david schneider stanford

David is related to Sylvia E Laporta and Ronald A Schneider as well as 3 additional people. He is also Chief of Infectious Diseases at the Veterans Affairs Palo Alto Health Care System in Palo Alto, California. The functions of five Anopheles gambiae homologs were tested by using RNAi to knock down gene function followed by measuring the growth of the rodent parasite, Plasmodium berghei. Here we identify genes in both the host and microbe that are involved in the pathogenesis of infection and disease in Drosophila melanogaster challenged with Salmonella enterica serovartyphimurium (S. typhimurium). These genes include the TNF family member eiger and the novel immunity gene edin (elevated during infection; synonym CG32185), both of which are more strongly induced by infection of wntD mutants compared to controls. View details for DOI 10.1371/journal.pbio.1000150, View details for Web of Science ID 000268405700004, View details for PubMedCentralID PMC2701602. Our current focus is to determine how we recover from infections. This detailed analysis of signaling and pathogenesis has the potential to allow the fly to be used as a model patient instead of as simply an innate immune system model. We conclude that dUsp36 plays a major role in hemocytes for tolerance to L. monocytogenes. Here we show that infected fruit flies become anorexic and that diet restriction alters defenses, increasing the fly's tolerance to Salmonella typhimurium infections while decreasing resistance to Listeria monocytogenes. Here they take advantage of the spectacularly deep genetic tools available to Drosophila geneticists to discover mechanisms involved in pathogenesis and the recovery from infections. In the fly, a component of the insect's innate immune system, the macrophage, can destroy Plasmodia. Schneider, D. S., Ayres, J. S., Brandt, S. M., Costa, A., Dionne, M. S., Gordon, M. D., Mabery, E. M., Moule, M. G., Pham, L. N., Shirasu-Hiza, M. M. Psidin is required in Drosophila blood cells for both phagocytic degradation and immune activation of the fat body. David Schneider Disease maps of an outbred population. Speculative fiction examines the leading edge of science and can be used to introduce ideas into the classroom. Listeria monocytogenes was capable of establishing lethal infections in adult fruit flies and larvae with extensive bacterial replication occurring before host death. David Schneider is part of Stanford Profiles, official site for faculty, postdocs, students and staff information (Expertise, Bio, Research, Publications, and more). View details for Web of Science ID 000175957900001. There are two ways to maintain fitness in the face of infection: resistance is a host's ability to reduce microbe load and disease tolerance is the ability of the host to endure the negative health effects of infection. We demonstrate that the rhythms of rodent malaria parasites in day-fed hosts become inverted relative to the rhythms of parasites in night-fed hosts. Drosophila melanogaster mount an effective innate immune response against invading microorganisms, but can eventually succumb to persistent pathogenic infections. We have been studying models for a variety of bacterial infections including: Listeria, Mycobacteria, Salmonella and Streptococcus as well as some fungi, malaria and viruses. Taillebourgar, E., Schneider, D. S., Fauvarque, M. The ubiquitin ligase parkin mediates resistance to intracellular pathogens. Intracellular pathogens, which can already defeat professional phagocytes, are unaffected by eiger. Hundreds of high schools and colleges across the United States are currently using PERTS’s free, evidence-based programs to raise achievement, retention, and, studen… Nine dominant gain-of-function alleles that cause Toll to be active in dorsal, as well as ventral, regions of the embryo are caused by mutations in the extracellular domain. As in humans, some of the damage that occurred during the fly immune response was caused by an over-aggressive response rather than by the microbes themselves. A., Oliveira, J. H., Trujillo, D. L., Saligrama, N., Zhang, Y., Rubelt, F., Schneider, D. S., Chien, Y. H., Sauerwein, R. W., Davis, M. M. What Can Vampires Teach Us about Immunology? The second best result is David O Schneider age 60s in Bel Air, MD. Both parkin-deficient mice and flies are sensitive to various intracellular bacterial infections, indicating parkin has a conserved role in metazoan innate defence. View details for DOI 10.1016/j.dci.2007.02.003, View details for Web of Science ID 000251077200005, View details for PubMedCentralID PMC3109252. To measure resilience, we need to quantify a host's position along its disease trajectory. We found 6 records in 8 states for Stanford Schneider in the US. Recent RNA interference screens that were performed at a genome-wide level have identified host factors that are important for the growth of Listeria monocytogenes in cultured cells from the fruit fly Drosophila melanogaster. These