Charles R. Brown
Ph.D., University of Chicago (Immunology)
M.S., University of Illinois (Animal Science)
B.S., Quincy College (Biological Sciences)
B.S., Quincy College (Chemistry)
Building Address: 315 Connaway Hall
Phone Number: 573-882-1628
Research Emphasis: 1) Host response to infection and (2) regulation of inflammatory diseases. The primary function of the immune response is to protect the host from harmful microbial invaders. The initial response of the host to microbial infection is to mobilize and recruit innate phagocytic cells (neutrophils and macrophages) to the site of infection where they will engulf and kill the invaders. If required, other more specialized immune cells (T calls and B cells) can be activated to join in the fight. Pathogenic microbes are able to thwart the immune response (at least for a while) and thus cause disease. Understanding the mechanisms used by the host immune response to remove pathogenic microbes, and those used by the microbes to combat this removal, is a primary focus of the lab.
Many of the diseases of the modern world (arthritis, heart disease, cancer, asthma, etc) are considered by many researchers to be caused by chronic inflammation. Inflammation is in general a beneficial response. It occurs in response injury or infection, mediates removal of microbes or irritants, and restores the tissue to its normal function. However, sometimes this process goes awry and the tissue fails to undergo resolution of the inflammation and chronic inflammatory disease ensues. In the past, resolution of inflammation was thought to be a passive event, the irritant was removed and the inflammation just “went away”. Now we know the resolution of inflammation, just like its development, is a tightly controlled process. However, little is known about how the resolution of inflammation is regulated. Bioactive lipids (eicosanoids) are known to be important regulators of inflammatory processes. How these compounds regulate both the development and resolution of inflammation is another primary focus of the lab.
Teaching Responsibilities: Course Director for Veterinary Immunology (VPB 5511/8451) Guest lecturer: Pathogenic Mechanisms in Veterinary Pathobiology (VPB 8436), Research Ethics (VPB 8641), Infection and Immunity (Micro 9001)
Brown, C.R., and E.A. Dennis. 2017. Infection with Borrelia burgdorferi induces lipid mediator production during Lyme arthritis. (Manuscript submitted).
Lasky, C.E., and C.R. Brown. 2017. Characterization of the cellular infiltrate into joints and hearts of C3H mice infected with Borrelia burgdorferi. (Manuscript submitted).
Lacey, C.A., L.L. Keleher, W.J. Mitchell, C.R. Brown, and J.A. Skyberg. 2016. Temporal role for MyD88 in joint inflammation in a novel model of Brucella-induced musculoskeletal inflammation and arthritis. Infect. Immun. 85: e00961-16.
Zhang, Y., R.M. Olson and C.R. Brown. 2016. Macrophage LTB4 drives efficient phagocytosis of Borrelia burgdorferi via BLT1 or BLT2. J. Lipid Res. 58:494-503.
Lasky, C.E., C.L. Pratt, K.A. Hilliard, J.L. Jones, and C.R. Brown. 2016. T cells exacerbate Lyme borreliosis in TLR2-deficient mice. Front. Immunol. 7:1-12. Article 468. PMCID: PMC5093308
Lacey, C.A., L.L. Keleher, W.J. Mitchell, C.R. Brown, and J.A. Skyberg. 2016. CXCR2 mediates Brucella-induced arthritis in IFN--deficient mice. J. Infect. Dis. 214:151-160. PMCID: PMC4907412
Lasky, C.E., K.E. Jamison, D.R. Sidelinger, C.L. Pratt, G. Zhang, and C.R. Brown. 2015. Infection of C3H IL-17RA-deficient mice with Borrelia burgdorferi does not affect their development of Lyme arthritis or carditis. Infect. Immun.83:2882-2888. PMCID: PMC4468557
