Our lab seeks to improve understanding of chronic bacterial infections and to devise new diagnostic and therapeutic approaches. We focus on the opportunistic pathogen Pseudomonas aeruginosa, other Gram negative organisms, and microbiome analyses to study chronic infections that afflict people with cystic fibrosis and other diseases.
We use genomic, evolutionary, and molecular biology approaches in multi-disciplinary research that involves microbiologists, genome scientists, physicians, immunologists, and clinical researchers. We are located in the School of Medicine at the University of Washington in Seattle.
People with cystic fibrosis develop lethal bacterial lung infections; studying these infections is a major focus of our lab. We use DNA-based (“microbiome”) analysis to better understand the causes of infection, genomics to study bacterial adaptations during infection, and proteomics to identify bacterial responses to lung conditions and treatments. We are also trying to better understand the growth of pathogens at chronic infection sites.
Our lab identified mechanisms of bacterial diversification in biofilms, which are matrix-encased bacterial aggregates. We are now studying genetic diversification of bacteria during chronic human infections. Our data indicate that P. aeruginosa strains infecting cystic fibrosis (CF) patients extensively diversify during infection, in large part due to the isolation of bacteria in different lung regions. We are currently investigating the effects of pathogen diversification on disease manifestations and on the development of drug resistance in CF and wound infections.
A key natural mechanism of host defense is the withholding of iron from pathogens. We are studying the metal gallium as a “Trojan horse” to disrupt bacterial iron metabolism. Because of its similarity to iron, gallium is imported by many bacteria. However, gallium cannot undergo the sequential reduction and oxidation critical for iron’s biologic functions. Based on positive phase 1 study results, we are now performing a phase 2 clinical trial, and we are studying the antimicrobial and anti-inflammatory mechanisms of gallium.
Antibiotic tolerance is decreased susceptibility of bacteria caused by phenotypic mechanisms, rather than due to the acquisition of resistance genes or gene mutations. Bacteria become antibiotic tolerant when aggregated, nutrient-deprived, or subjected to stress. Recent work from our lab showed that bacterial starvation triggers tolerance. We are now investigating how in vivo conditions may produce tolerance during infection.
Pradeep Singh, M.D., Prinicipal Investigator
Singh’s work seeks to improve understanding of chronic bacterial infections, particularly those afflicting people with cystic fibrosis. Work in the Singh lab is also directed toward understanding antibiotic activity, and on developing new anti-infective approaches.
Singh is an experienced mentor of trainees including PhD post-doctoral fellows, MD fellows in pulmonary and infectious disease, graduate students, undergraduates, and high school students. Singh is also the Director of the Cystic Fibrosis Research and Development program and Director of the Cystic Fibrosis Pilot and Feasibility grant program at the University of Washington
Cara Forsberg, Ph.D., Senior Fellow
Cara received her B.S. from the University of Michigan, where she studied lambdoid phage infection and phage exclusion systems with David Friedman. She received her graduate training in Michael Caparon’s laboratory at Washington University in St. Louis, studying the mechanism of cytolysin-mediated translocation, an effector translocation system used by Streptococcus pyogenes to intoxicate host cells.
Cara joined the Singh and Manoil labs in the summer of 2015. Her research is focused on understanding how Pseudomonas aeruginosa establishes a niche and initiates chronic infection in the lungs of patients with cystic fibrosis. She is also interested in identifying P. aeruginosa variants and changes in bacterial subpopulations that correlate with clinical outcomes.
Peter Jorth, Ph.D., Senior Fellow
My research focuses on understanding how bacterial diversity affects infectious disease progression. I completed my PhD in Microbiology at the University of Texas at Austin in Marvin Whiteley’s group. In graduate school, I used high-throughput RNA sequencing to investigate polymicrobial communities that cause periodontitis. During my postdoctoral studies, I have been using genome sequencing approaches to study Pseudomonas aeruginosa intraspecies diversity in cystic fibrosis infections. I am interested in 1) how P. aeruginosa evolves and diversifies during chronic infections and 2) how diversification affects antibiotic resistance and virulence.
Sarah Morgan, Ph.D., Senior Fellow
Sarah Morgan received a BS in Microbiology and a BS in Biochemistry from California Polytechnic State University, San Luis Obispo where she studied virulence factors in community-acquired methicillin-resistant Staphylococcus aureus. She received a PhD in Microbiology and Immunology for her work in the laboratory of Eric Krukonis studying how protein-DNA and protein-protein interactions modulate transcriptional activation of virulence factors in Vibrio cholerae.