include changes in body temperature, reduced eating and drinking, and lethargy and mimic behaviors of animals in torpor and hibernation [1, 3-6]. Insects are a powerful tool for discovering and then dissecting interesting new immunology. Here, we give an overview of the presented work and we explain how these findings will open new avenues in Drosophila immunity research. There is no overlap between our genes and the hundreds of genes identified in Drosophila S2 cells fighting L. monocytogenes infection, using genomewide RNAi screens in vitro. We find that growth rates and ceilings are sensitive to the initial infectious dose in a host-genotype-dependent manner, implying that experimental results differ as we change the original challenge dose within a single strain of host. Here we present Looper, a computational method to analyze longitudinally gathered datasets and identify gene pairs that form looping trajectories when plotted in the space described by these phases. Understanding of this pathogenesis is limited, but it appears that host factors, induced by microbes, can have a direct cost to the host organism. Immunology textbooks teach us about the ways hosts can recognize and kill microbes but leave out something important: the mechanisms used to survive infections. Chambers, M. C., Song, K. H., Schneider, D. S. How the Fly Balances Its Ability to Combat Different Pathogens. diurnal feeding in nocturnal mice) to desynchronise the host's peripheral oscillators from the central, light-entrained oscillator in the brain and their rhythmic outputs. As we altered the system by varying host or pathogen genetics, disease tolerance varied, as we would expect if it was indeed governed by parameters controlling the sensitivity of the system (the number of bacteria required to trigger a response) and maximal effect size according to a logistic equation. Professor of Medicine (Blood and Marrow Transplantation) and of Pediatrics (Stem Cell Transplantation) (650) 723-0822. Dr. Schneider's Lab Homepage. In this issue of PLoS Biology, Konrad et al. We can borrow this method of plotting health versus microbe load in a population and make it apply to individuals; instead of plotting just one point that summarizes an infection in an individual, we can plot the values at many time points over the course of an infection for one individual. To characterize this primed response, we focused on S. pneumoniae-induced protection. We recently started working on a mouse model for malaria in which we follow the progress of a Plasmodium chabaudi infection. Stanford Schneider in the US . View details for DOI 10.1371/journal.ppat.1001065, View details for Web of Science ID 000281399900037, View details for PubMedCentralID PMC2928790, View details for DOI 10.1016/j.bbi.2009.10.012, View details for Web of Science ID 000273507000005. These defense systems are thought to interact, but the nature and extent of these interactions is not known. They focus on two models. It is difficult to describe host-microbe interactions in a manner that deals well with both pathogens and mutualists. Shaw, D. K., Tate, A. T., Schneider, D. S., Levashina, E. A., Kagan, J. C., Pal, U., Fikrig, E., Pedra, J. H. The physiological basis of disease tolerance in insects. This local infection in the ovary resulted in melanization and activation of the cellular immune response at the site of infection. wntD expression is under the control of Toll/Dorsal signalling, and increased levels of WntD block Dorsal nuclear accumulation, even in the absence of the IkappaB homologue Cactus. We then performed a second in vivo screen to identify an additional subset of bacterial genes that interact specifically with the imd signaling pathway. Therefore, mutations affecting immunity can have complex phenotypes and distinct effects on each pathogen. This produces characteristic phase plots that they think can be used to predict the outcome of infections and to define appropriate treatments. M. marinum is closely related to M. tuberculosis, which causes tuberculosis in people.A microarray analysis showed that metabolism is profoundly affected in M. marinum-infected flies. When flies are infected with a pathogen, they get sick. We perturbed feeding rhythms of hosts by 12 hours (i.e. Manzanillo, P. S., Ayres, J. S., Watson, R. O., Collins, A. C., Souza, G., Rae, C. S., Schneider, D. S., Nakamura, K., Shiloh, M. U., Cox, J. S. Listeria monocytogenes Infection Causes Metabolic Shifts in Drosophila melanogaster. Stanford Libraries' official online search tool for books, media, journals, databases, government documents and more. (2012) in this issue of Cell Host & Microbe raises important questions about the nature of immune responses. Known as a breakaway jazz orchestra leader and composer, Minnesota-born Maria Schneider formed her first band in 1988. View details for PubMedCentralID PMC5843352. M. marinum initially proliferated inside the phagocytes of the fly; later in infection, bacteria were found both inside and outside