期刊
JOURNAL OF INFECTIOUS DISEASES
卷 204, 期 9, 页码 1349-1357出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jir544
关键词
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资金
- ICDDR, B: Centre for Health and Population Research
- National Institute of Allergy and Infectious Diseases, National Institutes of Health [U01 AI058935, RO3 AI063079, U01 AI077883]
- International Research Scientist Development Award [K01 TW07409, K01 TW07144]
- Charles H. Hood Foundation
- Howard Hughes Medical Institute
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.
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