Sarah’s research in the Singh lab focuses on understanding how the physiology of bacteria in chronic infections differs from that of acute infections. Sarah’s research projects include: (1) determining fitness requirements for Pseudomonas aeruginosa infection of chronic wounds and (2) identifying genes responsible for antibiotic treatment failure in a relapse model of meliodosis.
Matthew Radey, Ph.D., Senior Fellow
Matthew did his graduate work in information science and gradually made his way from clinical data systems to research bioinformatics and comparative genomics, focusing on sequencing, algorithms, and analysis methods. With labs at UW and other institutions, Matthew has worked on projects involving various microbial species, host interactions, metagenomic studies, and software applicable to a variety of use cases.
Matthew is currently pursuing a variety of projects involving Escherichia coli, Pseudomonas aeruginosa, bacterial secretion systems, and microbiome analysis. He is continually involved in the testing and development of software tools and methods.
Patrick R. Secor, Ph.D., Senior Fellow
Pat received his B.S. in biochemistry from Montana State University. As a PhD student at the Center for Biofilm Engineering at Montana State University in Garth James’ lab, he focused on host-pathogen interactions between keratinocytes and Staphylococcus aureus biofilms. He then moved to the University of Washington to start a postdoc in William Parks lab where he continued investigating host-pathogen interactions between the host and bacterial biofilms, focusing on how host matrix components promote biofilm assembly.
Pat’s current research interests are focused on how bacterial aggregation promotes chronic infection phenotypes. For example, crowded polymer-rich environments, such as those found in the airways of people with cystic fibrosis, cause bacteria to spontaneously aggregate, even when biofilm assembly functions are disabled. When host polymers force bacteria to aggregate, chronic infection phenotypes such as antibiotic tolerance are induced.
Richard Siehnel, Ph.D., Research Scientist
My research experience began at SUNY Buffalo investigating essential gene regulation, specifically the coordinated and balanced regulation of ribosomal genes in E. coli. As a postdoc and research scientist in Dr. Bob Hancock’s lab at UBC in Vancouver, I studied size exclusion limits for uptake of small molecules and porin activity and regulation. Combining these interests led to research in industry (Procter & Gamble Pharmaceuticals, Elitra Pharmaceuticals) investigating uptake mechanisms of antibacterial compounds and the use of genetic techniques to identify novel essential targets and design genetic screens for compounds active against these targets, followed by biochemical validation. In the Singh laboratory, I used a genetic screen to discover a previously uncharacterized negative regulator of quorum sensing in P. aeruginosa. I have also evaluated how certain genes might contribute to biofilm formation.
Currently I am collaborating on efforts to create and evaluate genetic alterations of clinical isolates from CF patients and other pathogens. Some projects include: evaluating virulence factors by making multiple, sequential gene knockouts of virulence genes and evaluating the mutants in infection models; adding genetic barcodes to P. aeruginosa strains that were newly-acquired in CF lung infections to allow tracking in competition experiments; the use of Gallium (a non-reducible substitute for iron) as an antibacterial agent and how it might behave synergistically or antagonistically with host defense mechanisms and commonly used antibacterial therapies; and bacterial persistence mechanisms.
Ellen Wilhelm, Research Coordinator
Ms. Wilhelm has over 20 years of experience in clinical research. She has expertise in Institutional Review Board (IRB) procedures, protocol management, study design and monitoring, informed consent, ethics in research and confidentiality, project and data management, and quality control and clinical research regulation.
Gilbert Bautista, Research Scientist
I received my Bachelors in Microbiology and Biochemistry from the University of Washington.
I am currently working on determining whether the environmental and genetic basis of persistence in Burkholderia thailandensis is responsible for treatment failure in infection relapse and in chronic infection. I am also working to identify biomarker genes in CF Pseudomonas aeruginosa isolates that predict its ability to establish a persistent airway infection.
Anina Ratjen, Research Scientist
I graduated from McGill University majoring in Anatomy and Cell Biology.
I am helping both Pat Secor, looking at antimicrobial tolerance of polymer-driven bacterial aggregates, and Katie Hisert, looking at the effects of Gallium on macrophages.
I am also currently involved in a study looking at the combined effect of antibiotics and ivacaftor on P. aeruginosas and S. aureus in patients with a R117H CFTR mutation in Dublin.
Sumedha Ravishankar, Research Scientist
I received my Bachelors degree in Microbial Biology from the University of California, Berkeley.
