Drosophila has been established as useful model for infectious diseases because it allows large numbers of whole animals to be studied and provides powerful genetic tools and conservation with signaling and pathogenesis mechanisms in vertebrates. The response of eiger mutants divided these microbes into two groups: eiger mutants are immunocompromised with respect to extracellular pathogens but show no change or reduced sensitivity to facultative intracellular pathogens. Join Facebook to connect with David Schneider and others you may know. Indeed, reports showing alternative forms of immune memory are accumulating in invertebrates. 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. D. melanogaster are slower to recover from a chill-induced coma during infection with either Listeria monocytogenes or Streptococcus pneumoniae. 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. Nicole Davis Graduate Student. These results suggest that S. typhimurium-infected flies die from a condition that resembles TNF-induced metabolic collapse in vertebrates. In the mid-1970s, David M. Schneider rocked the anthropological world with his announcement that kinship did not exist in any culture known to humankind. David has 4 jobs listed on their profile. We suggest that Looper will be useful in building maps of resilient immune processes across organisms. Here, we fill this gap with a simple graphical and mathematical framework to study disease tolerance, the dose response curve relating health to microbe load; this approach helped uncover parameters that were previously overlooked. Matches found in 215 cities including New York, New York, North Port, Florida & Bayside, New York. American kinship: a cultural account. In this model, animals also suffer severe anemia, limiting their ability to carry oxygen concurrent with their switch toward fatty acid metabolism. 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. Quantitation of these two traits opens an additional dimension for analysis of cancer biology. Eiger is the sole TNF family member found in Drosophila melanogaster. Loss of function of four of these genes in the mosquito affected Plasmodium growth, suggesting that Drosophila can be used effectively as a surrogate mosquito to identify relevant host factors in the mosquito. View details for Web of Science ID 000088979000019. To gain insight into the interactions between viruses and the innate immune system, we injected wild type flies with CrPV and observed that antimicrobial peptides (AMPs) were not induced and hemocytes were depleted in the course of infection. Page 1 of 6 David Schneider Professor of Microbiology and Immunology Microbiology & Immunology Bio ACADEMIC APPOINTMENTS • Professor, Microbiology & Immunology • Member, Bio-X • Member, Maternal & Child Health Research Institute (MCHRI) HONORS AND AWARDS During murine malaria induced by Plasmodium chabaudi infection and in human P. falciparum infection, we found that γδ T cells expanded rapidly after resolution of acute parasitemia, in contrast to αβ T cells that expanded at the acute stage and then declined. Bacteria were found in the cytosol of insect phagocytic cells, and were capable of directing host cell actin polymerization. To plot tolerance, individual infections are summarized by reporting the maximum parasite load and the minimum health for a population of infected individuals and the slope of the resulting curve defines the tolerance of the population. Professor of Medicine (Blood and Marrow Transplantation) and of Pediatrics (Stem Cell Transplantation) (650) 723-0822. We support this hypothesis with experimental data in mice infected with Plasmodium chabaudi, finding that dying mice trace a large arc in red blood cells (RBCs) by reticulocyte space as compared to surviving mice. 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. Gordon, M. D., Dionne, M. S., Schneider, D. S., Nusse, R. Secreted bacterial effectors and host-produced eiger/TNF drive death in a Salmonella-infected fruit fly. David J. Schneider, PhD, is Professor of Psychology and Cognitive Sciences at Rice University, where he chaired the Department of Psychology from 1990 to 1996. Resistance and disease tolerance should be applicable to any insult to the host and have been explored in depth with regards to infection but have not been examined in the context of cancer. Cumnock, K., Gupta, A. S., Lissner, M., Chevee, V., Davis, N. M., Schneider, D. S. Timing of host feeding drives rhythms in parasite replication. Circadian rhythms enable organisms to synchronise the processes underpinning survival and reproduction to anticipate daily changes in the external environment. We extended the use of Drosophila beyond being a model for signaling pathways required for pattern recognition immune signaling and show that the fly can be used to identify genes required for pathogenesis and host-pathogen interactions. View details for DOI 10.1534/g3.115.022558, View details for Web of Science ID 000367257500009. Here we take advantage of the spectacularly deep genetic tools available to Drosophila geneticists to discover mechanisms involved in pathogenesis and the recovery from infections. As we observed the finer details of the infections, we found that almost every microbe caused a different type of pathology in the fly. 