Simvastatin reduziert die TGF-β1-vermittelte Proliferation und Adhäsion von humanen intestinalen Lamina propria Fibroblasten (HILPF) aus fibrotischer Mukosa von Patienten mit Morbus Crohn und moduliert den Smad3-vermittelten TGF-β1 Signalweg

Background: Patients with endotracheal intubation or tracheostomy are subject to benign tracheal stenosis (TS), for which current therapies are unsatisfactory. We conducted a preliminary investigation of drugs and drug combinations for the prevention and treatment of TS in a rabbit model. Methods: Fifty-four rabbits were apportioned into nine groups according to treatment: sham-operated control; untreated TS model; amikacin; budesonide; erythromycin; penicillin; amikacin + budesonide; erythromycin + budesonide; and penicillin + budesonide. TS was induced by abrasion during surgery. The drugs were applied for 7 days before and 10 days after the surgery. Rabbits were killed on the eleventh day. Tracheal specimens were processed for determining alterations in the thicknesses of tracheal epithelium and lamina propria via hematoxylin and eosin. The tracheal mRNA (assessed by real-time quantitative polymerase chain reaction) expressions of the following fibrotic-related factors were determined: transforming growth factor-β1 (TGF- β1), collagen type I (COL1A1), collagen type III (COL3A1), and interleukin-17 (IL-17). The protein levels of TGF-β1, COL1A1, and COL3A1 were determined through immunohistochemistry and integrated optical densities. Results: Compared with all other groups, the untreated TS model had significantly thicker tracheal epithelium and lamina propria, and higher mRNA and protein levels of all targeted fibrotic factors. The mRNA and protein levels of the targeted fibrotic factors in all the drug-treated groups were lower than those of the untreated TS model, and differences were most significant in the erythromycin + budesonide group. Conclusions: Erythromycin combined with budesonide may reduce inflammation and modify fibrosis progression in TS after tracheal injury.

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Sequential BMP7/TGF-β1 signaling and microbiota instruct mucosal Langerhans cell differentiation

Journal of Experimental Medicine ◽

10.1084/jem.20171508 ◽

2018 ◽

Vol 215 (2) ◽

pp. 481-500 ◽

Cited By ~ 12

Author(s):

Tal Capucha ◽

Noam Koren ◽

Maria Nassar ◽

Oded Heyman ◽

Tsipora Nir ◽

...

Keyword(s):

Dendritic Cells ◽

Cell Differentiation ◽

Lamina Propria ◽

Langerhans Cells ◽

Tissue Destruction ◽

Step Process ◽

Mucosal Homeostasis ◽

Tgf Β1

Mucosal Langerhans cells (LCs) originate from pre–dendritic cells and monocytes. However, the mechanisms involved in their in situ development remain unclear. Here, we demonstrate that the differentiation of murine mucosal LCs is a two-step process. In the lamina propria, signaling via BMP7-ALK3 promotes translocation of LC precursors to the epithelium. Within the epithelium, TGF-β1 finalizes LC differentiation, and ALK5 is crucial to this process. Moreover, the local microbiota has a major impact on the development of mucosal LCs, whereas LCs in turn maintain mucosal homeostasis and prevent tissue destruction. These results reveal the differential and sequential role of TGF-β1 and BMP7 in LC differentiation and highlight the intimate interplay of LCs with the microbiota.

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Eosinophils from Murine Lamina Propria Induce Differentiation of Naïve T Cells into Regulatory T Cells via TGF-β1 and Retinoic Acid

PLoS ONE ◽

10.1371/journal.pone.0142881 ◽

2015 ◽

Vol 10 (11) ◽

pp. e0142881 ◽

Cited By ~ 12

Author(s):

Hong-Hu Chen ◽

Ai-Hua Sun ◽

David M. Ojcius ◽

Wei-Lin Hu ◽

Yu-Mei Ge ◽

...

Keyword(s):

T Cells ◽

Retinoic Acid ◽

Regulatory T Cells ◽

Lamina Propria ◽

Naive T Cells ◽

Naïve T Cells ◽

Tgf Β1

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Porcine Vocal Fold Lamina Propria-Derived Biomaterials Modulate TGF-β1-Mediated Fibroblast Activation in Vitro

ACS Biomaterials Science & Engineering ◽

10.1021/acsbiomaterials.9b01837 ◽

2020 ◽

Vol 6 (3) ◽

pp. 1690-1703 ◽

Cited By ~ 2

Author(s):

Camilo Mora-Navarro ◽

Andreea Badileanu ◽

Ana M. Gracioso Martins ◽

Emily W. Ozpinar ◽

Lewis Gaffney ◽

...

