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)
Zhang, Y. and C.R. Brown. 2012. Effect of 5-lipoxygenase-deficiency on phagocytosis in mouse leukocytes:the implication of chronic Lyme disease. Manuscript submitted.
Peters, K.N., J.M. Hughes Hanks, C.R. Brown, and D.M. Anderson. 2012. Early apoptosis of macrophages induced by injection of Yersinia pestis YopK promotes progression of primary pneumonic plague. PLoS Pathogen, Manuscript in revision.
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, In Press.
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.
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.
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.
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.
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.
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.
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
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.
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.
Brown, C.R., V.A. Blaho, K.L. Fritsche, and C.M. Loiacono. 2006. STAT1-deficiency exacerbates carditis but not arthritis during experimental Lyme borreliosis. J. Interferon Cytokine Res. 26:18-27.
Fritsche, K., R. Irons, L. Pompos, J. Janes, Z. Zheng, and C. Brown. 2005. Omega-3 poly-unsaturated fatty acid impairment of early host resistance against Listeria monocytogenes infection is independent of neutrophil infiltration and function. Cell. Immunol. 235:65-71.
Wilson, A.P., J.J. Thelen, J. Lakritz, C.R. Brown, and A.E. Marsh. 2004. The identification of a sequence related to apicomplexan enolase from Sarcocystis neurona. Parasitol. Res. 94:354-360.
Ray, A., D. Kumar, A. Shakya, C.R. Brown, and B.K. Ray. 2004. Serum amyloid A-activating factor-1 (SAF-1) transgenic mice are prone to develop a severe form of inflammation-induced arthritis. J. Immunol. 173:4684-4691.
Brown, C.R., V.A. Blaho, and C.M. Loiacono. 2004. Treatment of mice with the neutrophil-depleting antibody RB6-8C5 results in early development of experimental Lyme arthritis via the recruitment of Gr-1- PMN-like cells. Infect. Immun. 72:4956-4965.
Brown, C.R., V.A. Blaho, and C.M. Loiacono. 2003. Susceptibility to experimental Lyme arthritis correlates with KC and MCP-1 production in joints and requires neutrophil recruitment via CXCR2. J. Immunol.171:893-901.
Johnson, J.J., C.W. Roberts, C. Pope, F. Roberts, M.J. Kirisits, R. Estes, E. Mui, T. Krieger, C.R. Brown, J. Forman, and R. McLeod. 2002. In vitro correlates of Ld restricted resistance to Toxoplasmic encephalitis and their critical dependence on parasite strain. J. Immunol. 169:966-973.
Brown, C.R., and S.L. Reiner. 2000. Genes outside the major histocompatability complex control resistance and susceptibility to development of experimental Lyme arthritis. Med. Microbiol. Immunol. 198:85-90.
Brown, C.R., and S.L. Reiner. 2000. Bone-marrow chimeras reveal hemopoietic and nonhemopoietic control of resistance to experimental Lyme arthritis. J. Immunol.165:1446-1452.