LPLUNC1 modulates innate immune responses to vibrio cholerae

Ok S. Shin, Taher Uddin, Robert Citorik, Jennifer P. Wang, Patricia Della Pelle, Richard L. Kradin, Colin D. Bingle, Lynne Bingle, Andrew Camilli, Taufiqur R. Bhuiyan, Tahmina Shirin, Edward T. Ryan, Stephen B. Calderwood, Robert W. Finberg, Firdausi Qadri, Regina C. Larocque, Jason B. Harris

Research output: Contribution to journalArticlepeer-review

43 Citations (Scopus)


Background. Recent studies demonstrate that long palate, lung, and nasal epithelium clone 1 protein (LPLUNC1) is involved in immune responses to Vibrio cholerae, and that variations in the LPLUNC1 promoter influence susceptibility to severe cholera in humans. However, no functional role for LPLUNC1 has been identified.Metods.We investigated the role of LPLUNC1 in immune responses to V. cholerae, assessing its affect on bacterial growth and killing and on innate inflammatory responses to bacterial outer membrane components, including purified lipopolysaccharide (LPS) and outer membrane vesicles. We performed immunostaining for LPLUNC1 in duodenal biopsies from cholera patients and uninfected controls.Results.LPLUNC1 decreased proinflammatory innate immune responses to V. cholerae and Escherichia coli LPS. The effect of LPLUNC1 was dose-dependent and occurred in a TLR4-dependent manner. LPLUNC1 did not affect lipoprotein-mediated TLR2 activation. Immunostaining demonstrated expression of LPLUNC1 in Paneth cells in cholera patients and controls.Conclusions.Our results demonstrate that LPLUNC1 is expressed in Paneth cells and likely plays a role in modulating host inflammatory responses to V. cholerae infection. Attenuation of innate immune responses to LPS by LPLUNC1 may have implications for the maintenance of immune homeostasis in the intestine.

Original languageEnglish
Pages (from-to)1349-1357
Number of pages9
JournalJournal of Infectious Diseases
Issue number9
Publication statusPublished - 2011 Nov 1
Externally publishedYes

Bibliographical note

Funding Information:
Financial Support. This work was supported by the ICDDR,B: Centre for Health and Population Research; the National Institute of Allergy and Infectious Diseases, National Institutes of Health (U01 AI058935 to S. B. C., RO3 AI063079 to F. Q., and U01 AI077883 to E. T. R.); International Research Scientist Development Award (K01 TW07409 to J. B. H.); Charles H. Hood Foundation Child Health Research Award (J. B. H.); International Research Scientist Development Award (K01 TW07144 to R. C. L.); and Physician-Scientist Early Career Award from the Howard Hughes Medical Institute (R. C. L.). Potential conflicts of interest. All authors: No reported conflicts.

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases


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