Major Areas of Research
- The Systemic Capillary Leak Syndrome (Clarkson disease)
- Fungal-associated asthma
- Signal mechanisms of G protein-coupled receptors
The LVIS conducts broad and in-depth translational research that focuses on fundamental processes underlying allergic inflammation. Our research program includes studies aimed at mechanistic dissection of fungal associated-asthma and exploration of the pathogenesis of the rare vascular disorder resembling systemic anaphylaxis, a condition known as systemic capillary leak syndrome (SCLS, Clarkson disease). SCLS is a life-threatening disorder of unknown etiology in which patients experience spontaneous and recurrent episodes of hypovolemic shock and edema in the absence of allergic triggers. In the area of fungal asthma, we have identified a fungal protease allergen (Alp1) that is deposited in the airways of patients with severe asthma, and we have elucidated detailed mechanisms by which Alp1 promotes airway smooth muscle contraction and bronchoconstriction. Finally, ongoing studies in the LVIS include G protein-coupled receptor (GPCR)-dependent mechanisms of allergic inflammation, more specifically on the role of Regulators of G protein Signaling (RGS) proteins in lung and inflammatory cells.
Dr. Druey obtained his M.D. from Rush Medical College in Chicago, Illinois. In 1992, following a residency in internal medicine at The New York Hospital/Cornell Medical Center, Dr. Druey became a postdoctoral fellow in the NIAID Laboratory of Immunoregulation. He joined the Laboratory of Allergic Diseases in 1997 to become chief of the Molecular Signal Transduction Section. In 2020, the section was renamed the Lung and Vascular Inflammation Section.
Zhihui (Sherry) Xie, Ph.D., Staff Scientist
Eunice C. Chan, Ph.D., Biologist
Wong GS, Redes JL, Balenga N, McCullough M, Fuentes N, Gokhale A, Koziol-White C, Jude JA, Madigan LA, Chan EC, Jester WH, Biardel S, Flamand N, Panettieri RA Jr, Druey KM. RGS4 promotes allergen- and aspirin-associated airway hyperresponsiveness by inhibiting PGE2 biosynthesis. J Allergy Clin Immunol 2020 Mar 19;S0091-6749(20)30372-9.
Raza A, Xie Z, Chan EC, Chen WS, Scott LM, Eisch AR, Krementsov DN, Rosenberg HF, Parikh SM, Blankenhorn EP, Teuscher C, Druey KM. A natural mouse model reveals genetic determinants of Systemic Capillary Leak Syndrome (Clarkson disease). Commun Biol. 2019 Oct 31;2:398.
Redes JL, Basu T, Ram-Mohan S, Ghosh CC, Chan EC, Sek AC, Zhao M, Krishnan R, Rosenberg HF, Druey KM. Aspergillus fumigatus-Secreted Alkaline Protease 1 Mediates Airways Hyperresponsiveness in Severe Asthma. Immunohorizons 2019 Aug 6;3(8):368-377.
Chan EC, Ren C, Xie Z, Jude J, Barker T, Koziol-White CA, Ma M, Panettieri RA Jr, Wu D, Rosenberg HF, Druey KM. Regulator of G protein signaling 5 restricts neutrophil chemotaxis and trafficking. J Biol Chem. 2018 Aug 17;293(33):12690-12702
Xie Z, Chen WS, Yin Y, Chan EC, Terai K, Long LM, Myers TG, Dudek AZ, Druey KM. Adrenomedullin surges are linked to acute episodes of the systemic capillary leak syndrome (Clarkson Disease).(link is external) J Leukoc Biol 2018 Apr;103(4):74
Balenga NA, Klichinsky M, Xie Z, Chan EC, Zhao M, Jude J, Laviolette M, Panettieri RA Jr, Druey KM. A fungal protease allergen provokes airway hyper-responsiveness in asthma. Nat Commun 2015 Apr 13;6:6763.