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

scholarly journals SPDEF regulates goblet cell hyperplasia in the airway epithelium

2007 ◽  
Vol 117 (4) ◽  
pp. 978-988 ◽  
Author(s):  
Kwon-Sik Park ◽  
Thomas R. Korfhagen ◽  
Michael D. Bruno ◽  
Joseph A. Kitzmiller ◽  
Huajing Wan ◽  
...  
Keyword(s):  
Goblet Cell ◽  
Airway Epithelium ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia

scholarly journals Goblet Cell Hyperplasia Increases SARS-CoV-2 Infection in COPD

2020 ◽  
Author(s):  
Jaspreet K. Osan ◽  
Sattya N. Talukdar ◽  
Friederike Feldmann ◽  
Beth Ann DeMontigny ◽  
Kailey Jerome ◽  
...  
Keyword(s):  
Goblet Cell ◽  
Airway Epithelium ◽  
Critical Role ◽  
Syncytium Formation ◽  
Goblet Cells ◽  
Severe Illness ◽  
Chronic Obstructive ◽  
Cell Hyperplasia ◽  
Obstructive Pulmonary Disease ◽  
Goblet Cell Hyperplasia

SummarySARS-CoV-2 has become a major problem across the globe, with approximately 50 million cases and more than 1 million deaths and currently no approved treatment or vaccine. Chronic obstructive pulmonary disease (COPD) is one of the underlying conditions in adults of any age that place them at risk for developing severe illness associated with COVID-19. We established an airway epithelium model to study SARS-CoV-2 infection in healthy and COPD lung cells. We found that both the entry receptor ACE2 and the co-factor transmembrane protease TMPRSS2 are expressed at higher levels on nonciliated goblet cell, a novel target for SARS-CoV-2 infection. We observed that SARS-CoV-2 infected goblet cells and induced syncytium formation and cell sloughing. We also found that SARS-CoV-2 replication was increased in the COPD airway epithelium likely due to COPD associated goblet cell hyperplasia. Our results reveal goblet cells play a critical role in SARS-CoV-2 infection in the lung.

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 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

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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