Keyword(s):

Lamina Propria ◽

Vocal Fold ◽

Fibroblast Activation ◽

Tgf Β1

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Faculty Opinions recommendation of Eosinophils from Murine Lamina Propria Induce Differentiation of Naïve T Cells into Regulatory T Cells via TGF-β1 and Retinoic Acid.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.725949619.793533750 ◽

2017 ◽

Author(s):

Amy Klion

Keyword(s):

T Cells ◽

Retinoic Acid ◽

Regulatory T Cells ◽

Lamina Propria ◽

Naive T Cells ◽

Naïve T Cells ◽

Tgf Β1

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Evaluation of TGF-β1 and EGFR in Cleft Affected Lip Mucosa

Acta medica Lituanica ◽

10.15388/amed.2021.28.1.14 ◽

2021 ◽

Vol 28 (1) ◽

pp. 14

Author(s):

Olga Rimdenoka ◽

Māra Pilmane

Keyword(s):

Epithelial Cells ◽

Lamina Propria ◽

Oral Mucosa ◽

Rank Correlation ◽

Control Group ◽

Orofacial Cleft ◽

Tissue Samples ◽

Moderate Number ◽

Healthy Mucosa ◽

Tgf Β1

Background. The morphopathogenesis of orofacial cleft development is only partly understood; therefore, it is important to identify factors, which possibly could be involved in it. The aim of the study was to evaluate the distribution of TGF-β1 and EGFR-containing cells in cleft affected lip mucosa.Materials and Methods. The study group included lip mucosa tissue samples from 14 patients with orofacial cleft. The control group contained 11 healthy oral mucosa tissue samples. The tissue sections were stained by immunohistochemistry for TGF-β1 and EGFR. The expression of positive structures was graded semiquantitatively. IBM SPSS 26.0 was used for statistical analysis, Spearman`s rank correlation and Mann-Whitney U tests were performed.Results. Mostly few to moderate number (+/++) of TGF-β1-containing cells was found in epithelium, also the same number of fibroblasts and macrophages was seen in the lamina propria of cleft affected lip mucosa. Meanwhile, healthy oral mucosa on average demonstrated a moderate number (++) of TGF-β1-containing epithelial cells, fibroblasts, and macrophages. A variable, mostly indistinct number of EGFR-containing cells was seen in the epithelium of cleft affected lip mucosa, meanwhile, mostly no (0) EGFR positive cells were found in the epithelium of healthy mucosa. Statistically significantly less TGF-β1-containing cells were found in the epithelium of cleft affected lip mucosa than in the healthy mucosa (U=33.000; p=0.015). Also, the lamina propria of cleft affected lip mucosa showed statistically significantly less TGF-β1 immunoreactive fibroblasts and macrophages than the healthy mucosa (U=28.500; p=0.006).Conclusions. The decreased number of TGF-β1-containing epithelial cells, fibroblasts and macrophages in cleft affected lip mucosa proves the role of problematic tissue remodelation in the cleft pathogenesis. The distribution of EGFR in cleft affected and healthy mucosa is similar and possibly does not play a role in the cleft development of humans.

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Scanning Electron Microscopy of Human Jejunum in Whipple's Disease

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100079279 ◽

1977 ◽

Vol 35 ◽

pp. 354-355

Author(s):

John H. L. Watson ◽

C. N. Sun

Keyword(s):

Electron Microscopy ◽

Scanning Electron Microscopy ◽

Basement Membrane ◽

Lamina Propria ◽

Brush Border ◽

Whipple’S Disease ◽

Whipple's Disease ◽

Biopsy Specimens ◽

Brush Borders ◽

Scanning Electron

That the etiology of Whipple's disease could be bacterial was first suggested from electron micrographs in 1960. Evidence for binary fission of the bacteria, their phagocytosis by histiocytes in the lamina propria, their occurrence between and within the cells of the epithelium and on the brush border of the lumen were reported later. Scanning electron microscopy has been applied by us in an attempt to confirm the earlier observations by the new technique and to describe the bacterium further. Both transmission and scanning electron microscopy have been used concurrently to study the same biopsy specimens, and transmission observations have been used to confirm those made by scanning.The locations of the brush borders, the columnar epithelial cells, the basement membrane and the lamina propria beneath it were each easily identified by scanning electron microscopy. The lamina propria was completely filled with the wiener-shaped bacteria, Fig. 1.

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The protease phenotype and crystalline nature of the granules of intraepithelial mast cells in Trichinella spiralis-infected mice

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100140464 ◽

1995 ◽

Vol 53 ◽

pp. 818-819

Author(s):

D.S. Friend ◽

N. Ghildyal ◽

M.F. Gurish ◽

K.F. Austen ◽

R.L. Stevens

Keyword(s):

Small Intestine ◽

Mast Cells ◽

Epithelial Cells ◽

Lamina Propria ◽

Trichinella Spiralis ◽

Intestinal Epithelial ◽

Carboxypeptidase A ◽

C3h Mice ◽

Granule Morphology ◽

Crystalline Nature

Trichinella spiralis induces a profound mastocytosis and eosinophilia in the small intestine of the infected mouse. Mouse mast cells (MC) store in their granules various combinations of at least five chymotryptic chymases [designated mouse MC protease (mMCP) 1 to 5], two tryptic proteases designated mMCP-6 and mMCP-7 and an exopeptidase, carboxypeptidase A (mMC-CPA). Using antipeptide, protease -specific antibodies to these MC granule proteases, immunohistochemistry was done to determine the distribution, number and protease phenotype of the MCs in the small intestine and spleen 10 to >60 days after Trichinella infection of BALB/c and C3H mice. TEM was performed to evaluate the granule morphology of the MCs between intestinal epithelial cells and in the lamina propria (mucosal MCs) and in the submucosa, muscle and serosa of the intestine (submucosal MCs).As noted in the table below, the number of submucosal MCs remained constant throughout the study. In contrast, on day 14, the number of MCs in the mucosa increased ~25 fold. Increased numbers of MCs were observed between epithelial cells in the mucosal crypts, in the lamina propria and to a lesser extent, between epithelial cells of the intestinal villi.

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