期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 117, 期 8, 页码 2313-2324出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI26705
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Cell surface mucin glycoproteins are highly expressed by all mucosal tissues, yet their physiological role is currently unknown. We hypothesized that cell surface mucins protect mucosal cells from infection. A rapid progressive increase in gastrointestinal expression of mucin I (Muc1) cell surface mucin followed infection of mice with the bacterial pathogen Campylobacter jejuni. In the first week following oral infection, C jejuni was detected in the systemic organs of the vast majority of Mucl (-)/(-) mice but never in Muc1(+)/(+) mice. Although C jejuni entered gastrointestinal epithelial cells of both Mucl(-)/(-) and Mucl (+)/(+) mice, small intestinal damage as manifested by increased apoptosis and enucleated and shed villous epithelium was more common in Muc1(-)/(-) mice. Using radiation chimeras, we determined that prevention of systemic infection in wild-type mice was due exclusively to epithelial Mucl rather than Mucl on hematopoietic cells. Expression of MUC1-enhanced resistance to C. jejuni cytolethal distending toxin (CDT) in vitro and CDT null C. jejuni showed lower gastric colonization in Muc1(-)/(-) mice in vivo. We believe this is the first in vivo experimental study to demonstrate that cell surface mucins are a critical component of mucosal defence and that the study provides the foundation for exploration of their contribution to epithelial infectious and inflammatory diseases.
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