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Immunology & Infectious Disease

Immunology is the study of how animals react to foreign substances such as infectious agents and allergens. The host immune system consists of hundreds of molecules, cells, and lymphoid organs such as the bone marrow and spleen. Because we live in a sea of microbes, the immune system is constantly engaged in a battle that prevents microbes from invading and consuming the cells of our bodies. Immunology research at MSU focuses on improving our basic understanding of how the host immune system functions, such that new approaches can be developed to vaccinate against a broader spectrum of infectious diseases in people and animals, and so that new approaches can be developed to prevent detrimental immune responses such as asthma or organ transplant rejection.

Infectious diseases of humans and animals are caused by a wide spectrum of microorganisms including single-cell bacteria, multicellular parasites, viruses or infectious proteins known as ‘prions’ (i.e., causative agent of ‘mad cow disease’). Infectious disease research at MSU focuses on understanding the biology of each specific group of infectious agents and learning how these specific microbes produce disease when infections are established in people or animals.

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Montana State University

Division of Graduate Education

Molecular Biosciences Program

P.O. Box 172580
Bozeman, MT 59717-2580

(406) 994-6652 mbprogram@montana.edu

 

Molecular BIOSciences |> Immunology & Infectious Disease
|> Faculty |> Allen G Harmsen, Ph. D

Pulmonary immunology

Current Research

Research in the Harmsen Lab encompasses the areas of Pulmonary Immunology and Immunopathology. The lung is extremely susceptible to infection because of the constant deposition of potential pathogens in the airways that results from breathing contaminated air. Thus, the lung must respond to these pathogens quickly and intensely to avoid infection. Although these host immune and inflammatory responses usually are successful in preventing infection, these processes can also be damaging to the host. This is especially a problem for the lung because the delicate lace-like structure of lung tissue is easily damaged. In addition, misguided immune responses to inhaled noninfectious antigens, such as allergens, can directly cause serious diseases such as asthma and bronchitis.

The major goal of our research is to better understand how the lung immune responses can resist infections and yet limit "collateral" host damage caused by the immune response. In the process of studying these mechanisms of resistance and tissue damage, our lab utilizes animal models of disease. These include mouse models of influenza, Pneumocystis carinii pneumonia, and Streptococcus as well as bovine models of viral and bacterial pneumonia.

Recent Publications

Hall-Stoodley, L, G Watts, J Crowther, A Balagopal, J Torrelles, J Robinson-Cox, R Bargatze, A Harmsen, E Crouch and L Schlesinger. 2006. Mycobacterium tuberculosis binding to human Surfactant Poteins A and D, fibronectin and small airway epithelial cells under shear. Infect. Immun. 74:3587-96.

Bonnett, CR, EJ Cornish, AG Harmsen, and JB Burritt. 2006. Early neutrophil recruitment and aggregation in the murine lung inhibit germination of Aspergillus fumigatus conidia. Infect. Immun. 74:6528-39.

Moyron-Quiroz, JE, J Rangel-Moreno, L Hartson, MP Tighe, KD Klonowski, L Lefrancois, LS Caughly, AG Harmsen, FE Lund, and TD Randall. 2006. Persistence and responsiveness of immunologic memory in the absence of secondary lymphoid organs. Immunity. 4:643-54.

McNamee, LA and AG Harmsen. 2006. Both influenza-induced neutrophil dysfunction and neutrophil-independent mechanisms contribute to increased susceptibility to a secondary Streptococcus pneumoniae infection. Infect. Immun. 74:6707-21.

Rutkowski, MR and AG Harmsen. 2007. Trichomonas foetus: Pathogenesis of acute infection in normal, estradiol-treated, and stressed mice. Exp. Parasitol. 115: 143-59.

Rutkowski, MR, LA McNamee and AG Harmsen. 2007. Neutrophils and INOS are critical for early resistance to the establishment of Tritrichomonas foetus infection. J. Parasitol. Jun;93(3):562-74.

Kaiser, CR, ML Flenniken, AG Harmsen, AL Harmsen, M A Jutila, T Douglas, and M J Young. 2007. Biodistribution studies of protein cage nanoparticles demonstrate broad tissue distribution and rapid clearance in vivo. International J. Nanomedicine 2007;2(4):715-33.

Meissner, NN, M Rutkowski, A Harmsen, S Hann, AG Harmsen. 2007. Type I IFN-signaling and B cells maintain hematopoiesis during Pneumocystis infection of the lung. J. Immunol.178 (10) 6604-15.

Swain S, S Han, A Harmsen, K Shampeny, and AG Harmsen 2007. Pulmonary Hypertension Can Be A Sequela Of Prior Pneumocystis Pneumonia. Am J Pathol. 171:790-799.

Wiley, J.A. and Harmsen AG 2008. Pneumocystis Infection Enhances Antibody-Mediated Resistance to a Subsequent Influenza Infection. J Immunol 180: 5613-24. NIHMS 58413.

Haynes, J.R., Dokken L., Wiley J.A., Cawthon A.G., Bigger J., Harmsen A.G., Richardson C. 2009 Influenza-pseudotyped Gag virus-like particle vaccines provide broad protection against highly pathogenic avian influenza challenge. Vaccine 27(4): 530-41.

King, Q. O., B. Lei, and A. G. Harmsen. 2009. Pneumococcal Surface Protein A Contributes to Secondary Streptococcus pneumoniae Infection following Influenza Infection. J. Infect. Dis. 200:537–545. NIHMSID #138083.

Pittet, Lynnelle A., Hall-Stoodley ,Luanne, Rutkowski Melanie R., Harmsen ,Allen G. 2009. Influenza virus infection decreases tracheal mucociliary velocity and clearance of Streptococcus pneumoniae. Am Journal of Respiratory Cell and Molecular Biology. In Press.

Wiley, James A, Richert, Laura E., Swain, Steve, Harmsen, Ann L., Barnard, Dale L., Randall, Troy D., Jutila, Mark A, Douglas, Trevor, Broomell, Chris, Young, Mark, Harmsen, Allen G. 2009. Inducible Bronchus-associated Lymphoid Tissue Elicited by a Protein Cage Nanoparticle Enhances Protection in Mice Against Diverse Respiratory Viruses. PLoS ONE. manuscript #: 09-PONE-RA-11940. Published September 23, 2009.


 
Allen G Harmsen, Ph. D


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