Local Immune Changes in Early Stages of Inflammation and Carcinogenesis Correlate with the Collagen Scaffold Changes of the Colon Mucosa
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388971%3A_____%2F21%3A00542929" target="_blank" >RIV/61388971:_____/21:00542929 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/67985823:_____/21:00542929 RIV/68378041:_____/21:00542929 RIV/00064190:_____/21:N0000060 RIV/75010330:_____/21:00013475 a 3 dalších
Výsledek na webu
<a href="https://www.mdpi.com/2072-6694/13/10/2463" target="_blank" >https://www.mdpi.com/2072-6694/13/10/2463</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3390/cancers13102463" target="_blank" >10.3390/cancers13102463</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Local Immune Changes in Early Stages of Inflammation and Carcinogenesis Correlate with the Collagen Scaffold Changes of the Colon Mucosa
Popis výsledku v původním jazyce
Chronic colitis and colon cancer develop for alteration of the mucosa homeostatic regulation, also involving TGF-beta 1. Dextran sulphate sodium (DSS)-induced colitis and azoxymethane (AOM)-induced colorectal carcinogenesis animal models allow for the investigation of the pathological evolution steps. Since chronic inflammation is a common factor, we aimed to explore in rat models the colon mucosa immunological and structural conditions at one month after the end of the inductions, a transition period between acute effects and established lesions. We found, in comparison to healthy controls, downregulation of inflammatory cytokines (except IL-6) and of TGF-beta 1. At the same time, the collagen scaffold was significantly remodelled in both groups. We conclude that the pro-inflammatory cytokines, in front of a downregulated TGF-beta 1, sustained a smouldering inflammation with structural changes preparing the niche of both pathologies (ulcerative colitis with fibrosis, tumour). The collagen scaffold changes pointing to an unnoticed inflammation may be suggested as a possible pre-neoplastic condition marker.nnContinuous activation of the immune system inside a tissue can lead to remodelling of the tissue structure and creation of a specific microenvironment, such as during the tumour development. Chronic inflammation is a central player in stimulating changes that alter the tissue stroma and can lead to fibrotic evolution. In the colon mucosa, regulatory mechanisms, including TGF-beta 1, avoid damaging inflammation in front of the continuous challenge by the intestinal microbiome. Inducing either DSS colitis or AOM colorectal carcinogenesis in AVN-Wistar rats, we evaluated at one month after the end of each treatment whether immunological changes and remodelling of the collagen scaffold were already in development. At this time point, we found in both models a general downregulation of pro-inflammatory cytokines and even of TGF-beta 1, but not of IL-6.
Název v anglickém jazyce
Local Immune Changes in Early Stages of Inflammation and Carcinogenesis Correlate with the Collagen Scaffold Changes of the Colon Mucosa
Popis výsledku anglicky
Chronic colitis and colon cancer develop for alteration of the mucosa homeostatic regulation, also involving TGF-beta 1. Dextran sulphate sodium (DSS)-induced colitis and azoxymethane (AOM)-induced colorectal carcinogenesis animal models allow for the investigation of the pathological evolution steps. Since chronic inflammation is a common factor, we aimed to explore in rat models the colon mucosa immunological and structural conditions at one month after the end of the inductions, a transition period between acute effects and established lesions. We found, in comparison to healthy controls, downregulation of inflammatory cytokines (except IL-6) and of TGF-beta 1. At the same time, the collagen scaffold was significantly remodelled in both groups. We conclude that the pro-inflammatory cytokines, in front of a downregulated TGF-beta 1, sustained a smouldering inflammation with structural changes preparing the niche of both pathologies (ulcerative colitis with fibrosis, tumour). The collagen scaffold changes pointing to an unnoticed inflammation may be suggested as a possible pre-neoplastic condition marker.nnContinuous activation of the immune system inside a tissue can lead to remodelling of the tissue structure and creation of a specific microenvironment, such as during the tumour development. Chronic inflammation is a central player in stimulating changes that alter the tissue stroma and can lead to fibrotic evolution. In the colon mucosa, regulatory mechanisms, including TGF-beta 1, avoid damaging inflammation in front of the continuous challenge by the intestinal microbiome. Inducing either DSS colitis or AOM colorectal carcinogenesis in AVN-Wistar rats, we evaluated at one month after the end of each treatment whether immunological changes and remodelling of the collagen scaffold were already in development. At this time point, we found in both models a general downregulation of pro-inflammatory cytokines and even of TGF-beta 1, but not of IL-6.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10606 - Microbiology
Návaznosti výsledku
Projekt
<a href="/cs/project/IAA500200917" target="_blank" >IAA500200917: Genetická a imunologická studie časných stádií kolorektálního adenokarcinomu: prostředí zánětu na konvenčních vs germ free zvířecích modelech a na vzorcích z lidské tkáně</a><br>
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2021
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Cancers (Basel)
ISSN
2072-6694
e-ISSN
2072-6694
Svazek periodika
13
Číslo periodika v rámci svazku
10
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
19
Strana od-do
2463
Kód UT WoS článku
000654722200001
EID výsledku v databázi Scopus
2-s2.0-85105863368