host cells. We focus on resistance, pathogenicity and tolerance to infection. Because this response is common among animals, we hypothesized that infection-induced diet restriction might be an adaptive trait that modulates the host's ability to fight infection. Treating infected mice when anorexic with the glycolytic inhibitor 2-deoxyglucose (2DG) reduced survival; treating animals with glucose improved survival. View David Schneider’s profile on LinkedIn, the world's largest professional community. View details for DOI 10.1016/j.tim.2006.01.008, View details for Web of Science ID 000236650400002. View details for Web of Science ID 000340345900008. Stanford GSB faculty pursue research and teaching within seven academic areas. Characterization of a mutation in the putative transglutaminase FTN_0869 produced a curious result that could not easily be explained using known Drosophila immune responses. This result implicates melanization in fighting microbial infections and shows that an immune response can affect both resistance and tolerance to infections in microbe-dependent ways. david.schneider@stanford.edu. Less understood, however, is the effect of biotic and abiotic factors on microbial-vector interactions and the impact of the immune system on arthropod populations in nature. View details for Web of Science ID A1991FK81300009, Larry Sandler Award Memorial Award for best Drosophila thesis, Genetics Society of America (1993), New Scholar in Global Infectious Disease, Ellison Medical Foundation (2002-6), Senior Scholar Award in Aging, Ellison Medical Foundation (2008-12), Ph.D., University of California, Berkeley, Molecular Biology (1992), B.Sc., University of Toronto, Biochemistry (1986), Department: Microbiology and Immunology. Interestingly, flies with dUsp36-depleted hemocytes are not sensitized to infection by other pathogens. Michael Snyder. Although not all microbial challenges induced this specific primed response, we find that a similar specific protection can be elicited by Beauveria bassiana, a natural fly pathogen. Brenda Y. Torres A simple model of infection-induced pathology. These results suggest that S. typhimurium-infected flies die from a condition that resembles TNF-induced metabolic collapse in vertebrates. Linderman, J. These data indicate L. monocytogenes infection of fruit flies shares numerous features of mammalian infection, and thus that Drosophila has the potential to serve as a genetically tractable host system that will facilitate the analysis of host cellular responses to L. monocytogenes infection. Gordon, M. D., Ayres, J. S., Schneider, D. S., Nusse, R. Identification of drosophila mutants altering defense of and endurance to Listeria monocytogenes infection. Our data show that antiviral innate immune responses in flies infected with CrPV depend upon hemocytes and signaling through the Imd pathway. These results suggest that the fly can be used to study more than the immediate innate immune response to infection; it can also be used to understand the physiological consequences of infection and the immune response. He graduated from Wabash College in 1962 with majors in psychology and philosophy, and earned a doctorate in psychology from Stanford … The phagocytes of Drosophila encounter bacterial invaders early in infection and contribute to survival of infection. "The Stanford Economics Department has two central missions: to train students at the undergraduate and graduate level in the methods and ideas of modern economics, and to conduct both basic and applied research in economics that pushes forward the frontier of knowledge in the field." Furthermore, the wntD mutant phenotype is suppressed by loss of zygotic dorsal. However, the ubiquitin ligases responsible for catalysing ubiquitin chains that surround intracellular bacteria are poorly understood. Associates . If we just consider the host, there are many outputs that interest us: evolutionary fitness determining parameters like fecundity, survival and pathogen clearance as well as medically important health parameters like sleep, energy stores and appetite. These γδ T cells expressed specific cytokines, M-CSF, CCL5, CCL3, which are known to act on myeloid cells, indicating that this γδ T cell subset might have distinct functions. We find that in a Listeria monocytogenes/Drosophila melanogaster infection model, L. monocytogenes grows according to logistic kinetics, which means we can measure both a maximal growth rate and growth plateau for the microbe. We also found that bacteria colonized the ovary in a previously undescribed manner; bacteria were found in the posterior of the ovary, adjacent to the lateral oviduct. Research is sparked by intellectual curiosity and enriched by interactions with other academics and … We analyzed two publicly available, longitudinal human microarray datasets that describe self-resolving immune responses. David has 6 jobs listed on their profile. By engineering a gene knockout, we show that wntD loss-of-function mutants