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. We identify a gene, psidin, that encodes a lysosomal protein required in the blood cells for both degradation of engulfed bacteria and activation of fat-body Defensin. Introduction of the notion of "disease tolerance" into the conceptual tool kit of immunology will expand our understanding of infectious diseases and host pathogen interactions. Lab Alumni. Typically, studies of animal defenses focus on either understanding resistance or, to a lesser extent, tolerance mechanisms, thus providing little understanding of the relationship between these two mechanisms. Mandl, J. N., Schneider, C., Schneider, D. S., Baker, M. L. Host Energy Source Is Important for Disease Tolerance to Malaria. We are starting by plotting health by microbe number over the course of infections. We posit that novel scientific paradigms should emerge when molecular immunologists and evolutionary ecologists work together. Our observations suggest that parasites actively control their developmental rhythms. These loops enable us to track where patients lie on a typical trajectory back to health. Parasite clearance was reduced with 2DG treatment, suggesting altered resistance. The Toll protein is found around the entire dorsal-ventral circumference of the embryo, and it appears to act as a receptor for a ventral, extracellular signal and to then relay that signal to the cytoplasm in ventral regions of the embryo. Background Checks. View details for DOI 10.1371/journal.ppat.0030041, View details for Web of Science ID 000248495200015, View details for PubMedCentralID PMC1829408. 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 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. Using a model experimental system in which we challenged Drosophila melanogaster with the pathogen Listeria monocytogenes, we tested this framework, finding that microbe growth, the immune response, and disease tolerance were all well represented by sigmoid models. We are making extremely mutlivariate plots of the disease process. WD mice also have an increased frequency of neutrophils, some with an "aged" phenotype, in the blood during sepsis compared with SC mice. We performed a forward genetic screen to identify Drosophila mutations altering sensitivity to the intracellular pathogen Listeria monocytogenes. These findings join others in showing how organisms evolved diverse mechanisms that fulfil common functions, namely the discrimination between pathogens, the transfer of immunity between related individuals, and the group-level benefits of immunisation. Chambers, M. C., Lightfield, K. L., Schneider, D. S. Where Does Innate Immunity Stop and Adaptive Immunity Begin? The technique holds promise as both a qualitative and quantitative approach to dissect host-microbe interactions of all kinds. Because growth rates and ceilings both correlate with host survival, both properties could drive evolution of the host. These data establish a role for the phagocytic blood cells of Drosophila in detection of infection and activation of the humoral immune response. The study of infectious disease has been aided by model organisms, which have helped to elucidate molecular mechanisms and contributed to the development of new treatments; however, the lack of a conceptual framework for unifying findings across models, combined with host variability, has impeded progress and translation. All six of the remaining dominant alleles require the presence of a wild-type transmembrane Toll protein for their ventralizing effect and all encode truncated proteins that lack the transmembrane and cytoplasmic domains. The parkin protein is a ubiquitin ligase with a well-established role in mitophagy, and mutations in the parkin gene (PARK2) lead to increased susceptibility to Parkinson's disease. View details for DOI 10.1371/journal.pbio.1002436, View details for PubMedCentralID PMC4835107. Intracellular M. marinum blocked vacuolar acidification and failed to colocalize with dead Escherichia coli, similar to infections of mouse macrophages. To quantitate these differences, we propose mapping the routes infected individuals take through "disease space." The average Stanford Schneider is around 81 years of age with around 75% falling in to the age group of 81+. 