I am currently working on understanding the effect Tobramycin has on genetic variation in P. aeruginosa populations, identifying genes important for to antibiotic tolerance in B. thailandensis, and establishing a chronic murine infection model to be used for identifying potential biomarker genes for chronic P. aeruginosa infections.
Samantha Durfey, Graduate student
Sam grew up in the Adirondack Mountains of upstate NY. She then fled to the warmer winters of the University of Alabama — Tuscaloosa to complete her bachelor’s and master’s degrees in microbiology. She wrote her master’s thesis on work completed in Dr. Robert Findlay’s lab, developing a new method to produce a biofuel precursor from plant waste. In the Singh lab, Sam is interested in microbial evolution in chronic infections. She is currently working on a method to strain type a diverse population of bacteria in a high-throughput manner. Outside of the lab, Sam’s all-American mutt, Hallie, occupies most of her free time.
Mechanisms of antibiotic tolerance, and modeling bacterial growth in human secretions
Antibiotic tolerance describes the decreased susceptibility of bacteria caused by phenotypic mechanisms. Tolerance is fundamentally different from resistance, which is due to heritable genes or gene mutations. Bacteria become antibiotic-tolerant when aggregated, nutrient-deprived or subject to stress. Recent work from our lab showed that the bacterial response pathway that senses starvation triggers tolerance that is independent of growth arrest. We are now investigating how in vivo conditions can produce tolerance during infection, and modeling bacterial aggregation in human secretions.
Genetic diversification of bacteria human infections
Our lab identified mechanisms of bacterial diversification in laboratory biofilms, which are surface-attached and matrix-enchased bacterial aggregates. We are now studying genetic diversification of bacteria during chronic human infections. Our data indicate that single P. aeruginosa strains living in in the lungs of cystic fibrosis patients extensively diversify during infection, in large part due to the isolation of bacteria in different lung regions. We are currently investigating the effects of pathogen diversification on disease manifestation and drug resistance.
Our lab is currently recruiting postdocs with interest in these areas:
Restoring CFTR Function Reduces Airway Bacteria and Inflammation in People With Cystic Fibrosis and Chronic Lung Infections. Hisert KB, Heltshe SL, Pope C, Jorth P, Wu X, Edwards RM, Radey M, Accurso FJ, Wolter DJ, Cooke G, Adam RJ, Carter S, Grogan B, Launspach JL, Donnelly SC, Gallagher C, Bruce JL, Stoltz D, Welsh MJ, Hoffman LR, McKone EF, Singh PK, In press, Am J Respir Crit Care Med. 2017
In vivo protein interaction network analysis reveals porin-localized antibiotic inactivation in antibiotic resistant bacteria. Wu X; Chavez J, Schweppe DK, Zheng C, Weisbrod C, Eng J, Murali A, Lee S, Ramage E, Gallagher L, Kulasekara H, Edrozo M, Kamischke C, Brittnacher M, Miller SI, Singh PK, Manoil C, Bruce JE. Nat Commun. 2016 Nov 11;7:13414
Filamentous bacteriophage produced by Pseudomonas aeruginosa alters the inflammatory response and promotes non-invasive infection in vivo. Secor PR, Michaels LA, Smigiel KS, Rohani MG, Jennings LK Hisert KB, Arrigoni A, Braun KR, Birkland TP; Lai Y, Hallstrant TR, Bollyky PL, Singh PK, Parks WC. Infect Immun. 2016 Dec 29;85(1).
Ivacaftor-induced proteomic changes suggest monocyte defects may contribute to the pathogenesis of cystic fibrosis. Hisert KB, Schoenfelt KQ, Cooke, G, Grogan B, Launspach JL, Gallagher CG, Donnelly SC, McKone EF, Welsh MJ, Singh PK, Becker L. Am J Respir Cell Mol Bio, Am J Respir Cell Mol Biol. 2016 Apr;54(4):594-7. doi: 10.1165/rcmb.2015-0322LE.
Acute Administration of Ivacaftor to People with Cystic Fibrosis and a G551D-CFTR Mutation Reveals Smooth Muscle Abnormalities. Adam RJ, Hisert KB, Jonathan D. Dodd JD, Grogan B, Barnes JK, Gallagher CG, Sieren JP, Gross TJ, Fischer AJ, Cavanaugh JE,
Hoffman EA, Singh PK, Welsh MJ, McKone EF, Stoltz DA. JCI Insight. 2016 Apr 7;1(4):e86183.
