Enhancement by cholera toxin of IgA secretion from intestinal crypt epithelium.

Cryptdin mRNA codes for the apparent precursor to a corticostatin/defensin-related peptide that accumulates to high levels in mouse intestinal crypt epithelium during postnatal development. The primary structure, intestinal cell distribution, and developmental appearance of cryptdin mRNA have been determined. Cryptdin mRNA is 450-480 nucleotides long. Translation of the partial cryptdin cDNA sequence reveals a 70-amino acid open reading frame that includes 32 carboxy-terminal residues that align with those in the consensus sequence, C.CR...C....ER..G.C....CCR, which is a common feature of leukocyte defensins and lung corticostatins (Selsted, M. E., D. M. Brown, R. J. DeLange, S. S. L. Harwig, and R. I. Lehrer. 1985. J. Biol. Chem. 260:4579-4584; Zhu, Q., J. Hu, S. Mulay, F. Esch, S. Shimasaki, and S. Solomon. 1988. Proc. Natl. Acad. Sci. USA. 85:592-596). In situ hybridization of cryptdin cDNA to paraformaldehyde-fixed, frozen sections of adult jejunum and ileum showed intense and specific labeling of epithelial cells in the base of all crypts. Analysis of sections from suckling mice showed that cryptdin mRNA is detectable in 10-20% of crypts in 10-d-old mice, in approximately 80% of crypts in 16-d-old mice, and in all crypts of mice 20 d and older. During the fourth week, the sequence accumulates in crypts to the maximal adult level. Cryptdin mRNA content in adult small intestine is independent both of T cell involvement and luminal bacteria. The role of cryptdin in small bowel physiology remains to be determined: cryptdin may inhibit bacterial translocation, modulate intestinal hormone synthesis, influence hormonal sensitivity of the intestinal epithelium, or exhibit a multiplicity of related activities.

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Studies on Small Intestinal Crypt Epithelium

Gastroenterology ◽

10.1016/s0016-5085(19)34696-7 ◽

1964 ◽

Vol 47 (5) ◽

pp. 480-495 ◽

Cited By ~ 40

Author(s):

Jerry S. Trier

Keyword(s):

Intestinal Crypt ◽

Crypt Epithelium ◽

Small Intestinal

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Apoptosis of intestinal crypt epithelium after Cryptosporidium parvum infection

Journal of Infection and Chemotherapy ◽

10.1007/s10156-003-0259-1 ◽

2003 ◽

Vol 9 (3) ◽

pp. 278-281 ◽

Cited By ~ 35

Author(s):

Takeshi Sasahara ◽

Tomoko Sekiguchi ◽

Yoshinori Satoh ◽

Hidero Kitasato ◽

Matsuhisa Inoue ◽

...

Keyword(s):

Cryptosporidium Parvum ◽

Intestinal Crypt ◽

Crypt Epithelium

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STUDIES ON SMALL INTESTINAL CRYPT EPITHELIUM

The Journal of Cell Biology ◽

10.1083/jcb.18.3.599 ◽

1963 ◽

Vol 18 (3) ◽

pp. 599-620 ◽

Cited By ~ 92

Author(s):

Jerry S. Trier

Keyword(s):

Endoplasmic Reticulum ◽

Cytoplasmic Membrane ◽

Secretory Granules ◽

Goblet Cells ◽

Paneth Cells ◽

Intestinal Crypt ◽

Crypt Epithelium ◽

Dense Bodies ◽

Undifferentiated Cells ◽

Small Intestinal

Small intestinal crypt epithelium obtained from normal fasting humans by peroral biopsy of the mucosa was studied with the electron microscope. Paneth cells were identified at the base of the crypts by their elaborate highly organized endoplasmic reticulum, large secretory granules, and small lysosome-like dense bodies within the cytoplasm. Undifferentiated cells were characterized by smaller cytoplasmic membrane-bounded granules which were presumed to be secretory in nature, a less elaborate endoplasmic reticulum, many unattached ribosomes and, in some cells, the presence of glycogen. Some undifferentiated cells at the base of the crypts contained lobulated nuclei and striking paranuclear accumulations of mitochondria. Membrane-bounded cytoplasmic fragments, probably originating from undifferentiated and Paneth cells, were frequently apparent within crypt lumina. Of the goblet cells, some were seen actively secreting mucus. In these, apical mucus appeared to exude into the crypt lumen between gaps in the microvilli. The membrane formerly surrounding the apical mucus appeared to fuse with and become part of the plasma membrane of the cell, suggesting a merocrine secretory mechanism. Enterochromaffin cells were identified by their location between the basal regions of other crypt cells and by their unique intracytoplasmic granules.

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IFN-γ and IL-17A regulate intestinal crypt production of CXCL10 in the healthy and inflamed colon

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00208.2019 ◽

2020 ◽

Vol 318 (3) ◽

pp. G479-G489 ◽

Cited By ~ 3

Author(s):

Travis Walrath ◽

Robert A. Malizia ◽

Xinjun Zhu ◽

Stephen P. Sharp ◽

Shanti S. D'Souza ◽

...

Keyword(s):

Intestinal Inflammation ◽

Ex Vivo ◽

Colonic Crypt ◽

Intestinal Crypt ◽

Colon Crypt ◽

Crypt Epithelium ◽

Negative Effect ◽

Cytokine Milieu ◽

Ifn Γ

During intestinal inflammation, immature cells within the intestinal crypt are called upon to replenish lost epithelial cell populations, promote tissue regeneration, and restore barrier integrity. Inflammatory mediators including TH1/TH17-associated cytokines influence tissue health and regenerative processes, yet how these cytokines directly influence the colon crypt epithelium and whether the crypt remains responsive to these cytokines during active damage and repair, remain unclear. Here, using laser-capture microdissection and primary colon organoid culture, we show that the cytokine milieu regulates the ability of the colonic crypt epithelium to participate in proinflammatory signaling. IFN-γ induces the TH1-recruiting, proinflammatory chemokine CXCL10/IP10 in primary murine intestinal crypt epithelium. CXCL10 was also induced in colonic organoids derived from mice with active, experimentally induced colitis, suggesting that the crypt can actively secrete CXCL10 in select cytokine environments during colitis. Colon expression of cxcl10 further increased during infectious and noninfectious colitis in Il17a−/− mice, demonstrating that IL-17A exerts a negative effect on CXCL10 in vivo. Furthermore, IL-17A directly antagonized CXCL10 production in ex vivo organoid cultures derived from healthy murine colons. Interestingly, direct antagonism of CXCL10 was not observed in organoids derived from colitic mouse colons bearing active lesions. These data, highlighting the complex interplay between the cytokine milieu and crypt epithelia, demonstrate proinflammatory chemokines can be induced within the colonic crypt and suggest the crypt remains responsive to cytokine modulation during inflammation. NEW & NOTEWORTHY Upon damage, the intestinal epithelium regenerates to restore barrier function. Here we observe that the local colonic cytokine milieu controls the production of procolitic chemokines within the crypt base and colon crypts remain responsive to cytokines during inflammation. IFN-γ promotes, while IL-17 antagonizes, CXCL10 production in healthy colonic crypts, while responses to cytokines differ in inflamed colon epithelium. These data reveal novel insight into colon crypt responses and inflammation-relevant alterations in signaling.

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