Charles R. Brown, PhD

Professor

  • Ph.D., University of Chicago (Immunology)
  • M.S., University of Illinois (Animal Science)
  • B.S., Quincy College (Biological Sciences)
  • B.S., Quincy College (Chemistry)
Charles R. Brown

Building Address: 315 Connaway Hall
Phone Number: 573-882-1628
Email: brownchar@missouri.edu

RESEARCH INTERESTS

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

Course Director: Veterinary Immunology (VPB 5511/8451)
Course Director: Intro to Immunology I (VPB 3551)
Microbiology Capstone Course (V_PBio 4980)
Infection and Immunity (Microb 9449)

SELECTED PUBLICATIONS (since 2016)

Jackson, C.D., K.A. Hilliard, and C.R. Brown. 2023 . 12/15-lipoxygenase activity promotes efficient inflammation resolution in a murine model of Lyme arthritis. Front. Immunol . 14:1144172.

Ho, K-V, N. Efrat, K.L. Schreiber, P.H. Vo, M.N. De Canha, A.B. van Staden, B.D. Payne, C.B. Oosthuizen, D. Twilley, Z. Lei, L.W. Sumner, C.R. Brown, N. Lall, and C.H. Lin. 2022. Assessing anti-inflammatory activities and compounds Switchgrass (Panicum virgatum). Agriculture 12:936.

Ho, K-V., K.L. Schreiber, J. Park, P. Vo, Z. Lei, L.W. Sumner, C.R. Brown, and C.H. Lin. 2020. Identification and quantification of bioactive molecules inhibiting pro-inflammatory cytokine production in spent coffee grounds using metabolomics analyses. Front. Pharmacol. 11:229.

Hilliard, K.A., V.A. Blaho, C.D. Jackson and C.R. Brown. 2020. Leukotriene B4 receptor BLT1 signaling is critical for neutrophil apoptosis and resolution of experimental Lyme arthritis. FASEB J. 34:2840-2852.

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 pro-inflammatory cytokine production from LPS-stimulated human pro-monocytic line U-937. Front. Pharmacol. 10:1059 1-11.

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

Brown, C.R., and E.A. Dennis. 2017. Borrelia burgdorferi infection induces lipid mediator production during Lyme arthritis. Biochimie141:86-90 .

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.

Zhang, Y., R.M. Olson and C.R. Brown. 2017. Macrophage LTB 4 drives efficient phagocytosis of Borrelia burgdorferi via BLT1 or BLT2. J. Lipid Res. 58:694-503.

Lasky, C.E., C.L. Pratt, K.A. Hilliard, J.J. Jones, and C.R. Brown. 2016. T cells exacerbate Lyme borreliosis in TLR2-deficient mice. Front. Immunol. 7:1-12. Article 468.

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.