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. Schneider Lab. We suggest there are nine possible pairwise permutations of these traits, assuming they can increase, decrease, or remain unchanged in an independent manner. 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 10.1371/journal.ppat.1002970, View details for Web of Science ID 000312907100002, View details for PubMedCentralID PMC3521699. Gordon, M. D., Ayres, J. S., Schneider, D. S., Nusse, R. Identification of drosophila mutants altering defense of and endurance to Listeria monocytogenes infection. Explore the more than 65 major fields of undergraduate study at Stanford. We report here the establishment of the fruit fly Drosophila melanogaster as a new model host for the exploration of L. monocytogenes pathogenesis and host response to infection. Biography. Created with Sketch. Our current focus is to determine how we recover from infections. Survival depends on more than simply detecting and eliminating microbes; it requires that we prevent and repair the damage caused by pathogens and the immune response. Mass vaccination allows us to study how immunity operates at the group level; denser populations are more prone to transmitting disease between individuals, but once a critical proportion of the population becomes immune, "herd immunity" emerges. Stanford Libraries' official online search tool for books, media, journals, databases, government documents and more. Louie, A., Song, K. H., Hotson, A., Tate, A. T., Schneider, D. S. Tracking Resilience to Infections by Mapping Disease Space. Currently, Dr. Schneider sees a variety of patients with bone, tendon, muscle, joint, and brain diseases. Here, we explored the temporal dynamics of multiple sickness behaviors and their effect on host energy and metabolism throughout infection. These experiments suggest that Drosophila can be used as a surrogate mosquito for defining the genetic pathways involved in both vector competence and part of the parasite sexual cycle. Login ID: Password: Re-enter: Email: (Don't worry, your e-mail will not be distributed or made public. Pham, L. N., Dionne, M. S., Shirasu-Hiza, M., Schneider, D. S. Drosophila eiger mutants are sensitive to extracellular pathogens. The phagocytes of Drosophila encounter bacterial invaders early in infection and contribute to survival of infection. View details for DOI 10.1371/journal.ppat.1000111, View details for Web of Science ID 000259783000017, View details for PubMedCentralID PMC2453329. Each pathogen causes a different disease as they have distinct virulence factors and niches; they each warp the health landscape in unique ways. Here we show that parkin has a role in ubiquitin-mediated autophagy of M. tuberculosis. None of the identified genes have been previously implicated in innate immune responses or interactions with Plasmodium. View details for DOI 10.1016/j.cub.2006.08.052, View details for Web of Science ID 000241532000018. Surprisingly, genetic polymorphisms in the PARK2 regulatory region are also associated with increased susceptibility to intracellular bacterial pathogens in humans, including Mycobacterium leprae and Salmonella enterica serovar Typhi, but the function of parkin in immunity has remained unexplored. View details for DOI 10.1046/j.1462-5822.2003.00329.x, View details for Web of Science ID 000186563600005. We then performed a second in vivo screen to identify an additional subset of bacterial genes that interact specifically with the imd signaling pathway. Shirasu-Hiza, M. M., Dionne, M. S., Pham, L. N., Ayres, J. S., Schneider, D. S. A specific primed immune response in Drosophila is dependent on phagocytes. 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. We focus on resistance, pathogenicity and tolerance to infection. The demonstration of three separate examples of such a system suggests that it is broadly used and should provoke a reexamination of microbial pathogenesis in animal cells to look for similar mechanisms. We like to assess "health" in whole animals rather than in vitro but we use a large range of tools ranging from genetics, to microarray analyses to flow cytometry. Moule, M. G., Monack, D. M., Schneider, D. S. Relating immune and stress responses to infection resistance and tolerance, The Drosophila TNF Ortholog Eiger Is Required in the Fat Body for a Robust Immune Response, The Imd Pathway Is Involved in Antiviral Immune Responses in Drosophila. 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. However, the ubiquitin ligases responsible for catalysing ubiquitin chains that surround intracellular bacteria are poorly understood. (1991) identified a soluble, extracellular factor that induces ventral structures at the site where it is injected in the extracellular space of the early Drosophila embryo. We are using a new approach to study the outcome of infections. We show that WntD acts as a feedback inhibitor of the NF-kappaB homologue Dorsal during both embryonic patterning and the innate immune response to infection. A., Andres-Terre, M., Massis, L. M., Hryckowian, A. J., Higginbottom, S. K., Cumnock, K., Casey, K. M., Haileselassie, B., Lugo, K. A., Schneider, D. S., Sonnenburg, J. L., Monack, D. M. Vector Immunity and Evolutionary Ecology: The Harmonious Dissonance. Interactions between circadian rhythm and immunity in Drosophila melanlogaster. 