Innate immune response mechanisms in the intestinal epithelium: potential roles for mast cells and goblet cells in the expulsion of adultTrichinella spiralis

Parasitology ◽  
2008 ◽  
Vol 135 (6) ◽  
pp. 655-670 ◽  
Author(s):  
P. A. KNIGHT ◽  
J. K. BROWN ◽  
A. D. PEMBERTON
Keyword(s):  
Mast Cell ◽  
Goblet Cell ◽  
Intestinal Epithelium ◽  
Trichinella Spiralis ◽  
Goblet Cells ◽  
Mucosal Mast Cell ◽  
Cell Hyperplasia ◽  
Goblet Cell Differentiation ◽  
Mucosal T Cells ◽  
Mast Cell Hyperplasia

SUMMARYGastrointestinal infection with the nematodeTrichinella spiralisis accompanied by a rapid and reversible expansion of the mucosal mast cell and goblet cell populations in the intestinal epithelium, which is associated with the release of their mediators into the gut lumen. Both goblet cell and mast cell hyperplasia are highly dependent on mucosal T-cells and augmented by the cytokines IL-4 and IL-13. However, the contribution of both mast and goblet cells, and the mediators they produce, to the expulsion of the adults ofT. spiralisis only beginning to be elucidated through studies predominantly employingT. spiralis-mouse models. In the present article, we review the factors proposed to controlT. spiralis-induced mucosal mast cell (MMC) and goblet cell differentiation in the small intestine, and focus on some key MMC and goblet cell effector molecules which may contribute to the expulsion of adult worms and/or inhibition of larval development.

scholarly journals Stem cell factor contributes to intestinal mucosal mast cell hyperplasia in rats infected with Nippostrongylus brasiliensis or Trichinella spiralis, but anti-stem cell factor treatment decreases parasite egg production during N brasiliensis infection

Blood ◽  
1995 ◽  
Vol 86 (5) ◽  
pp. 1968-1976 ◽  
Author(s):  
GF Newlands ◽  
HR Miller ◽  
A MacKellar ◽  
SJ Galli
Keyword(s):  
Mast Cell ◽  
Stem Cell ◽  
Stem Cell Factor ◽  
Egg Production ◽  
Trichinella Spiralis ◽  
Mucosal Mast Cell ◽  
Nippostrongylus Brasiliensis ◽  
Cell Hyperplasia ◽  
Interesting Possibility ◽  
Mast Cell Hyperplasia

We assessed the effects of the c-kit ligand, stem cell factor (SCF), in the jejunal mucosal mast cell hyperplasia that occurs during infection with the intestinal nematodes, Nippostrongylus brasiliensis or Trichinella spiralis in rats. Compared with vehicle-treated rats, rats treated with SCF (25 micrograms/kg/d, intravenous [i.v.] for 14 days) during N brasiliensis infection exhibited significantly higher levels of the rat mucosal mast cell (MMC)-associated protease, rat mast cell protease II (RMCP II) in the jejunum and serum on day 8 of infection, but not on days 10 or 15 of infection. By contrast, in comparison to rats treated with normal sheep IgG, rats treated with a polyclonal sheep antirat SCF antibody exhibited markedly decreased numbers of jejunal MMCs, levels of jejunal RMCP II, and serum concentrations of RMCP II during infection with either nematode, particularly at the earlier intervals of infection (< or = day 10). Taken together, these findings indicate that SCF importantly contributes to MMC hyperplasia and/or survival during N brasiliensis or T spiralis infection in rats, but that levels of endogenous SCF are adequate to sustain near maximal MMC hyperplasia during infection with these nematodes. Notably, treatment of rats with SCF somewhat increased, and treatment with anti- SCF significantly decreased, parasite egg production during N brasiliensis infection. This finding raises the interesting possibility that certain activities of intestinal MMCs may contribute to parasite fecundity during infection with this nematode.

scholarly journals Indoles from the commensal microbiota act via the AHR and IL-10 to tune the cellular composition of the colonic epithelium during aging

2020 ◽  
Vol 117 (35) ◽  
pp. 21519-21526 ◽  
Author(s):  
Domonica N. Powell ◽  
Alyson Swimm ◽  
Robert Sonowal ◽  
Alexis Bretin ◽  
Andrew T. Gewirtz ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Goblet Cell ◽  
Intestinal Epithelium ◽  
Dynamic Structure ◽  
Goblet Cells ◽  
Type I ◽  
Cellular Composition ◽  
Type I Ifn ◽  
Commensal Microbiota ◽  
Goblet Cell Differentiation

The intestinal epithelium is a highly dynamic structure that rejuvenates in response to acute stressors and can undergo alterations in cellular composition as animals age. The microbiota, acting via secreted factors related to indole, appear to regulate the sensitivity of the epithelium to stressors and promote epithelial repair via IL-22 and type I IFN signaling. As animals age, the cellular composition of the intestinal epithelium changes, resulting in a decreased proportion of goblet cells in the colon. We show that colonization of young or geriatric mice with bacteria that secrete indoles and various derivatives or administration of the indole derivative indole-3 aldehyde increases proliferation of epithelial cells and promotes goblet cell differentiation, reversing an effect of aging. To induce goblet cell differentiation, indole acts via the xenobiotic aryl hydrocarbon receptor to increase expression of the cytokine IL-10. However, the effects of indoles on goblet cells do not depend on type I IFN or on IL-22 signaling, pathways responsible for protection against acute stressors. Thus, indoles derived from the commensal microbiota regulate intestinal homeostasis, especially during aging, via mechanisms distinct from those used during responses to acute stressors. Indoles may have utility as an intervention to limit the decline of barrier integrity and the resulting systemic inflammation that occurs with aging.

