The Lencer laboratory studies the cell and molecular biology of vesicular transport in polarized epithelial cells and regulation of ion transport in the intestine. These studies relate to how intestinal epithelial cells interact with the luminal and sub-epithelial micro-environment, and to the biology of bacterial pathogenesis and host defense at mucosal surfaces.
The lab has discovered how some enteric bacterial toxins breech the intestinal epithelial barrier and enter host epithelial cells to cause disease. These toxins hijack the cellular and molecular mechanisms of retrograde membrane transport to move from the luminal cell surface into the endoplasmic reticulum (ER) of affected cells, the total reverse of protein biosynthesis.
In another project, the lab studies the cell and molecular biology of the MHC Class I-like IgG receptor FcRn. FcRn transports IgG across mucosal surfaces where it may function in immune surveillance and host defense.
In a third area of interest, the lab aims to understand the mechanisms and regulation of intestinal Cl- secretion, the initial ion transport event in secretory diarrhea.
The Lencer Lab is also conducting research projects on oral and pulmonary delivery of protein therapeutics and on clotrimazole for the treatment of inflammatory bowel disease.
About Wayne Lencer
Wayne Lencer received his MD degree from Boston University School of Medicine. He completed an internship and residency at Boston City Hospital, a clinical and research fellowship at Harvard Medical School/Boston Children's Hospital and a fellowship in cell biology and biophysics at Massachusetts General Hospital, HMS and University of California San Francisco.
Dr. Lencer is the recipient of the Samuel J. Meltzer Basic Research Award from the American Digestive Health Foundation and a Harvard Medical School Teaching Award.
- Chinnapen, D.J., Chinnapen, H., Saslowsky, D. and Lencer, W.I. (2007) Rafting with cholera toxin: endocytosis and trafficking from plasma membrane to ER. FEMS Microbiol Lett. 266: 129-137.
- Dickinson BL, Claypool SM, D'Angelo JA, Aiken ML, Venu N, Yen EH, Wagner JS, Borawski JA, Pierce AT, Hershberg R, Blumberg RS, Lencer WI. 2008. Ca2+-dependent Calmodulin Binding to FcRn Affects Immunoglobulin G Transport in the Transcytotic Pathway. Mol Biol Cell 19:414-423.
- Qiao SW, Kobayashi K, Johansen FE, Sollid LM, Andersen JT, Milford E, Roopenian DC, Lencer WI, Blumberg RS. 2008. Dependence of antibody-mediated presentation of antigen on FcRn. Proc Natl Acad Sci U S A 105:9337-9342. PMCID: PMC2453734
- Saslowsky DE, Lencer WI. 2008. Conversion of apical plasma membrane sphingomyelin to ceramide attenuates the intoxication of host cells by cholera toxin. Cell Microbiol 10:67-80.
- Lencer WI. 2008. Patching a leaky intestine. N Engl J Med 359:526-528. In process.
- Wolf AA, Jobling MG, Saslowsky DE, Kern E, Drake KR, Kenworthy AK, Holmes RK, Lencer WI. 2008. Attenuated endocytosis and toxicity of a mutant cholera toxin with decreased ability to cluster ganglioside GM1 molecules. Infect Immun 76:1476-1484. PMCID: PMC2292862