Host-Microbe Protein Interactions during Bacterial Infection. Schweppe DK, Harding C, Chavez JD, Wu X, Ramage E, Singh PK, Manoil C, Bruce JE. Chem Biol. 2015 Nov 19;22(11):1521-30. doi: 10.1016/j.chembiol.2015.09.015. Epub 2015 Nov 5. PMID: 26548613
Probing the protein interaction network of Pseudomonas aeruginosa cells by chemical cross-linking mass spectrometry. Navare AT, Chavez JD ,Zheng C, Weisbrod CR, Eng JK, Siehnel R, Singh PK, Manoil C, Bruce JE, Structure 2015 Apr 7;23(4):762-73. doi: 10.1016/j.str.2015.01.022. Epub 2015 Mar 19. PMID: 25800553.
General and condition-specific essential genes of Pseudomonas aeruginosa. Lee S, Gallagher L, Thongdee B, Staudinger B, Lippman S, Singh PK, Manoil C Proc Natl Acad Sci USA. 2015 Apr 21;112(16):5189-94. doi: 10.1073/pnas.1422186112. Epub 2015 Apr 6.
Dynamic Proteome Response of Pseudomonas aeruginosa to Tobramycin Antibiotic Treatment. Wu X, Held K, Zheng C, Staudinger BJ, Chavez JD, Weisbrod CR, Eng JK, Singh PK, Manoil C, Bruce JE. Mol Cell Proteomics. 2015 Aug;14(8):2126-37. doi: 10.1074/mcp.M115.050161. Epub 2015 May 27.
Gallium Compounds Exhibit Potential as New Therapeutic Agents against Mycobacterium abscessus. Abdalla MY, Switzer BL, Goss CH, Aitken ML, Singh PK, Britigan BE. Antimicrob Agents Chemother. 2015 Aug;59(8):4826-34. doi: 10.1128/AAC.00331-15. Epub 2015 Jun 1.
Precision-engineering the Pseudomonas aeruginosa genome with two-step allelic exchange. Hmelo L, Borlee BR, Almblad H, Randall TE, Love ME, Yang JJ, Irie Y, Tseng BS, Storek KM, Siehnel RJ, P. Howell LS, Singh PK, Tolker-Nielsen T, Parsek MR, and Harrison JJ. Nature Protocols, 2015 Nov;10(11):1820-41
Regional Bacterial Adaptations in Chronically Infected Cystic Fibrosis Lungs. Staudinger BJ, Wu X, Jorth P, Hisert K, Garudathri J, Hayden H, Harding C, Radey MC, Barrington W, Goddard AF, Angermeyer A, Brittnacher MJ, Shendure J, Kitzmam J, Fligner C, Aitken ML, Manoil C, Bruce JE, Yahr TL, and Singh PK, Cell Host and Microbe, 2015 Sep 9;18(3):307-19. Cover article
Host-Microbe Protein Interactions during Bacterial Infection. Schweppe DK, Singh PK, Manoil C, Bruce JE. Chemistry & Biology 2015 Nov 19;22(11):1521-30.
Filamentous Bacteriophage Promote Biofilm Assembly and Function. Secor PR, Sweere JM, Michaels LA, Malkovskiy AV, Lazzareschi D, Katznelson E, Rajadas J, Birnbaum ME, Arrigoni A, Braun KR, Evanko SP, Stevens DA, Kaminsky W, Singh PK, Parks WC, Bollyky PL. Cell Host Microbe. 2015 Nov 11;18(5):549-59.
Rapid Evolution of Culture-Resistant Bacteria During Adaptation to Biofilm Growth. Penterman J, Nguyen D, Staudinger B, Anderson E, Greenberg EP, Lam JS, and Singh, PK. Cell Reports. 2014 Jan 30;6(2):293-300. doi: 10.1016/j.celrep.2013.12.019. Epub 2014 Jan 9. PMID: 24412364
Conditions Associated with the CF Defect Promote Chronic P. aeruginosa Infection. Staudinger B, Muller JF, Halldórsson S, Boles BR, Angermeyer A, Nguyen D, Rosen H, Baldursson O, Gottfreðsson M, Guðmundsson GH, and Singh PK. Am J Respir Crit Care Med. 2014 Apr 1;189(7):812-24. doi: 10.1164/rccm.201312-2142OC. PMID: 24467627
Biological cost of pyocin production during the SOS response in Pseudomonas aeruginosa. Penterman J, Singh PK, Walker GC. J Bacteriol. 2014 Jul 14. pii: JB.01889-14.
