Department of Veterinary Pathobiology

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: Veterinary Immunology (VPB 5511/8451)
Course Director: Intro to Immunology I (VPB 3551)
Infection and Immunity (Microb 9449)
Advanced Microbial Pathogenesis (Microb 9404)
Research Ethics (VPB 8641)

Selected Publications: (since 2010)

Hilliard, K.A., V.A. Blaho, C.D. Jackson, and C.R. Brown. 2019. Leukotriene B4 receptor BLT1 signaling is critical for neutrophil apoptosis and resolution of experimental Lyme arthritis. FASEB J. Article in press. PMCID In Progress

Ho K.V., K.L. Schreiber, D.C. Vu, S.M. Rottinghaus, D.E. Jackson, C.R. Brown, Z. Lei, L.W. Sumner, M.V. Coggeshall, and C.H. Lin. 2019. Black walnut (Juglans nigra) extracts inhibit proinflammatory cytokine production from lipopolysaccharide-stimulated human promonocytic cell line U-937. Front. Pharmacol. 10:1059. PMCID: PMC6761373

Hilliard, K.A., and C.R. Brown. 2019. Treatment of B. burgdorferi-infected mice with apoptotic cells attenuates Lyme arthritis via PPARg. J. Immunol. 202:1798-1806. PMCID In Progress

Brown, C.R., and E.A. Dennis. 2017. Infection with Borrelia burgdorferi induces lipid mediator production during Lyme arthritis. Biochimie 141:86-90. PMCID: PMC5610093

Lacey, C.A., W.J. Mitchell, C.R. Brown, and J.A. Skyberg. 2017. Temporal role for MyD88 in joint inflammation in a novel model of Brucella-induced musculoskeletal inflammation and arthritis. Infect. Immun. 85:e00961-16. PMCID: PMC5328475

Zhang, Y., R.M. Olson and C.R. Brown. 2017. Macrophage LTB4 drives efficient phagocytosis of Borrelia burgdorferi via BLT1 or BLT2.  J. Lipid Res. 58:494-503. PMCID: PMC5335579

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-g-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 interleukin 17 receptor A-deficient C3H mice with Borrelia burgdorferi does not affect their development of Lyme arthritis and 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., J.M. Hughes Hanks, C.R. Brown, and D.M. Anderson. 2013. Early apoptosis of macrophages induced 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


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