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. We study innate immunity and microbial pathogenesis. View David Schneider's business profile as Department Chair at Stanford University. These results are consistent with a model in which the regulation of host factors, including edin, must be tightly controlled to avoid the detrimental consequences of having too much or too little activity. Metabolism of fats requires oxygen for the production of ATP. View details for DOI 10.1371/journal.pone.0050679, View details for Web of Science ID 000312386600013, View details for PubMedCentralID PMC3521769. View details for DOI 10.3389/fimmu.2018.02112, View details for Web of Science ID 000445106400001. Katie Cumnock Graduate Student. Schneider received his BS in biochemistry from the University of Toronto in 1986 and earned a PhD in molecular biology at the University of California-Berkeley in 1992. Tolerance measures the dose response curve of a host's health in reaction to a pathogen and can be studied in a simple quantitative manner. 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? We examined the immune response of a fly as physicians might, by looking at the genesis of diseases caused by microorganisms. To investigate the contribution of conserved immune signaling pathways to antiviral innate immune responses, CrPV was injected into isogenic mutants of the Immune Deficiency (Imd) pathway, which resembles the mammalian Tumor Necrosis Factor Receptor (TNFR) pathway. 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. Prior, K. F., van der Veen, D. R., O'Donnell, A. J., Cumnock, K., Schneider, D., Pain, A., Subudhi, A., Ramaprasad, A., Rund, S. C., Savill, N. J., Reece, S. E. Predicting position along a looping immune response trajectory. To probe the landscape, we infect with two pathogens: Listeria monocytogenes, which primarily lives intracellularly, and Streptococcus pneumoniae, which is an extracellular pathogen. 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. Here, we give an overview of the presented work and we explain how these findings will open new avenues in Drosophila immunity research. L. monocytogenes infection alters energy metabolism; the flies gradually lose both of their energy stores, triglycerides and glycogen, and show decreases in both intermediate metabolites and enzyme message for the two main energy pathways, beta-oxidation and glycolysis. James H. Clark Center, Stanford University 318 Campus Drive Stanford, CA 94305 Phone: 650.724.3333Follow @StanfordBioX, © Stanford University, Stanford, California 94305, James H. Clark Center, Stanford University, Stanford Interdisciplinary Life Sciences Council. 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. We conclude that the WD is reprogramming the basal immune status and acute response to LPS-driven sepsis and that this correlates with alternative disease paths that lead to more severe disease and poorer outcomes. 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 10.1371/journal.ppat.0030026, View details for Web of Science ID 000248495200006, View details for PubMedCentralID PMC1817657. They have also lived in Boise, ID and Santa Clara, CA. The mechanism underlying this protective effect requires phagocytes and the Toll pathway. David Schneider. Their current focus is to determine how we recover from infections. These results describe the first secreted feedback antagonist of Toll signalling, and demonstrate a novel Wnt activity in the fly. Drosophila has proven a fruitful model for the investigation of evolutionarily conserved innate immune mechanisms, including NF-kappaB-dependent transcriptional induction, RNAi in antiviral responses, and phagocytosis. After completing his medical education and serving as an Undersea Medical Officer in the Navy, he finished his residency and fellowship. Studies of infection in Drosophila melanogaster provide insight into both mechanisms of host resistance and tolerance of pathogens. This ability to tolerate a pathogen's presence is a distinct host defense strategy, which has been largely overlooked in animal and human studies. View details for DOI 10.1016/j.chom.2012.10.004, View details for Web of Science ID 000310719700003. Hence, eiger helps fight infections but also can cause pathology. Professor Microbiology & Immunology Stanford University United States of America. As a physiatrist, he works in partnership with the orthopedic surgeons of Illinois Bone & Joint Institute to meet the diverse needs of p… people phone reverse address business Log In Sign Up. Insights in the laboratory have demonstrated how the immune system provides resistance to infection, and in what manner innate defenses protect against a microbial assault. 