Metabolic dysfunction drives a unique pro-inflammatory phenotype in human adipose tissue macrophages. Kratz M, Hisert K, Hagman E, Peris E, Schoenfelt K, Coats B, Kuzma J, Larson I, Billing P, Landerholm RW, Crouthamel M, Singh PK, and Becker L. Cell Metabolism. 2014 Oct 7;20(4):614-25. (Cover article).
The extracellular matrix protects Pseudomonas aeruginosa biofilms by limiting the penetration of tobramycin. Tseng BS, Zhang W, Harrison JJ, Quach TP, Song JL, Penterman J, Singh PK, Chopp DL, Packman AI, Parsek MR. Environ Microbiol. 2013 May 13.
Future Directions in Early Cystic Fibrosis Lung Disease Research. Ramsey BW, Schlegel SB, Accurso FJ, Boucher RC, Cutting GR, Engelhardt JF, Guggino WB, Karp CL, Knowles MR, Kolls JK, LiPuma JJ, Lynch S, McCray PB, Rubenstein RC, Singh PK, Sorscher E, Welsh MJ. Am J Respir Crit Care Med. 2012 Apr 15;185(8):887-92.
Time Course Study of Delayed Wound Healing in a Biofilm-Challenged Diabetic Mouse Model. Zhao G, Hochwalt P, Usui M, Underwood R, Singh PK, James G, Stewart P, Olerud J, Fleckman P. Wound Repair and Regeneration. Wound Repair Regen. 2012 May-Jun;20(3):342-52.
Direct sampling of cystic fibrosis lungs indicates that DNA-based analyses of upper airway specimens can misrepresent infecting populations. Goddard, A F, Staudinger, B J, Dowd SE, Datar A, Wolcott RD, Aitken ML, Fligner CL, and Singh, PK; Proc Natl Acad Sci U S A. 2012 Aug 21;109(34):13769-74.
PLUNC: A multifunctional surfactant of the airways. Bartlett J, Gakhar L, Penterman J, Singh PK, Mallampalli RK, Porter E, McCray PB: Biochem Soc Trans. 2011 Aug 1;39(4):1012-6
Active starvation responses mediate antibiotic tolerance in biofilms and nutrient limited bacteria. Nguyen D, Lepine F, Datar A, Bauerle E, Olakanmi O, Beer K, McKay G, Siehnel R, Schafhauser J, Britigan B and Singh, PK. Science Nov 18; 334(6058):982-6.
2010 and earlier
Azithromycin maintains airway epithelial integrity during Pseudomonas aeruginosa infections. Halldorsson S, Gudjonsson T, Gottfredsson M, Singh PK, Baldursson O: Am. J. Resp. Cell. Mol. Bio. 2010 Jan;42(1):62-8. Cover article
PLUNC is a Novel Surfactant Protein Secreted by Conducting Airway Epithelia. Gakhar L, Bartlett JA, Penterman J, Mizrachi D, Singh PK, Mallampalli RK, Ramaswamy S, McCray PB. PLOS ONE, 2010 Feb 9;5(2):e9098
A unique regulator controls the activation threshold of quorum-regulated genes in Pseudomonas aeruginosa. Siehnel R, Traxler B, Parsek, M, Schaefer A, Singh PK. Proc Natl Acad Sci. 2010 Apr 27;107(17):7916-21.
Delayed Wound Healing in Diabetic (db/db) Mouse with Pseudomonas aeruginosa Biofilm Infections, A Model for the Study of Chronic Wounds. Wound Repair Regen. Zhao G, Hochwalt P, Usui M, Underwood R, Singh PK, James G, Stewart P, Olerud J, Fleckman P: 2010 Sep-Oct;18(5):467-77.
Targeting bacterial stress responses to enhance antibiotic action. Lee S, Hinz A, Bauerle E, Angermyer A, Juhaszova, K, Kaneko Y, Singh PK, Manoil C: Proc Natl Acad Sci 2009 Aug 25;106(34):14570-5.
Endogenous Oxidative Stress Produces Diversity and Adaptability in Biofilm Communities. Boles BR and Singh PK: Proc Natl Acad Sci U S A. 2008 Aug 26;105(34):12503-8.
The transition metal gallium disrupts iron metabolism in P. aeruginosa and has anti-microbial and anti-biofilm action. Kaneko Y, Thoendel M, Olakanmi O, Britigan BE, Singh PK: J. Clin. Invest. Apr;117(4):877-88, 2007.
