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Endocytosis in enterocytes

Endozytose in Enterozyten

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Summary

Endocytosis is a fundamental cell biological process, which carries out essential functions in a polarized epithelial cell such as enterocytes provided with a huge surface area of the brush border membrane. Major tasks of enterocytes, which are regulated by endocytic signals, are digestion and absorption of nutrients and drugs/pharmacological agents, barrier permeability to microorganism, toxins and antigens, and transcytotic crosstalk between intestinal lumen and lamina propria cells with access to the circulation.

Investigations on inflammatory bowel diseases such as food allergy, celiac disease, Crohn’s disease, and ulcerative colitis focus on immune processes originating within enterocytes as antigen presenting cells. Thus the initiation of oral tolerance, that is, the binding of food antigens to MHC class II proteins, might be localized within late endosomes of enterocytes. Furthermore, the late endosomal compartment of enterocytes seems to be involved in the processing of luminal antigens during the pathogenesis of celiac disease and inflammatory bowel diseases. Investigations of inherited diseases such as microvillus inclusion disease have revealed a pathogenetic defect in the autophagocytotic and/or recycling pathway of enterocytes.

Our progress in the cell and molecular biological understanding of the endocytosis and the methodical opportunities of translational research offer now new therapeutic options for patients suffering from endocytosis-related diseases of enterocytes.

Zusammenfassung

Endozytose ist ein fundamentaler zellbiologischer Prozess mit essentiellen Funktionen für polarisierte Epithelzellen wie Enterozyten, die mit einer Bürstensaummembran ausgestattet sind. Wichtige Aufgaben der Enterozyten, die durch endozytische Signale gesteuert werden, sind Verdauung und Resorption von Nährstoffen und (pharmakologischen) Wirkstoffen, Barrierefunktion und Permeabilitätssteuerung gegenüber Mikroorganismen, Toxinen und Antigenen sowie transzytotischer "crosstalk" zwischen Darmlumen und Zellen der Lamina propria.

Die Erforschung entzündlicher Darmerkrankungen wie Nahrungsmittelallergien, Zöliakie, Morbus Crohn und Colitis ulcerosa schließt Immunprozesse ein, die ihren Ursprung in Enterozyten als antigenpräsentierenden Zellen nehmen. So könnte die Initiierung oraler Toleranz, d.h. die Bindung von Nahrungsmittelantigenen an MHC II Proteine, in späten Endosomen von Enterozyten lokalisiert sein. Weiterhin scheint in Enterozyten das späte endosomale Kompartiment durch Prozessierung luminaler Antigene in der Pathogenese der Zöliakie und chronisch-entzündlicher Darmerkrankungen (M. Crohn, Colitis ulzerosa) eine Rolle zu spielen. Pathogenetische Defekte der Autophagozytose und/oder endosomalen Recyclings von Enterozyten wurden auch in angeborenen Erkrankungen wie der Microvillus-Inklusion-Erkrankung gefunden.

Das verbesserte zell- und molekularbiologische Verständnis der Endozytose und die methodischen Möglichkeiten der translationalen Forschung geben Patienten mit Endozytose-assoziierten Erkrankungen Hoffnung auf neue therapeutische Optionen.

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Authors and Affiliations

  1. Department of General Pediatrics and Neonatology, Zentrum für Kinderheilkunde und Jugendmedizin UKGM, Standort Gießen/Justus-Liebig University, Feulgenstr. 12, 35392, Gießen, Germany

    Klaus-Peter Zimmer & Jan de Laffolie

  2. Department of Translational Medical Science, University of Naples, Federico II, Via S. Pansini 5, 80131, Napoli, Italy

    Maria Vittoria Barone

  3. Department of Physiological Chemistry, University of Veterinary Medicine, Buenteweg 17, 30559, Hannover, Germany

    Hassan Y. Naim

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  1. Klaus-Peter Zimmer
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  2. Jan de Laffolie
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Correspondence to Klaus-Peter Zimmer.

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K.-P. Zimmer, J. de Laffolie, M. V. Barone, and H. Y. Naim declare that there are no actual or potential conflicts of interest in relation to this article.

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Zimmer, KP., de Laffolie, J., Barone, M. et al. Endocytosis in enterocytes. Wien Med Wochenschr 166, 205–210 (2016). https://doi.org/10.1007/s10354-016-0448-z

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