Goblet Cell Hyperplasia in the Airway of Nippostrongylus brasiliensis-Infected Rats

Respiration ◽  
2000 ◽  
Vol 67 (5) ◽  
pp. 565-569 ◽  
Author(s):  
Masaki Tomita ◽  
Takahiko Kobayashi ◽  
Hiroshi Itoh ◽  
Toshio Onitsuka ◽  
Yukifumi Nawa
Keyword(s):  
Goblet Cell ◽  
Nippostrongylus Brasiliensis ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia

scholarly journals The development of an in vitro 3D model of goblet cell hyperplasia using MUC5AC expression and repeated whole aerosol exposures

2021 ◽  
Author(s):  
Linsey E. Haswell ◽  
David Smart ◽  
Tomasz Jaunky ◽  
Andrew Baxter ◽  
Simone Santopietro ◽  
...  
Keyword(s):  
Goblet Cell ◽  
3D Model ◽  
Cell Hyperplasia ◽  
Goblet 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.

scholarly journals Intermittent Oral Coadministration of a Gamma Secretase Inhibitor with Dexamethasone Mitigates Intestinal Goblet Cell Hyperplasia in Rats

2013 ◽  
Vol 42 (2) ◽  
pp. 422-434 ◽  
Author(s):  
Shirley A. Aguirre ◽  
Ling Liu ◽  
Natilie A. Hosea ◽  
Wesley Scott ◽  
Jeffrey R. May ◽  
...  
Keyword(s):  
Goblet Cell ◽  
Gamma Secretase ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia ◽  
Secretase Inhibitor ◽  
Gamma Secretase Inhibitor

scholarly journals Hypoxia-inducible factor-1 signalling promotes goblet cell hyperplasia in airway epithelium

2011 ◽  
Vol 224 (2) ◽  
pp. 203-211 ◽  
Author(s):  
Vasiliy V Polosukhin ◽  
Justin M Cates ◽  
William E Lawson ◽  
Aaron P Milstone ◽  
Anton G Matafonov ◽  
...  
Keyword(s):  
Goblet Cell ◽  
Airway Epithelium ◽  
Hypoxia Inducible Factor ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia ◽  
Hypoxia Inducible Factor 1

Goblet Cell Hyperplasia is not Epithelial-Autonomous in the Cftr Knockout Intestine

2021 ◽  
Author(s):  
Nancy M Walker ◽  
Jinghua Liu ◽  
Sarah M Young ◽  
Rowena A Woode ◽  
Lane L. Clarke
Keyword(s):  
Cell Differentiation ◽  
Goblet Cell ◽  
Ex Vivo ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia ◽  
Cell Numbers ◽  
Markers Of Inflammation ◽  
Tlr4 Agonist ◽  
Goblet Cell Differentiation ◽  
Mucosal Morphology

Goblet cell hyperplasia is an important manifestation of cystic fibrosis (CF) disease in epithelial-lined organs. Explants of CF airway epithelium show normalization of goblet cell numbers; therefore we hypothesized that small intestinal enteroids from Cftr knockout (KO) mice would not exhibit goblet cell hyperplasia. Toll-like receptors 2 and 4 (Tlr2, Tlr4) were investigated as markers of inflammation and influence on goblet cell differentiation. Ex vivo studies found goblet cell hyperplasia in Cftr KO jejunum as compared to wild-type (WT). IL-13, SAM pointed domain-containing ETS transcription factor (Spdef), Tlr2 and Tlr4 protein expression was increased in Cftr KO intestine relative to WT. In contrast, WT and Cftr KO enteroids did not exhibit differences in basal or IL-13-stimulated goblet cell numbers, or differences in expression of Tlr2, Tlr4 and Spdef. Ileal goblet cell numbers in Cftr KO/Tlr4 KO and Cftr KO/Tlr2 KO mice were not different from Cftr KO mice, but enumeration was confounded by altered mucosal morphology. Treatment with Tlr4 agonist LPS did not affect goblet cell numbers in WT or Cftr KO enteroids, whereas the Tlr2 agonist Pam3Csk4 stimulated goblet cell hyperplasia in both genotypes. Pam3Csk4 stimulation of goblet cell numbers was associated with suppression of Notch1 and Neurog3 expression and upregulated determinants of goblet cell differentiation. We conclude that goblet cell hyperplasia and inflammation of the Cftr KO small intestine are not exhibited by enteroids, indicating that this manifestation of CF intestinal disease is not epithelial-automatous but secondary to the altered CF intestinal environment.

scholarly journals IL-12 gene transfer alters gut physiology and host immunity in nematode-infected mice

2001 ◽  
Vol 281 (1) ◽  
pp. G102-G110 ◽  
Author(s):  
Waliul I. Khan ◽  
Patricia A. Blennerhassett ◽  
Yikang Deng ◽  
Jack Gauldie ◽  
Bruce A. Vallance ◽  
...  
Keyword(s):  
Immune Response ◽  
Goblet Cell ◽  
Recombinant Adenovirus ◽  
Trichinella Spiralis ◽  
Nematode Infection ◽  
Interleukin 12 ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia ◽  
Worm Expulsion ◽  
Ifn Γ

Immune responses elicited by nematode parasite infections are characterized by T helper 2 (Th2) cell induction. The immunologic basis for changes in intestinal physiology accompanying nematode infection is poorly understood. This study examined whether worm expulsion and associated goblet cell hyperplasia and muscle contractility share a similar immune basis by shifting the response from Th2 to Th1 using interleukin-12 (IL-12) overexpression. We used a single administration of recombinant adenovirus vector expressing IL-12 (Ad5IL-12) in Trichinella spiralis-infected mice. Ad5IL-12 administered 1 day after infection prolonged worm survival and inhibited infection-induced muscle hypercontractility and goblet cell hyperplasia. This was correlated with upregulated interferon-γ (IFN-γ) expression and downregulated IL-13 expression in the muscularis externa layer. We also observed increased IFN-γ production and decreased IL-4 and IL-13 production from in vitro stimulated spleen and mesenteric lymph node cells of infected Ad5IL-12-treated mice. These results indicate that transfer and overexpression of the IL-12 gene during Th2-based nematode infection shifts the immune response toward Th1 and delays worm expulsion. Moreover, the immune response shift abrogated the physiological responses to infection, attenuating both muscle hypercontractility and goblet cell hyperplasia. These findings strongly indicate that worm expulsion, muscle hypercontractility, and goblet cell hyperplasia share a common immunologic basis and may be causally linked.

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