Bacterial neuraminidase facilitates mucosal infection by participating in biofilm production. Soong, G, Muir A, Gomez M, Reddy B, Planet P, Singh PK, Kaneko Y, Wolfgang MC, Prince A: J. Clin. Invest. Aug;116(8):2297-2305, 2006.
Mucin-Pseudomonas aeruginosa interactions promote biofilm formation and antibiotic resistance. Landry RM, An D, Hupp JT, Singh PK, Parsek MR:. Mol. Microbiol., Jan;59(1):142-51, 2006.
Evolving stealth: genetic adaptation of Pseudomonas aeruginosa during cystic fibrosis infections. Nguyen D, Singh PK., Proc Natl Acad Sci U S A. 2006 May 30;103(22):8305-6.
Pseudomonas aeruginosa acquires biofilm-like properties within airway epithelial cells. Garcia-Medina R, Dunne WM, Singh PK, Brody SL: Infect. Immun. Dec;73(12):8298-305, 2005.
Genetic variation in biofilms and the insurance effects of diversity. Boles BR, Thoendel M, Singh PK: Microbiology, 151(Pt 9):2816-8, 2005.
Rhamnolipids Mediate Detachment of Pseudomonas aeruginosa from Biofilms. Boles BR, Thoendel M, Singh PK: Mol. Micrbiol., 57(5):1210-23, 2005. Cover article
Cystic Fibrosis Sputum Supports Growth and Cues Key Aspects of Pseudomonas aeruginosa. Physiology. Palmer KL, Mashburn LM, Singh PK, Whiteley M: J Bacteriol, 187(15):5267-77, 2005.
Iron Sequestration by Human Lactoferrin Stimulates P. aeruginosa Surface Motility and Blocks Biofilm Formation. Singh PK: BioMetals 17(3):267-70, 2004.
Boles BR, Thoendel M, Singh PK: Self-Generated Diversity Produces “Insurance Effects” in Biofilm Communities. Proc. Natl. Acad. Sci. USA, 101(47):16630-5, 2004.
Bacterial Biofilms: An Emerging Link to Disease Pathogenesis. Parsek MR, Singh PK:, Annu. Rev. Microbiol., 57:677-701, 2003.
A Component of Innate Immunity Prevents Bacterial Biofilm Development. Singh PK, Parsek MR, Greenberg EP, Welsh MJ: Nature, 417:552-5, 2002.
ExsD is a Negative Regulator of the Pseudomonas aeruginosa Type III Section Regulon. McCaw ML, Lykken L, Singh PK, and Yahr, TL: Mol. Microbiol, 46:1123-1133, 2002.
Antimicrobial Peptides and Proteins in the Innate Defense of the Airway Surface. Travis SM, Singh PK, Welsh MJ; Curr. Opin. Immunol., 13(1):89-95, 2001.
Lactoferrin, An Antimicrobial Factor of Human Airways, Prevents Biofilm Formation by P. aeruginosa. Singh PK, Parsek MR, Welsh MJ, Greenberg EP: Pediatr. Pulmonol., 32:282, 2001.
Synergistic and Additive Killing by Antimicrobial Factors Found in Human Airway Surface Liquid. Singh PK, Tack BF, McCray PB, Welsh MJ: Am. J. Physiol., 279(5):L799-L805, 2000.
Quorum-Sensing Signals Indicate that Cystic Fibrosis Lungs are Infected with Bacterial Biofilms. Singh PK, Schaefer AL, Parsek MR, Moninger TO, Welsh MJ, Greenberg EP: Nature, 407(6805):762-764, 2000.
Activity of Abundant Antimicrobials of the Human Airway. Travis SM, Conway B-AD, Zabner J, Smith JJ, Anderson NN, Singh PK, Greenberg EP, Welsh MJ: Am. J. Respir. Cell Mol. Biol., 20(5):872-879, 1999.
Production of ß-Defensins by Human Airway Epithelia. Singh PK, Jia H-P, Wiles K, Hesselberth J, Liu L, Conway B-A D, Greenberg EP, Valore EV, Welsh MJ, Ganz T, Tack BF, McCray PB Jr: Proc. Natl. Acad. Sci. USA, 95(25):14961-14966, 1998.
Our lab finds these links useful:
UW Box 357735
Seattle WA 98195
1705 NE Pacific St
Seattle WA 98195
Pradeep Singh, MD, Professor
office: (206) 221-7151
lab: (206) 221-7702