The Allen laboratory studies the fundamental biology of phagocytes, both neutrophils and macrophages, and manipulation of their function by the Gram-negative bacterial pathogens Helicobacter pylori and Francisella tularensis. H. pylori lives in the human stomach and is the primary cause of peptic ulcers and gastric cancer. Notably, this pathogen elicits a chronic, neutrophil-dominant inflammatory response that fails to control the infection and instead promotes tissue destruction and disease. Our goal is to elucidate the mechanisms that allow H. pylori to thrive in a neutrophil-rich environment. Current projects are related to our discovery that H. pylori exploits neutrophil plasticity as part of its virulence strategy, eliciting N1-like subtype differentiation that is notable for profound nuclear hypersegmentation. F. tularensis is an intracellular pathogen that replicates in the cytosol of host cells and causes tularemia. Current studies focus on the roles of capsule and bacterial lipoproteins in virulence and links between cell metabolism and inflammation.
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M616B Medical Sciences Building
Columbia, MO 65212
- Mechanisms of phagocytosis and phagosome maturation.
- Signal transduction pathways in phagocytes.
- Mechanisms of NADPH oxidase regulation and perturbation by pathogenic microbes.
- Neutrophil phenotypic plasticity in host defense and cancer.
- Perturbation of neutrophil function and lifespan by Helicobacter pylori.
- Pathogenesis of tularemia with a focus on macrophages and neutrophils.
- Roles of F. tularensis O-antigen and capsule in virulence.
- Metabolic reprogramming of host cells by bacterial pathogens and consequences for virulence and inflammation.
- Muscle macrophage activation state in nociceptor signaling and fibromyalgia
Areas of Expertise
- Human neutrophils
- Human and murine macrophages
- NADPH oxidase
- Bacterial pathogensis
- Mechansims of cell death
- Neutrophil plasticity
- Regulation of inflammation
Education & Training
Postdoctoral Fellow, Laboratory of Cellular Physiology and Immunology, and Laboratory of Signal Transduction, The Rockefeller University
PhD, Biochemistry, University of Wisconsin-Madison
MS, Biochemistry, University of California-Riverside
BS, Biochemistry, University of California-Riverside
Awards & Honors
- 2019-2023 Member, FASEB Board of Directors
- 2018-2020 Kate Daum Professorship, University of Iowa
- 2018-2019 President of the Society for Leukocyte Biology
- 2018-pres. Fellow of the American Academy of Microbiology
- 2016-2017 President-Elect of the Society for Leukocyte Biology
- 2016-2020 Associate Director, Center for Immunology and Immune Based Diseases, U. Iowa
- 2013 Chair, Phagocytes Gordon Research Conference, June 9-14, 2013.
- 2011 Vice Chair, Gordon Research Conference on Phagocytes, June 19-24, 2011
- 2009-2012 Treasurer of the Society for Leukocyte Biology (2 terms, elected position).
- 2003-2005 Nominating Committee of the Society for Leukocyte Biology (Chair in 2005)
- 1997-1998 Biosciences Initiative Award, University of Iowa
- 1992-1995 NIH/NIAID Individual Postdoctoral Fellowship F32 NRSA
- 1991-1992 Charles H. Revson Fellow, The Rockefeller University
- Allen, L.-A.H. and Criss, A.K. (2019) Cell intrinsic functions of neutrophils and their modulation by pathogens. Curr. Opin. Immunol. 60:124-129. PMID: 31302568.
- Kinkead, L. C., Whitmore, L. C., McCracken, J. M., Fletcher, J. R., Ketelsen, B. B., Kaufman, J. W., Jones, B. D., Weiss, D. S., Barker, J. H. & Allen, L.-A. H. (2018). Bacterial lipoproteins and other factors released by Francisella tularensis modulate human neutrophil lifespan: Effects of a TLR1 SNP on apoptosis inhibition. Cellular Microbiology, 20(2). PMID: 29063667.
- Whitmore, L. C., Weems, M. N. & Allen, L.-A. H. (2017). Cutting Edge: Helicobacter pylori Induces Nuclear Hypersegmentation and Subtype Differentiation of Human Neutrophils In Vitro. J. Immunol., 198(5), 1793-1797. PMID: 28148734.
- Long, M. E., Lindemann, S. R., Rasmussen, J. A., Jones, B. D. & Allen, L.-A.H. (2013). Disruption of Francisella tularensis Schu S4 iglI, iglJ, and pdpC genes results in attenuation for growth in human macrophages and in vivo virulence in mice and reveals a unique phenotype for pdpC. Infect. Immun., 81(3), 850-61. PMID: 23275090.