David S. Weiss

ORCID: 0000-0003-0980-7866
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About
Contact & Profiles
Research Areas
  • Antibiotic Resistance in Bacteria
  • Vibrio bacteria research studies
  • CRISPR and Genetic Engineering
  • Bacterial Genetics and Biotechnology
  • Antibiotics Pharmacokinetics and Efficacy
  • Bacillus and Francisella bacterial research
  • Immune Response and Inflammation
  • Gut microbiota and health
  • Bacteriophages and microbial interactions
  • Bacterial Identification and Susceptibility Testing
  • Escherichia coli research studies
  • Bacterial biofilms and quorum sensing
  • Pharmaceutical and Antibiotic Environmental Impacts
  • Inflammasome and immune disorders
  • Antibiotic Use and Resistance
  • RNA and protein synthesis mechanisms
  • Pneumonia and Respiratory Infections
  • Liver Disease Diagnosis and Treatment
  • Mycobacterium research and diagnosis
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Clostridium difficile and Clostridium perfringens research
  • Cystic Fibrosis Research Advances
  • Advanced biosensing and bioanalysis techniques
  • Enterobacteriaceae and Cronobacter Research
  • Cell death mechanisms and regulation

Emory University
2016-2025

Emory Healthcare
2013-2025

Carl von Ossietzky Universität Oldenburg
2024

Georgia Department of Public Health
2022-2024

Emory and Henry College
2012-2023

CNR de la Résistance aux Antibiotiques
2022-2023

AID Atlanta
2013-2023

Agilent Technologies (United States)
2023

Atlanta VA Medical Center
2016-2022

Emory National Primate Research Center
2012-2021

Neutrophils engulf and kill bacteria when their antimicrobial granules fuse with the phagosome. Here, we describe that, upon activation, neutrophils release granule proteins chromatin that together form extracellular fibers bind Gram-positive -negative bacteria. These neutrophil traps (NETs) degrade virulence factors NETs are abundant in vivo experimental dysentery spontaneous human appendicitis, two examples of acute inflammation. appear to be a innate response binds microorganisms,...

10.1126/science.1092385 article EN Science 2004-03-04

Francisella tularensis is a highly infectious gram-negative coccobacillus that causes the zoonosis tularemia. This bacterial pathogen plague-like disease in humans after exposure to as few 10 cells. Many of mechanisms by which innate immune system fights are unknown. Here we show wild-type Francisella, reach cytosol, but not mutants remain localized vacuole, induced host defense response macrophages, dependent on caspase-1 and death-fold containing adaptor protein ASC. Caspase-1 ASC...

10.1084/jem.20050977 article EN The Journal of Experimental Medicine 2005-10-17

Francisella tularensis is a pathogenic bacterium whose virulence linked to its ability replicate within the host cell cytosol. Entry into macrophage cytosol activates host-protective multimolecular complex called inflammasome release proinflammatory cytokines interleukin (IL)-1β and -18 trigger caspase-1–dependent death. In this study, we show that cytosolic F. subspecies novicida (F. novicida) induces type I interferon (IFN) response essential for caspase-1 activation, inflammasome-mediated...

10.1084/jem.20062665 article EN The Journal of Experimental Medicine 2007-04-23

Francisella tularensis subverts the immune system to rapidly grow within mammalian hosts, often causing tularemia, a fatal disease. This pathogen targets cytosol of macrophages where it replicates by using genes encoded in pathogenicity island. However, bacteria are recognized host's ASC/caspase-1 pathway, which is essential for host defense, and leads macrophage cell death proinflammatory cytokine production. We used microarray-based negative selection screen identify that contribute growth...

10.1073/pnas.0609675104 article EN Proceedings of the National Academy of Sciences 2007-03-28

Significance The clustered, regularly interspaced, short palindromic repeats associated endonuclease, Cas9, has quickly become a revolutionary tool in genome engineering. Utilizing small guiding RNAs, Cas9 can be targeted to specific DNA sequences of interest, where it catalyzes cleavage. We now demonstrate that from the Gram-negative bacterium Francisella novicida (FnCas9) reprogrammed target RNA substrate, +ssRNA virus, hepatitis C eukaryotic cells. Further, this targeting results...

10.1073/pnas.1422340112 article EN Proceedings of the National Academy of Sciences 2015-04-27

Multidrug-resistant organism (MDRO) colonization is a fundamental challenge in antimicrobial resistance. Limited studies have shown that fecal microbiota transplantation (FMT) can reduce MDRO colonization, but its mechanisms are poorly understood. We conducted randomized, controlled trial of FMT for decolonization renal transplant recipients called PREMIX (NCT02922816). Eleven participants were enrolled and randomized 1:1 to or an observation period followed by delayed if stool cultures...

