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Decreased expression of Paneth cell antimicrobial peptides coincide with bacterial translocation after starvation
Author(s) -
Hodin Caroline M,
Lenaerts Kaatje,
Haan JaccoJuri,
Grootjans Joep,
Hadfoune M'hamed,
Hooper Lora V,
Heineman Eric,
Buurman Wim A
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.117.8
Subject(s) - paneth cell , chromosomal translocation , lysozyme , enteral administration , bacterial translocation , microbiology and biotechnology , biology , bacteria , medicine , immunology , small intestine , endocrinology , biochemistry , parenteral nutrition , gene , genetics
The lack of enteral feeding, with or without parenteral nutritional support has been reported to result in increased translocation of bacteria, which is considered to play an important role in the high morbidity and mortality rates of critical illnesses such as acute pancreatitis. Recently, Paneth cells, important constituents of the innate intestinal immunity, were shown to be crucial in host protection against invasion of both commensal and pathogenic bacteria. This study investigates the influence of food deprivation on Paneth cell function and small intestinal integrity. Significant decreases in RNA expression of lysozyme (p< 0.01), cryptdin (p< 0.05) and RegIIIγ (p<0.05) were seen after 48 hours of food deprivation in C57BL/6 mice (n=15/group). Accordingly, protein expression of lysozyme and the precursor form of RegIIIγ were also shown to decrease significantly (p<0.01, p<0.05 respectively). Furthermore, increased bacterial translocation to mesenteric lymph nodes occurred (p<0.01), while HE staining showed normal intestinal architecture, distribution and expression of respectively tight junction proteins zonula occludens‐1 and claudin‐3 were unchanged. In conclusion, the current study demonstrates that enteral starvation causes Paneth cell dysfunction paralleled by increased bacterial translocation without disturbances of the small intestinal physical barrier.