone Loss; Periodontal Diseases; Periodontal Resorption; Periodontitis; Peritonitis; Pharmaceutic Preparations; Pharmaceutical Preparations; Phosphatidylinositol 3-Kinase; Phosphatidylinositol-3-OH Kinase; Phosphoinositide 3-Hydroxykinase; Play; Porphyromonas gingivalis; Protein Kinase A; Proteins; PtdIns 3-Kinase; Publishing; Receptor Protein; Research; Research Proposals; Role; Signal Pathway; Signal Transduction; Signal Transduction Systems; Signaling; Structure; Systemic disease; TIL4; TLR protein; TLR2; TLR2 receptor; Testing; Therapeutic; Toll-Like Receptor 2; Toll-like receptors; Toll/Interleukin 1 Receptor-Like 4; Toll/Interleukin 1 Receptor-Like Protein 4; Type I Phosphatidylinositol Kinase; Type III Phosphoinositide 3-Kinase; Virulence; Virulence Factors; Virulent; Virus-HIV; Work; adaptive immunity; anti-microbial; antimicrobial; atheromatosis; atherosclerotic vascular disease; base; biological signal transduction; bone loss; cAMP-Dependent Protein Kinases; chemokine receptor; chronic disease/disorder; chronic disorder; cultured cell line; cytohesin-1; design; designing; disease/disorder; drug/agent; fight against; fimbria; fimbrillin; gene product; host response; immunoresponse; in vivo; macrophage; microbial; microbicidal; microbicide; mouse model; mutant; novel; pathogen; pathway; periodontal disorder; periodontium disease; periodontium disorder; periodontopathogen; prevent; preventing; public health relevance; receptor; response; social role
Project start date: 2003-04-01
Project end date: 2013-07-31
Budget start date: 1-AUG-2010
Budget end date: 31-JUL-2011
PFA/PA: PA-07-070
5R01DE015254-08 (2010): $340659
5R01DE015254-07 (2009): $344100
Sponsored Links Excellgen http://Excellgen.com
2R01DE015254-06A1 (2008): $344100
Oral Pathogen Exploitation Of Innate Recognition As A Function Of Age
Georgios Hajishengallis, Associate Professor
Periodontics, Endodontics And Dental Hygieneuniversity Of Louisville
Grant 5R01DE018292-03 from National Institute Of Dental & Craniofacial Research IRG: ZDE1
Abstract: Innate immunity is present from birth and represents the inherited resistance to infection. Microbial infection is detected by pattern-recognition receptors (PRRs) through recognition of microbe-associated molecular patterns (MAMPs). Since MAMPs are conserved in a wide range of pathogenic or commensal organisms, it is not clear how PRR-MAMP interactions per se lead to differential host responses to pathogens and commensals. This application proposes that pathogens exploit selective pattern recognition pathways in ways that perturb the otherwise homeostatic PRR-MAMP interactions, leading to chronic persistence of the pathogen and nonproductive inflammation. This outcome is detrimental especially to the elderly host due to age-related alterations in pattern-recognition mechanisms. In this regard, it is proposed that pathway-specific alterations in innate recognition render the aging innate immune system more amenable to exploitation by pathogens than its younger counterpart. Taking advantage of the accessibility and relevance of the oral cavity in host-microbial interactions, these concepts will be investigated in the context of periodontitis and the model pathogen Porphyromonas gingivalis. P. gingivalis interacts via its surface fimbriae with the CD14/Toll-like receptor 2 recognition complex and induces phosphatidylinositol-3-kinase signaling for activating the adhesive capacity of CR3, a monocytic beta2 integrin with PRR capabilities. Although this proadhesive pathway promotes the migratory activity of monocytes, it has surprisingly been co-opted by P. gingivalis for exploiting CR3. By means of immunological, genetic, and biophysical techniques, as well as a mouse periodontitis model, these studies will test the hypothesis that the interaction of P. gingivalis with activated CR3 leads to pathogen internalization, suppression of normal defense clearing mechanisms, inhibition of apoptosis, and promotion of intracellular persistence. Moreover, it is hypothesized that the inducibility of this co-opted pathway becomes higher with age leading to enhanced immune evasion by P. gingivalis and potentially increased periodontal disease activity. This study has been designed not only for answering fundamental questions in innate immunity, but also for facilitating the development of novel immunomodulatory concepts at a translational level. Indeed, only by knowing how the innate response is deregulated by pathogens, could effective immunomodulatory strategies be implemented for redirecting the oral mucosal immune defense to the benefit of the elderly host. While the proposed experimental model focuses on a periodontal pathogen, the fundamental concept of immune evasion by corruption of PRR function and how this process changes with advancing age may be applicable to infections of less accessible mucosal tracts such as the respiratory, gastrointestinal, and genitourinary tracts
Keywords: aging Bacteroides gingivalis, apoptosis, base, birth, bone, concept, gastrointestinal system, genetics, human, immune response, immune system, immunity, infection, inflammation, integrin, intracellular, lead, ligand, macrophage, model, monocyte, mutant, organism, periodontitis, peritonitis, phosphatidylinositol, phosphatidylinositol 3 kinase, pilus, receptor, role, suppression, toll like receptor, virulence clinical research
Project start date: 2007-03-06
Project end date: 2012-02-28
1R01DE018292-01 (2007): $325600
Georgios Hajishengallis
University Of Pennsylvania
Project start date: 2003-04-01
Project end date: 2013-07-31
ORAL IMMUNITY AND ADJUVANT RECEPTORS
Georgios Hajishengallis, Associate Professor
University Of Louisville, Office Of Grants Management, Louisville, Ky 40292
Grant 5R01DE017138-05 from National Institute Of Dental & Craniofacial Research
Keywords: No Project Terms available
Project start date: 2006-02-01
Project end date: 2011-01-31
Budget start date: 1-FEB-2010
Budget end date: 31-JAN-2011
5R01DE017138-05 (2010): $346100
Georgios Hajishengallis
University Of Pennsylvania
Project start date: 2010-09-27
Project end date: 2013-08-31
Oral Immunity And Adjuvant Receptors
Georgios Hajishengallis, Associate Professor
Periodontics, Endodontics And Dental Hygieneuniversity Of Louisville
Grant 5R01DE017138-04 from National Institute Of Dental & Craniofacial Research IRG: ODCS
Keywords: ganglioside, immunity, receptor Streptococcus mutans, adhesin, antibody, antigen, antigen presenting cell, art, base, cell, cell line, cell proliferation, cholera toxin, cytokine, dendritic cell, enterotoxin, fluorescence microscopy, fluorescence resonance energy transfer, health /scientific organization, human, immune response, immunization, immunoprecipitation, infection, interdisciplinary collaboration, intracellular, ligand, lipid raft, model, molecular /cellular imaging, monocyte, motivation, mucosal immunity, mutant, play, point mutation, protein, receptor expression, role, tissue, toll like receptor, toxin, transcription factor, vaccine clinical research
Project start date: 2006-02-01
Project end date: 2011-01-31
Pattern Recognition Of P. Gingivalis Virulence Factors
Georgios Hajishengallis
Microbiology, Immunology And Parasitologylouisiana State Univ Hsc New Orleans
5R01DE015254-02 (2005): $207330
Sponsored Links Excellgen http://Excellgen.com