have immune defects and exhibit increased levels of Toll/Dorsal signalling. Two pattern recognition pathways, Toll and immune deficiency (Imd), were found to detect, and respond to, infections. David Schneider - Professor of Microbiology and Immunology . The purified protein is smaller than the primary translation product of spätzle, suggesting that proteolytic processing of Spätzle on the ventral side of the embryo is required to generate the localized, active form of the protein. View details for DOI 10.1126/science.1214935, View details for Web of Science ID 000300931800037. This online memorial is dedicated to Stanford Dean Schneider. We infected the fruit fly Drosophila melanogaster with M. marinum. Regulating the nuclear factor-kappaB (NF-kappaB) family of transcription factors is of critical importance to animals, with consequences of misregulation that include cancer, chronic inflammatory diseases and developmental defects. Here we describe how two components of the fly's immune response, melanization and phagocytosis, contribute to the health landscape generated by the transcription factor ets21c (CG2914) and its putative effector, the signaling molecule wntD (CG8458). We chose to examine the fly ovary because we found bacterial infection had a striking effect on fly reproduction. Hosts use a variety of effector pathways to fight infections and these effectors are brought to bear differentially. In particular, host anorexia has been shown to be beneficial or detrimental depending on the infection [7, 8]. Our interest is in characterizing how bacterial pathogenesis affects various physiologies of the fly. This idea provides us with a new model to study shock-like biology in a genetically manipulable host. We suggest there are nine possible pairwise permutations of these traits, assuming they can increase, decrease, or remain unchanged in an independent manner. Studies in Drosophila melanogaster have proved fruitful in determining the signals used to control NF-kappaB proteins, beginning with the discovery that the Toll/NF-kappaB pathway, in addition to patterning the dorsal-ventral axis of the fly embryo, defines a major component of the innate immune response in both Drosophila and mammals. A Macrophage Colony-Stimulating-Factor-Producing γδ T Cell Subset Prevents Malarial Parasitemic Recurrence. Interactions between circadian rhythm and immunity in Drosophila melanlogaster. Our study is the first examination of the metabolic consequences of infection in a genetically tractable invertebrate and gives insight into the metabolic consequences of mycobacterial infection, implicating impaired insulin signaling as a key mediator of these events. We examined the immune response of a fly as physicians might, by looking at the genesis of diseases caused by microorganisms. A 'read' is counted each time someone views a publication summary (such as the title, abstract, and list of authors), clicks on a figure, or views or downloads the full-text. We focus on two models. However, despite metabolism's powerful ability to alter the course of infections, little is known about what being "sick" means metabolically. Environments which affect immunity not only include diet and metabolism, but also social interactions and the animal's microbiota. Despite evidence that γδ T cells play an important role during malaria, their precise role remains unclear. This protective effect exhibits coarse specificity for S. pneumoniae and persists for the life of the fly. View details for Web of Science ID 000268076900013. We report a level of complexity in the fly's immune response that has strong ecological implications. David's blog; Topological network of mouse and human malaria. They continue to work on fruit flies as a model for microbial pathogenesis. Using loops derived from training data, we found that we could predict the time of perturbation in withheld test samples with accuracies of 94% in the human monocyte data, and 65-83% within the same cohort and in two independent cohorts of YF17D vaccinated individuals. present an example of fungus-specific immune responses in social ants that lead to the active immunisation of nestmates by infected individuals. Deletion of the gene encoding the secreted bacterial effect or Salmonella leucine-rich (PslrP)changes an acute and lethal infection to one that is persistent and less deadly. These loops enable us to track where patients lie on a typical trajectory back to health. View details for DOI 10.1371/journal.ppat.0030026, View details for Web of Science ID 000248495200006, View details for PubMedCentralID PMC1817657. Circadian rhythms enable organisms to synchronise the processes underpinning survival and reproduction to anticipate daily changes in the external environment. View details for DOI 10.1016/j.chom.2012.10.004, View details for Web of Science ID 000310719700003. Faculty Advisor(s): Carolyn Bertozzi, Noah Burns, Tony Wyss-Coray Jiuzhi "Gillian" Sun. The observation that mutants with defects in the humoral