Major Areas of Research
- Cellular mechanisms of Inflammation in vivo
- Inflammatory cytokine and lipid mediator networks in host resistance
- Role of innate effector cells in host resistance to tuberculosis
- Role of inflammation in host-directed therapies and vaccine-adjuvant design
The Inflammation and Innate Immunity Unit (IIIU) investigates the function and regulation of inflammatory cytokines and lipid mediators during pulmonary infections, the immunological mechanisms of host protective versus host detrimental inflammation, and the translation of basic observations into host-directed immunotherapies.
In vivo cellular immunological techniques such as highly dimensional multi-parameter flow cytometry are employed in mouse models of pulmonary infection, chief among them Mycobacterium tuberculosis. Findings and hypotheses derived from the mouse model are tested in patient material to advance our understanding of the underlying pathological mechanisms and to aid in the design of novel treatment strategies. In turn, observations in patient material will be studied in appropriate animal models.
Research in the IIIU is based on the hypothesis that during infection distinct arms of innate inflammatory responses establish counter regulatory cytokine and lipid mediator networks that ultimately determine the outcome of infection. Understanding different classes of inflammation and the corresponding innate effector cells, lipids, and cytokines that orchestrate protective versus detrimental inflammatory responses will provide critical insight for the development of new treatment strategies for a variety of inflammatory diseases, including non-infectious chronic inflammatory conditions.
Dr. Mayer-Barber received her diploma in biology from the University of Würzburg, Germany, in 2002. In 2003 she came to the United States for her Ph.D. thesis work in the laboratory of Dr. Markus Mohrs at the Trudeau Institute in Saranac Lake, New York. There she specialized on multi-parameter flow-cytometry analysis of pulmonary CD4 effector T cells after viral and parasitic infections and studied immune cell-derived interferon responses in vivo. She obtained her doctoral degree (Doctor rerum naturalium: Dr. rer. nat.) in 2006 from the University of Würzburg, Germany and joined NIAID in 2007 as a postdoctoral fellow in the Laboratory of Parasitic Diseases. There she studied pulmonary innate effector cells, such as inflammatory monocytes and dendritic cells, and delineated the role of inflammatory mediators like IL-1, type I Interferons and prostaglandins in host resistance to tuberculosis. Dr. Mayer-Barber was awarded the Earl Stadtman Tenure-Track Investigator position in the NIAID Laboratory of Clinical Infectious Diseases in 2015.
Kimber Meyer, Post-Bac IRTA
Claire Tocheny, Post-Bac IRTA
Andrea Bohrer, Senior Scientist
Mayer-Barber KD, Yan B. Clash of the Cytokine Titans: counter-regulation of interleukin-1 and type I interferon-mediated inflammatory responses. Cell Mol Immunol. 2016 Jun 6. Epub ahead of print.
Mayer-Barber KD, Sher A. Cytokine and lipid mediator networks in tuberculosis. Immunol Rev. 2015 Mar;264(1):264-75.
Sionov E, Mayer-Barber KD, Chang YC, Kauffman KD, Eckhaus MA, Salazaar AM, Barber DL, Kwon-Chung KJ. Type I IFN Induction via Poly-ICLC Protects Mice against Cryptococcosis. PLoS Pathog. 2015 Aug 7;11(8):e1005040. *shared first-authorship
Mayer-Barber KD, Andrade BB, Oland SD, Amaral EP, Barber DL, Gonzales J, Derrick SC, Shi R, Kumar NP, Wei W, Yuan X, Zhang G, Cai Y, Babu S, Catalfamo M, Salazar AM, Via LE, Barry CE 3rd, Sher A. Host-directed therapy of tuberculosis based on interleukin-1 and type I interferon crosstalk. Nature. 2014 Jul 3;511(7507):99-103. *corresponding author
Redford PS, Mayer-Barber KD, McNab FW, Stavropoulos E, Wack A, Sher A, O’Garra A. Influenza A virus impairs control of Mycobacterium tuberculosis coinfection through a type I interferon receptor-dependent pathway. J Infect Dis. 2014 Jan 15;209(2):270-4. *shared first-authorship
Mayer-Barber KD *, Andrade BB, Barber DL, Hieny S, Feng CG, Caspar P, White S, Gordon S, Sher A. Innate and adaptive interferons suppress IL-1α and IL-1β production by distinct pulmonary myeloid subsets during Mycobacterium tuberculosis infection. Immunity. 2011 Dec 23;35(6):1023-34. *corresponding author