Zhou Zhu M.D., Ph.D.
Associate Professor of Pediatrics (Immunology) and of Medicine (Immunology)
siglecs; eosinophils (Siglec-8); neutrophils (Siglec-9); apoptosis; pulmonary diseases such as asthma and COPD
Glycobiology of inflammatory lung diseases
Siglec-8 in eosinophil inflammation and asthma
Siglec-9 in neutrophil inflammation and COPD
SHP-1 regulation of allergic and inflammatory diseases
Role of SHIP-1 in anaphylaxis and asthma
Pulmonary inflammation is an important immune response that underlies many diseases, including asthma and COPD. Cytokines, chemokines, and other factors play important roles in initiation, regulation, and resolution of inflammation in the lung. Our laboratory is interested in understanding the molecular mechanisms and specific pathways that regulate inflammation. Our studies involve clinical samples including tissues and cells from patients and we utilize animal models of allergen induced, cytokine induced, and spontaneous inflammatory responses in the lung. These include allergen sensitization and challenge models, transgenic models in which specific cytokines or factors are targeted to the lung, and natural mutant models. Using these models and techniques we will be able to identify novel molecules and pathways that mediate or regulate pulmonary inflammation.
Extensive Research Description
Another area of research is in understanding the regulatory mechanisms in food allergy and anaphylaxis. During allergen-triggered responses, for example in anaphylaxis, activation of immune cells, release of mediators, and tissue and cellular responses are involved but are highly regulated by many factors. Using animal models of anaphylaxis we are identifying some of these factors, processes and the underlying mechanisms. Findings from these studies will help us to understand, and enable us to modify and improve the anaphylactic processes.
- Wang, Y., Z. Zhu, T. D. Church, N. L. Lugogo, D. Francisco, J. L. Ingram, M. Huggins, D. Beaver, J. R. Wright, and M. Kraft. 2012. Role of SHP-1 in the regulation of Mycoplasma pneumoniae-induced inflammation in asthmatic airway epithelial cells. J Immunol 188:3371-3381.
- Aloulou, M., S. B. Mkaddem, M. Biarnes-Pelicot, T. Boussetta, H. Souchet, E. Rossato, M. Benhamou, B. Crestani, Z. Zhu, U. Blank, P. Launay, and R. C. Monteiro. 2012. IgG1 and IVIg induce inhibitory ITAM signaling through FcgammaRIII controlling inflammatory responses. Blood 119:3084-3096.
- Cho, S. H., S. Y. Oh, Z. Zhu, J. Lee, and A. P. Lane. 2012. Spontaneous eosinophilic nasal inflammation in a genetically-mutant mouse: comparative study with an allergic inflammation model. PLoS ONE 7(4):e35114.
- Yu, J., M. H. Oh, J. U. Park, A. C. Myers, C. Dong, Z. Zhu, and T. Zheng. 2012. Epicutaneous exposure to staphylococcal superantigen enterotoxin B enhances allergic lung inflammation via an IL-17A dependent mechanism. PLoS One 7(7):e39032.
- Zhou, L., S. Y. Oh, Y. Zhou, B. Yuan, F. Wu, M. H. Oh, Y. Wang, C. Takemoto, N. Van Rooijen, T. Zheng, and Z. Zhu. 2013. SHP-1 Regulation of Mast Cell Function in Allergic Inflammation and Anaphylaxis. PLoS One 8:e55763.
- Kim, Y. S., E. J. Choi, W. H. Lee, S. J. Choi, T. Y. Roh, J. Park, Y. K. Jee, Z. Zhu, Y. Y. Koh, Y. S. Gho, and Y. K. Kim. 2013. Extracellular vesicles, especially derived from Gram-negative bacteria, in indoor dust induce neutrophilic pulmonary inflammation associated with both Th1 and Th17 cell responses. Clin Exp Allergy 43:443-454.
- Kiwamoto, T., M. E. Brummet, F. Wu, M. G. Motari, D. F. Smith, R. L. Schnaar, Z. Zhu, and B. S. Bochner. 2013. Mice deficient in the St3gal3 gene product alpha2,3 sialyltransferase (ST3Gal-III) exhibit enhanced allergic eosinophilic airway inflammation. J Allergy Clin Immunol (E-Published July 2, 2013).
- Oh, M. H., S. Y. Oh, J. N. Lu, H. F. Lou, A. C. Myers, Z. Zhu, and T. Zheng. 2013. TRPA1-Dependent Pruritus in IL-13-Induced Chronic Atopic Dermatitis. J Immunol (Accepted).