photo of Patrick Geraghty

Patrick Geraghty, PhD

Research Assistant Professor
Division of Pulmonary and Critical Care Medicine.
Associate Program Director of Research and Academic Development, Department of Internal Medicine.

Education and Training

Positions held:

  • Associate Program Director Internal Medicine Residency Program, SUNY Downstate Health Sciences University, Brooklyn, 2019-ongoing
  • Assistant Professor, SUNY Downstate Health Sciences University, Brooklyn, 2015-ongoing
  • Associate Research Scientist (Dept of Medicine) Mount Sinai Roosevelt Hospital, Mount Sinai Health Systems, New York, 2014-2015
  • Associate Research Scientist (Dept of Medicine) St. Luke's Roosevelt Hospital, New York, 2011-2014


  • Postdoctoral Research T32 Fellow, Columbia University College of Physicians and Surgeons, New York, 2007-2011
  • Postdoctoral Research Scientist, Royal College of Surgeons in Ireland, Dublin, Ireland, 2004-2007

Graduate School:

  • Microbiology PhD, National University of Ireland, Maynooth, Co. Kildare, Ireland, 2000-2004

Career/Research Interests

The primary interest of my research is to investigate immune responses in healthy and diseased lungs. I am particularly interested in immune responses in three lung diseases, chronic obstructive pulmonary disease (COPD), alpha-1 antitrypsin deficiency, and pulmonary fibrosis. The long-term goal of my research is to identify key players associated with lung damage and resolution of sustained inflammation. We employ several approaches to studying lung diseases, including transgenic and knock-out mouse models, cigarette smoke animal exposure models, pulmonary viral infection animal models, pulmonary function testing in mice, primary mammalian cell culture systems, flow cytometry and immunohistochemistry. We provide basic research techniques training to pulmonary fellows, internal medicine residents, and students. The major active research topics within the lab are:

Resolution of lung inflammation by phosphatases.

Despite the role of phosphatases being extensively characterized in multiple organs and diseases, the role of phosphatases in the lung is limited; especially in cigarette smoke exposure and lung infection models. Viral infections are considered a major driving factor of COPD exacerbations and thus contribute disease morbidity and mortality. We primarily focus on one phosphatase, protein phosphatase 2A (PP2A), and we have identified that PP2A regulates several key responses linked to disease progression, such as apoptosis, and cytokine production. However, phosphatase responses are desensitized in the lung by prolonged cigarette smoke exposure and leave the lung more susceptible to enhanced damage due to prolonged inflammation. We perform molecular and medicinal techniques to target new therapies to treat the diseased lung.

Targeting lung S100A9-associated inflammation.

Elevated expression of S100A9, a damage-associated molecular pattern molecule, is observed in COPD and alpha-1 antitrypsin deficient patients. We have identified that S100A9 signaling significantly impacts lung damage. We study the function and signaling mechanisms of S100A9 in multiple lung diseases and using molecular and medicinal techniques we have identified that targeting S100A9 signaling may be a promising therapeutic approach.

Dr. Geraghty’s research is funded by The Flight Attendant Medical Research Institute (FAMRI), The Alpha-1 Foundation, The Department of Defense, NIH, Medical Research Council (MRC) – UK, and SUNY Downstate University Funds.