10.1126/scitranslmed.abo2750 article EN Science Translational Medicine 2023-11-01

To unravel the strategy by which Brucella abortus establishes chronic infections, we explored its early interaction with innate immunity.Brucella did not induce proinflammatory responses as demonstrated absence of leukocyte recruitment, humoral or cellular blood changes in mice. hampered neutrophil (PMN) function and PMN depletion influence course infection. barely induced cytokines consumed complement, was strongly resistant to bactericidal peptides, extracts serum. LPS (BrLPS),...

10.1371/journal.pone.0000631 article EN cc-by PLoS ONE 2007-07-17

Toll-like receptors (TLRs) are evolutionarily conserved proteins that recognize microbial molecules and initiate host defense. To investigate how TLRs work together to fight infections, we tested the role of in defense against Gram-negative bacterial pathogen, Salmonella. We show TLR4 is critical for early cytokine production killing bacteria by murine macrophages. Interestingly, later on, TLR2, but not TLR4, required macrophage responses. Myeloid differentiation factor 88, an adaptor...

10.4049/jimmunol.172.7.4463 article EN The Journal of Immunology 2004-04-01

The Secret Life of a Vaccine Antigen-specific CD8 ÷ T cells play central role in the adaptive immune response to viral infections and cancer. Ravindran et al. (p. 313 , published online 5 December) studied successful yellow fever virus vaccine YF-17D gain insight into its mechanism action. activated nutrient deprivation sensor, GCN2 kinase, dendritic cells. In transgenic mouse models, activation promoted autophagy antigen cross-presentation, enhancing virus-specific cell response. findings...

10.1126/science.1246829 article EN Science 2013-12-06

ABSTRACT Acinetobacter baumannii is an opportunistic pathogen that a cause of clinically significant nosocomial infections. Increasingly, clinical isolates A. are extensively resistant to numerous antibiotics, and the use polymyxin antibiotics against these infections often final treatment option. Historically, polymyxins have been thought kill bacteria through membrane lysis. Here, we present alternative mechanism based on data demonstrating induce rapid cell death hydroxyl radical...

10.1128/aac.00756-12 article EN Antimicrobial Agents and Chemotherapy 2012-08-21

The facultative intracellular bacterium Francisella tularensis causes the zoonotic disease tularemia. F. resides within host macrophages in vivo, and this ability is essential for pathogenesis. transcription factor MglA required expression of several genes that are necessary replication virulence mice. We hypothesized identification MglA-regulated genome by transcriptional profiling wild-type mglA mutant bacteria would lead to discovery new factors utilized tularensis. A total 102 were...

10.1128/iai.01250-06 article EN Infection and Immunity 2006-11-21

Cationic antimicrobial peptides (CAMPs) are important innate immune defenses that inhibit colonization by pathogens and contribute to clearance of infections. Gram-negative bacterial a major target, yet many them have evolved mechanisms resist these antimicrobials. These resistance can be critical contributors virulence often crucial for survival within the host. Here, we summarize methods used bacteria CAMPs. Understanding may lead new therapeutic strategies against with extensive CAMP resistance.

10.3390/antibiotics4010018 article EN cc-by Antibiotics 2014-12-25

ABSTRACT Antibiotic resistance is a growing crisis and grave threat to human health. It projected that antibiotic-resistant infections will lead 10 million annual deaths worldwide by the year 2050. Among most significant threats are carbapenem-resistant Enterobacteriaceae (CRE), including Klebsiella pneumoniae (CRKP), which mortality rates as high 40 50%. Few treatment options available treat CRKP, polymyxin antibiotic colistin often “last-line” therapy. However, increasing. Here, we...

10.1128/mbio.02448-17 article EN cc-by mBio 2018-03-05

ABSTRACT The alarming rise in antibiotic resistance has led to an increase patient mortality and health care costs. This problem is compounded by the absence of new antibiotics close regulatory approval. Acinetobacter baumannii a human pathogen that causes infections primarily patients intensive units (ICUs) highly resistant. Colistin one last-line for treating A. infections; however, colistin-resistant strains are becoming increasingly common. cationic attacks negatively charged bacterial...

10.1128/mbio.00021-13 article EN cc-by-nc-sa mBio 2013-05-22
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