immune response are further immunocompromised by blocking phagocytosis, and thus inhibiting the cellular immune response, shows that the Drosophila cellular and humoral immune responses act in concert to fight infection. Stanford Live, in compliance with the university’s decision, is moving to cancel large-scale performances within this time frame. In this year's Drosophila Research Conference, which was held in San Diego (March 30-April 3) and sponsored by the Genetics Society of America, the immunity and pathogenesis session comprised seven platform presentations and 34 posters that highlighted the latest advances in Drosophila infection and immunity field. Brandt, S. M., Jaramillo-Gutierrez, G., Kumar, S., Barillas-Mury, C., Schneider, D. S. Models of infectious diseases in the fruit fly Drosophila melanogaster, Pathogenesis of Listeria-infected Drosophila wntD mutants is associated with elevated levels of the novel immunity gene edin. Here, we examine how host circadian rhythms influence rhythms in the asexual replication of malaria parasites. Western diet regulates immune status and the response to LPS-driven sepsis independent of diet-associated microbiome. We posit that novel scientific paradigms should emerge when molecular immunologists and evolutionary ecologists work together. Loss-of-function mutations in several Imd pathway genes displayed increased sensitivity to CrPV infection and higher CrPV loads. View details for DOI 10.1534/g3.115.022558, View details for Web of Science ID 000367257500009. In this study, we examined the pathogen Francisella novicida and identified new bacterial virulence factors that interact with different parts of the Drosophila melanogaster innate immune system. Fly infections are complex and there are few simple rules that can predict how an infected fly might fare. Immunology is a well-defined field in which the mechanisms behind resistance to infection are dissected. The site facilitates research and collaboration in academic endeavors. Our results reveal that the host's peripheral rhythms (associated with the timing of feeding and metabolism), but not rhythms driven by the central, light-entrained circadian oscillator in the brain, determine the timing (phase) of parasite rhythms. One obvious mechanism affecting tolerance is the intensity of an immune response; an overly exuberant immune response can cause collateral damage through immune effectors and because of the energy allocated away from other physiological functions. We propose a model in which Salmonella secreted effectors stimulate the fly and thus cause an immune response that is damaging both to the bacteria and, subsequently, to the host. Brennan, C. A., Delaney, J. R., Schneider, D. S., Anderson, K. V. Bacterial infection of fly ovaries reduces egg production and induces local hernocyte activation, Akt and foxo dysregulation contribute to infection-induced wasting in Drosophila. Upon infection, Drosophila mounts an immune response including antimicrobial peptide production and autophagy activation. The physiological response of the fly was modified further by Eiger, insulin, Wnt inhibitor of dorsal (WntD) and nitric oxide (NO) signaling. Here we describe a method for inhibiting phagocytosis in Drosophila blood cells (hemocytes) by injecting polystyrene beads into the body cavity. Drosophila melanogaster, like other invertebrates, relies solely on its innate immune response to fight invading microbes; by definition, innate immunity lacks adaptive characteristics. Here, we show that eiger is made in the fly's fat body during a Salmonella typhimurium infection. They also become hyperglycemic. Health is a multidimensional landscape. Here we show that by making a single mutation in the gene encoding a protease, CG3066, active in the melanization cascade in Drosophila melanogaster, we observe the full spectrum of changes; these mutant flies show increases and decreases in their resistance and tolerance properties when challenged with a variety of pathogens. Bio-X Affiliated Faculty . We argue that every process that affects immunity should be considered as part of the immune response and that it is the broad phenomena discovered in insects that will be translated to other organisms rather than fine mechanistic details. Finally, in contrast to all other bacteria examined, mycobacteria failed to elicit the production of antimicrobial peptides in Drosophila.We believe that this system should be a useful genetically tractable model for mycobacterial infection. Dr. Schneider's laboratory study innate immunity and microbial pathogenesis. These studies provide a foundation for the identification of host factors and virulence mechanisms. View details for DOI 10.1371/journal.pone.0007436, View details for Web of Science ID 000270847800002, View details for PubMedCentralID PMC2758544. Site of infection in the fly, a component of the Toll pathway is not commonly studied first secreted antagonist... 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