Gao Lab

The research activities in Gao’s laboratory are focusing on revealing the molecular mechanisms that regulate inflammatory events during acute lung injury, sepsis, and inflammatory bone diseases. Specially, we are identifying the function of complements and their receptors in acute lung injury, sepsis, and inflammatory bone diseases. We are dissecting the function of transcription factors, cytokines and their networks of interaction, which underlie the inflammatory process in airway injury and bone.

One project we developed is determining the role of transcription factors including STAT3 and C/EBP in acute lung injury induced by immune complexes, LPS, and pneumonia. We have demonstrated that STAT3 plays a complex role in acute lung injury. We show that transcription factor C/EBP may be a key downstream molecule of STAT3. Furthermore, our study suggests that STAT3 acetylation seems to regulate its activities. We are currently testing the hypothesis that STAT3 exerts its regulatory function during acute lung injury by activating multiple target genes, which differentially regulate FcRs and TLR4-mediated inflammatory responses in the lung. In collaborating with Professor Charles Serhan’s group, we are determining the role of lipid mediators in acute lung injury. Our studies have been supported by two NIH grants from NHLBI.

Another project that we are working on is characterization of the roles of SOCS3 signaling and the C5a receptors, C5aR and C5L2, in the inflammation-associated bone diseases. We have demonstrated that osteoblasts express both C5aR and C5L2, and unexpectedly, we found that C5a down-regulated LPS-induced IL-6 release from osteoblasts. Our hypothesis is that osteoblasts can exert their functions like macrophages during inflammation, and C5a/C5aRs signaling may play an important role in inflammatory bone diseases by regulating TLR-mediated inflammatory responses. Furthermore, our recent work demonstrated that SOCS3 plays an important regulatory role in osteoblast inflammatory response.

Principal Investigator

Hongwei Gao, M.D., Ph.D.

Hongwei Gao

Hongwei Gao, M.D., Ph.D. is an Assistant Professor of Anaesthesia at Harvard Medical School.

The long-term objective of my lab is to dissect the cellular and molecular mechanisms that regulate immune and inflammatory events during lung injury and multi-organ failure in sepsis. In recent years, it has become clear that the complement system plays an important immunoregulatory role at the interface of innate and acquired immunity during inflammation. Our research uses a combination of cell biology, molecular biology, immunology, and experimental pathology to identify the function of complement, especially C5a and its receptors, in acute lung injury and pulmonary dysfunction during sepsis. We are also interested in dissecting the function of transcription factors, cytokines and their networks of interaction, which underlie the inflammatory process in airway injury. Ultimately, a more complete knowledge of the causative mechanisms in airway injury and multi-organ failure will promote the goal of devising more effective strategies for the prevention and treatment of lung diseases and sepsis.

  • Postdoctoral Fellow, Pathology, University of Michigan.
  • Ph.D., Microbiology and Molecular Genetics, Michigan State University
  • M.D., Joint Eight-Year-Program, Nankai University and Tianjin Medical University

Current Personnel 2012–2013

  • Hanna H. TangHanna H. Tang, MD, Ph.D. Research Fellow
  • Yan-Lan LiuYan-Lan Liu, M.D. Research Fellow
  • Chunguang YanChunguang Yan, B.Sc. Ph.D. Graduate Student
  • Ximo WangXimo Wang, M.D., Ph.D. Visiting Professor – Professor and Vice President Tianjin Ren-Min Hospital NanKai University Affiliated Hospital
  • Heather KearneyHeather Kearney Support Staff

Select Recent Publications

  • Yan, C., Cao, J., Wu, M., Zhang, W., Jiang, T., Yoshimura, A., Gao, H. “Suppressor of cytokine signaling 3 inhibits LPS-induced IL-6 expression by suppressing CCAAT/enhancer-binding protein β activity.” J. Biol. Chem. 2010; 285(48):37227-39.
  • Wu, M., Huang, H., Zhang, W., Skannan, S., Weaver, A., Mckibben, M., Herington, D., Zeng, H., Gao, H. “Host DNA repair proteins in response to P. aeruginosa in lung epithelial cells and in mice.” Infection and Immunity 2011; 79(1):75-87.
  • Yuan, K, Huang, C, Fox, J, Gaid, M, Weaver, A, Li, GP, Singh, BB, Gao, H, Wu, M. “Elevated inflammatory response in Caveolin-1 deficient mice with P. aeruginosa infection is mediated by STAT3 and NF-{kappa}B.” J. Biol. Chem. 2011; 286(24):21814-25.
  • Tang, H., Yan, C., Sarma, J.V., Haura, E.B., Wu, M., Gao, H. “An essential role for Stat3 in regulating IgG immune complex-induced pulmonary inflammation.” FASEB J. 2011, Dec;25(12):4292-300.
  • “C5a-regulated CCAAT/enhancer binding protein β and -δ are essential in Fcγ receptor- mediated inflammatory cytokine and chemokine production in macrophages.” Yan C, Zhu M, Staiger J, Johnson PF, Gao H. J Biol Chem. 2012 Jan 27;287(5):3217-30.
  • Yuan, K., Huang, C., Zhang, B., Yin, Q., Fox III, J., Laturnus, D., Carlson, E., Gao, H., Wu, M. “Autophagy plays an essential role in the clearance of P. aeruginosa by alveolar macrophages.” J Cell Sci. 2012, 15;125(Pt 2):507-15.
  • Yan C, Wang X, Cao J, Wu M, Gao H. “CCAAT/Enhancer-Binding Protein gamma Is a Critical Regulator of IL-1beta-Induced IL-6 Production in Alveolar Epithelial Cells.” PLoS One 2012, 7:e35492.
  • Guo, Q., Shen, N., Yuan, K., Li, J., Wu, H., Zeng, Y., FoxIII, J., Bansal, AK, Singh, B., Gao, H., Wu, M. “Caveolin-1 plays a critical role in host immunity against Klebsiella pneumoniae by regulating STAT5 and Akt activity.” European Journal of Immunology. 2012, 42:1-13.
  • Yan, C., Wu, M., Cao J., Tang, H., Zhu, M., Johnson, P.F. Gao, H. “Critical Role for CCAAT/Enhancer Binding Protein β in Immune Complex-Induced Acute Lung Injury.” J Immunol. 2012 Aug 1;189(3):1480-90.


Members of the Gao Lab can be reached at 617-525-5021