scholarly journals Expression Profiling Reveals Novel Innate and Inflammatory Responses in the Jejunal Epithelial Compartment during Infection with Trichinella spiralis

2004 ◽  
Vol 72 (10) ◽  
pp. 6076-6086 ◽  
Author(s):  
Pamela A. Knight ◽  
Alan D. Pemberton ◽  
Kevin A. Robertson ◽  
Douglas J. Roy ◽  
Steven H. Wright ◽  
...  
Keyword(s):  
Mast Cell ◽  
Goblet Cell ◽  
Expression Profiling ◽  
Time Course ◽  
Inflammatory Responses ◽  
Trichinella Spiralis ◽  
Mucosal Mast Cell ◽  
Screening Process ◽  
Mucin Gene ◽  
Enhanced Production

ABSTRACT Infection with intestinal nematodes induces profound pathological changes to the gut that are associated with eventual parasite expulsion. We have applied expression profiling as an initial screening process with oligonucleotide microarrays (Affymetrix MG-U74AV2 gene chips) and time course kinetics to investigate gene transcription triggered by the intraepithelial nematode Trichinella spiralis in jejunal epithelium from BALB/c mice. Of the 4,114 genes detected, 2,617 were present in all uninfected and T. spiralis-infected replicates, 8% of which were notably upregulated, whereas 12% were downregulated at the time of worm expulsion (day 14 postinfection). Upregulation of goblet cell mucin gene transcripts intestinal mucin gene 3 (MUC3), calcium chloride channel 5 (CLCA5), and goblet cell gene 4 (GOB4) is consistent with enhanced production and alteration of mucus, whereas a 60- to 70-fold upregulation of transcripts for mast cell proteases 1 and 2 (MCPT-1 and -2) is consistent with intraepithelial mucosal mast cell recruitment. Importantly, there was novel expression of sialyltransferase 4C (SIAT4C), small proline-rich protein 2A (SPRR2A), and resistin-like molecule β (RELMβ) on day 14 postinfection. In contrast, DNase I and regenerating protein 3 (REG3) transcripts were substantially downregulated. Time course analyses revealed early (within 48 h of infection) induction of Siat4c, Sprr2A, and Relmβ and later (within 120 h) induction of Mcpt-1 and -2. The findings demonstrate early innate responses and later inflammatory changes within the epithelium. The early epithelial responses may be associated both with repair (Sprr2A) and with the development of innate immunity (Siat4c and Relmβ).

Pharmacologic inhibition of Notch signaling suppresses food antigen–induced mucosal mast cell hyperplasia

2017 ◽  
Vol 139 (3) ◽  
pp. 987-996.e10 ◽  
Author(s):  
Asuka Honjo ◽  
Nobuhiro Nakano ◽  
Susumu Yamazaki ◽  
Mutsuko Hara ◽  
Koichiro Uchida ◽  
...  
Keyword(s):  
Mast Cell ◽  
Notch Signaling ◽  
Mucosal Mast Cell ◽  
Cell Hyperplasia ◽  
Food Antigen ◽  
Mast Cell Hyperplasia ◽  
Pharmacologic Inhibition

scholarly journals Hepatic mucosal mast cell hyperplasia in rats with secondary biliary cirrhosis

Hepatology ◽  
1996 ◽  
Vol 23 (4) ◽  
pp. 888-895 ◽  
Author(s):  
K P Rioux ◽  
K A Sharkey ◽  
J L Wallace ◽  
M G Swain
Keyword(s):  
Mast Cell ◽  
Mucosal Mast Cell ◽  
Biliary Cirrhosis ◽  
Cell Hyperplasia ◽  
Secondary Biliary Cirrhosis ◽  
Mast Cell Hyperplasia

scholarly journals Molecular cloning of mouse intestinal trefoil factor and its expression during goblet cell changes

1995 ◽  
Vol 311 (1) ◽  
pp. 293-297 ◽  
Author(s):  
M Tomita ◽  
H Itoh ◽  
N Ishikawa ◽  
A Higa ◽  
H Ide ◽  
...  
Keyword(s):  
Goblet Cell ◽  
Goblet Cells ◽  
Recovery Phase ◽  
Nippostrongylus Brasiliensis ◽  
Trefoil Factor ◽  
Intestinal Trefoil Factor ◽  
Cell Hyperplasia ◽  
Reverse Transcription Pcr ◽  
Rapid Amplification ◽  
Mitf Expression

A cDNA encoding mouse intestinal trefoil factor (mITF) was successfully cloned and sequenced from the small intestine of C57BL/6 mouse by using the combination of reverse transcription-PCR and rapid amplification of cDNA ends methods. The gene was, similar to rat and human ITFs, mainly expressed in the small and large intestine. The mITF expression was up-regulated during the recovery phase after depletion of goblet cells in acetic acid-induced colitis. On the other hand, the expression in the jejunum was not altered, while goblet cell hyperplasia was induced by Nippostrongylus brasiliensis infection. These results suggest that the mITF expression did not simply correlate with the number of goblet cells. The mITF may play an important role in the maintenance and repair of mucosal function of the rectum. Additionally, the mITF in the jejunum may play a role in alteration of the physicochemical nature of goblet cell mucins, thereby affecting the establishment of intestinal helminths.

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