Starvation compromises paneth cells

C.M.I. Hodin, K. Lenaerts, J. Grootjans, J. de Haan, M.h. Hadfoune, F.K. Verheyen, H. Kiyama, E. Heineman, W.A. Buurman*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Lack of enteral feeding, with or without parenteral nutritional support, is associated with increased intestinal permeability and translocation of bacteria. Such translocation is thought to be important in the high morbidity and mortality rates of patients who receive nothing by mouth. Recently, Paneth cells, important constituents of innate intestinal immunity, were found 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 in a mouse starvation model. Quantitative PCR showed significant decreases in mRNA expression of typical Paneth cell antimicrobials, lysozyme, cryptdin, and RegIIIgamma, in ileal tissue after 48 hours of food deprivation. Protein expression levels of lysozyme and RegIIIgamma precursor were also significantly diminished, as shown by Western blot analysis and IHC. Late degenerative autophagolysosomes and aberrant Paneth cell granules in starved mice were evident by electron microscopy, Western blot analysis, and quantitative PCR. Furthermore, increased bacterial translocation to mesenteric lymph nodes coincided with Paneth cell abnormalities. The current study demonstrates the occurrence of Paneth cell abnormalities during enteral starvation. Such changes may contribute to loss of epithelial barrier function, causing the apparent bacterial translocation in enteral starvation.
Original languageEnglish
Pages (from-to)2885-2893
JournalAmerican Journal of Pathology
Issue number6
Publication statusPublished - 1 Jan 2011


Dive into the research topics of 'Starvation compromises paneth cells'. Together they form a unique fingerprint.

Cite this