  1. Railwah, C., Lora, A., Zahid, K., Goldenberg, H., Campos, M., Wyman, A., Jundi B., Ploszaj, M., Rivas, M., Dabo, A.J., Majka, S.M., Foronjy, R., El Gazzar, M., and Geraghty, P. Cigarette smoke induction of S100A9 contributes to chronic obstructive pulmonary disease. Am J Physiol Lung Cell Mol Physiol. (2020) Dec 1;319(6):L1021-L1035. doi: 10.1152/ajplung.00207.2020.
  2. Gupta, G., Baumlin, N., Poon, J., Ahmed, B., Chiang, Y.-P., Railwah, C., Kim, M.D., Rivas, M., Goldenberg, H., Elgamal, Z., Salathe, M., Panwala, A.A., Dabo, A., Huan, C., Foronjy, R., Jiang, X.-C., Wadgaonkar, R., and Geraghty, P. Airway resistance caused by sphingomyelin synthase 2 insufficiency in response to cigarette smoke. J. Respir. Cell Mol. Biol. (2020) Mar;62(3):342-353. doi: 10.1165/rcmb.2019-0133OC
  3. Campos, M.A., Geraghty, P., Escobar, L.A., Holt, G., Donna, E., Mendes, E., Newby, P.R., Ma, S., Luna-Diaz, L.V., Turino, G.M., Stockley, R.A. The biological effects of double-dose alpha-1 antitrypsin augmentation therapy: A pilot study. Am J Respir Crit Care Med. (2019) Aug 1;200(3):318-326. doi: 10.1164/rccm.201901-0010OC.
  4. Doherty, D.F., Nath, S., Poon, J., Foronjy, R.F., Ohlmeyer, M., Dabo, A.J., Salathe, M., Birrell, Belvisi, M.M., Baumlin, N., Kim, M.D., Weldon, S., Taggart, C. and Geraghty, P. Protein Phosphatase 2A Reduces Cigarette Smoke-Induced Cathepsin S and Loss of Lung Function. Am J Respir Crit Care Med. (2019) Jul 1;200(1):51-62. doi: 10.1164/rccm.201808-1518OC.
  5. Nath, S., Ohlmeyer, M., Salathe, M.A., Poon, J., Baumlin, N., Foronjy, R.F. and Geraghty, P. Chronic cigarette smoke exposure subdues PP2A activity by enhancing expression of the oncogene CIP2A. J. Respir. Cell Mol. Biol., (2018) Dec;59(6):695-705. doi: 10.1165/rcmb.2018-0173OC.
  6. Geraghty, P., Hadas, E., Kim, B.-H., Dabo, A.J., Volsky, D.J. and Robert Foronjy, F. HIV infection model of chronic obstructive pulmonary disease in mice. Am J Physiol Lung Cell Mol Physiol. (2017) Apr 1;312(4):L500-L509. doi: 10.1152/ajplung.00431.2016. Epub 2017 Jan 19.
  7. Foronjy, R., Salathe, M., Dabo, A.J., Baumlin, N., Cummins, N., Eden, E. and Geraghty, P. TLR9 expression is required for the development of cigarette smoke-induced emphysema in mice. Am J Physiol Lung Cell Mol Physiol. (2016) Jul 1;311(1):L154-66. doi: 10.1152/ajplung.00073.2016. Epub 2016 Jun 10.
  8. Foronjy, R.F., Ochieng, P.O., Salathe, M.A., Dabo, A.J., Eden, E., Baumlin, N., Cummins, N., Barik, S., Campos, M., Thorp, E.B. and Geraghty, P. Protein tyrosine phosphatase 1B negatively regulates S100A9-mediated lung damage during respiratory syncytial virus exacerbations. Mucosal Immunol. (2016) Sep;9(5):1317-29. doi: 10.1038/mi.2015.138. Epub 2016 Jan 27.
  9. Foronjy, R.F., Taggart, C.C., Dabo, A.J., Weldon, S., Cummins, N. and Geraghty, P. Type I interferons induce lung protease responses following respiratory syncytial virus infection via RIG-I-like receptors. Mucosal Immunol. (2015) Jan;8(1):161-75. doi: 10.1038/mi.2014.54. Epub 2014 Jul 9.
  10. Geraghty, P., Eden, E., Pillai, M., Campos, M., McElvaney, N.G. and Foronjy, R.F. α-1 antitrypsin activates protein phosphatase 2A (PP2A) to counter lung inflammatory responses. Am J Respir Crit Care Med. (2014) Dec 1;190(11):1229-42. doi: 10.1164/rccm.201405-0872OC.
  11. Brehm, A., Geraghty, P., Campos, M. Gaffney, A., Eden, E., Jiang, X.C., D’Armiento, J.M. and Foronjy, R.F. Cathepsin G degradation of phospholipid transfer protein (PLTP) augments pulmonary inflammation. FASEB J. 2014 Feb 28;9(2):e90567. doi: 10.1371/journal.pone.0090567.
  12. Foronjy, R.F., Taggart, C.C., Dabo, A.J., Weldon, S. and Geraghty, P. Respiratory syncytial virus infections enhance cigarette smoke induced COPD in mice. PLoS One. (2014) Feb 28;9(2):e90567. doi: 10.1371/journal.pone.0090567. eCollection 2014.
  13. Geraghty, P., Hardigan, A. and Foronjy, R.F. Cigarette smoke activates the proto-oncogene c-Src to promote airway inflammation and lung tissue destruction. J. Respir. Cell Mol. Biol., (2014) 2014 Mar;50(3):559-70. doi: 10.1165/rcmb.2013-0258OC.
  14. Geraghty, P., Hardigan, A., Wallace, A.M., Mirochnitchenko, O., Thankachen, J., Arellanos, L., Thompson, V., D’Armiento, J.M. and Foronjy, R.F. The GPx1-PTP1B-PP2A axis: a key determinant of airway inflammation and alveolar destruction. Am J Respir Cell Mol Biol. (2013) Nov;49(5):721-30. doi: 10.1165/rcmb.2013-0026OC.
  15. Geraghty, P., Dabo, A.J. and D'Armiento, J. TLR4 Protein Contributes to Cigarette Smoke-induced Matrix Metalloproteinase-1 (MMP-1) Expression in Chronic Obstructive Pulmonary Disease. J Biol Chem. (2011) 286 (34): 30211-8.

For a complete list of my contributions to science, please visit my National Library of Medicine Bibliography