Lasky, C.E., R.M. Olson, and C.R. Brown. 2015. Macrophage polarization during murine Lyme borreliosis. Infect. Immun. 83:2627-2635. PMCID: PMC4468556
Pratt, C.L., and C.R. Brown. 2014. The role of eicosanoids in experimental Lyme arthritis. Front. Cell. Infect. Microbiol. 4:1-6. PMCID: PMC4036060
Peters, K.N., M.O. Dhariwala, J.M. Hughes Hanks, C.R. Brown, and D.M. Anderson. 2013. Early apoptosis of macrophages modulated by injection of Yersinia pestis YopK promotes progression of primary pneumonic plague. PLoS Pathogens, 9:e1003324. PMCID: PMC3636031
von Moltke, J., N.J. Trinidad, M. Moayeri, A.F. Kintzer, S.B. Wang, N. van Rooijen, C.R. Brown, B.A. Krantz, S.H. Leppla, K. Gronert, R.E.Vance. 2012. Rapid induction of lipid mediators is a novel effector function of the inflammasome in vivo. Nature 490:107-111. PMCID: PMC3465483
Dumlao, D.S., A.M., Cunningham, L.E. Wax, P.C. Norris, J. M. Hughes Hanks, R.E. Halpin, K.M. Lett, V.A. Blaho, W.J. Mitchell, K.L. Fritsche, E.A. Dennis, and C.R. Brown. 2012. Dietary fish oil substitution alters the eicosanoid profile in ankle joints of mice during Lyme infection. J. Nutrit. 142:1582-1589. PMCID: PMC3397342
Eisele, N.A., C.R. Brown, and D.M. Anderson. 2012. Phagocytes and humoral immunity to pneumonic plague. Adv. Exp. Med. Biol. 954: 165-171.
Blaho, V.A., Y. Zhang, J.M. Hughes-Hanks, and C.R. Brown. 2011. 5-Lipoxygenase-deficient mice infected with B. burgdorferi develop persistent arthritis. J. Immunol. 186:3076-3084. PMCID: PMC3346295
Eisele, N.A., H. Lee-Lewis, C. Besch-Williford, C.R. Brown, and D.M. Anderson. 2011. Chemokine receptor CXCR2 mediates bacterial clearance rather than neutrophil recruitment in a murine model of pneumonic plague. Am. J. Pathol. 178:1190-1200. PMCID: PMC3070576
Ritzman, A.M., J. M. Hughes-Hanks, V.A. Blaho, L.E. Wax, W.J. Mitchell, and C.R. Brown. 2010. The chemokine receptor CXCR2 ligand KC (CXCL1) mediates neutrophil recruitment and is critical for development of both experimental Lyme arthritis and carditis. Infect. Immun.78:4593-4600. PMCID: PMC2976349
Bai, F., K.-F. Kong, J. Dai, F. Qian, L. Zhang, C.R. Brown, E. Fikrig, and R.R. Montgomery. 2010. A paradoxical role for neutrophils in the pathogenesis of West Nile Virus. J. Infect. Dis. 202:1804-1812. PMCID: PMC3053000
Blaho, V.A., M.W. Buczynski, E.A. Dennis, and C.R. Brown. 2009. Cyclooxygenase-1 orchestrates the humoral immune response via regulation of IL-17. J. Immunol.183:5644-5653. PMCID: PMC2857380
Blaho, V.A., M.W. Buczynski, C.R. Brown, and E.A. Dennis. 2009. Lipidomic analysis of dynamic eicosanoid responses during the induction and resolution of Lyme arthritis. J. Biol. Chem. 284:21599-21612. PMCID: PMC2755884
Brown, C.R., A.Y-C. Lai, Callen, S.T., V.A. Blaho, J.M. Hughes, and W.J. Mitchell. 2008. Adenoviral delivery of IL-10 fails to attenuate experimental Lyme disease. Infect. Immun. 76:5500-5507. PMCID: PMC2583579
Blaho, V.A., W.J. Mitchell, and C.R. Brown. 2008. Arthritis develops but fails to resolve during inhibition of cyclooxygenase-2 in a murine model of Lyme disease. Arthritis Rheum. 58:1485-1495.
Xu, Q., S.V Seemanapalli, K.E. Reif, C.R. Brown, and F.T. Liang. 2007. Increasing the recruitment of neutrophils to the site of infection dramatically attenuates Borrelia burgdorferi infectivity. J. Immunol. 178:5109-5115.
Montgomery, R.R., C. Booth, X. Wang, V.A. Blaho, S.E. Malawista, and C.R. Brown. 2007. Recruitment of macrophages and polymorphonuclear leukocytes in Lyme carditis. Infect. Immun. 75:613-620. PMCID: PMC1828503