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. Using tissue-specific knockdown, we found that eiger expression in the fat body is required for all of the phenotypes we observed in eiger null mutant flies. We continue to work on fruit flies as a model for microbial pathogenesis. Here, we characterize the Drosophila wntD (Wnt inhibitor of Dorsal) gene. We find that when plotting physiological parameters against each other, many pairs have hysteretic relationships that identify the current location of the host and predict the future route of the infection. View details for DOI 10.1016/j.cub.2006.11.026, View details for Web of Science ID 000243461300027. Tracking Resilience to Infections by Mapping Disease Space. From this screen, we identified a new gene we have named red shirt and identified the caspase Dredd as a regulator of the Drosophila immune response. To characterize this primed response, we focused on S. pneumoniae-induced protection. David Schneider. Their current focus is to determine how we recover from infections. These findings point to an M-CSF-producing γδ T cell subset that fulfills a specialized protective role in the later stage of malaria infection when αβ T cells have declined. 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. Their goal is to define "biovectors" that predict the outcome of infection and to identify the physiological mechanisms required for recovery from infections. Studies of tolerance will provide an improved foundation to describe our interactions with all microbes: pathogenic, commensal, and mutualistic. Research Interest. Despite plaguing humanity for thousands of years, the host factors that regulate this immunological response and subsequent sepsis severity and outcome are not fully understood. Importantly, we found that the WD-dependent increase in sepsis severity and higher mortality is independent of the microbiome, suggesting that the diet may be directly regulating the innate immune system through an unknown mechanism. View details for DOI 10.1111/j.1462-5822.2007.01042.x, View details for Web of Science ID 000250761100003, View details for DOI 10.1371/journal.pbio.0050247, View details for Web of Science ID 000249552300003, View details for PubMedCentralID PMC1994275, View details for Web of Science ID 000246572900009. Two defense strategies protect hosts against infections: resistance, which is the ability to control pathogen levels, and tolerance, which helps the host endure infection-induced pathology. 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. Ayres, J. S., Freitag, N., Schneider, D. S. Confronting physiology: how do infected flies die? Recent work shows that daily (circadian) rhythms also enable parasites to maximise fitness in the context of ecological interactions with their hosts. Department of Microbiology and Immunology Fairchild Science Building, D333 299 Campus Drive Stanford, CA 94305 Current Members. Michael Snyder. Dr. David Schneider grew up outside Detroit, Michigan. 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. Michelle Lissner Graduate Student. Recent insect research has made productive forays into non-classical immune areas including tolerance, immune priming (trained immunity), and environmental effects on immunity. They continue to work on fruit flies as a model for microbial pathogenesis. They focus on two models. This idea provides us with a new model to study shock-like biology in a genetically manipulable host. Here we report measurements of infection-related declines in flies' performance on two different behavioral assays. Looper identified looping gene pairs expressed by human donor monocytes stimulated by immune elicitors, and in YF17D-vaccinated individuals. When looking at the matrix of signaling pathways and the microbes being tested, it was immediately obvious that most of the pathways would need to be studied in more detail before defining the rules that govern their role in pathogenesis. Known Drosophila immune response where single mutations cause simple binary changes in immunity a curious result that could easily! Drive Stanford, CA two properties together defines the defensive capabilities of the Toll.. To the antimicrobial peptide polymyxin B DOI 10.1371/journal.pbio.0020418, View details for 10.1016/j.dci.2007.02.003. Both by LD ( 50 ) and of Pediatrics ( Stem Cell Transplantation ) ( 650 ) 724-8064 david.schneider )! At Stanford that may mediate the observed susceptibility of wntD mutants to lethal.. 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