Smouldering inflammation: from tissue remodeling to cancer niche

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61988987%3A17110%2F23%3AA2402NIK" target="_blank" >RIV/61988987:17110/23:A2402NIK - isvavai.cz</a>

Výsledek na webu

<a href="https://www.webofscience.com/wos/woscc/full-record/WOS:001058863800022" target="_blank" >https://www.webofscience.com/wos/woscc/full-record/WOS:001058863800022</a>

DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Smouldering inflammation: from tissue remodeling to cancer niche

Popis výsledku v původním jazyce

Long lasting chronic inflammation induces progressive fibrosis of the involved tissues. Chronic inflammation, a leading factor in many pathological processes, can address cancer establishment and evolution. Local changes of immune activation inside a tissue, if maintained and supported by the environment, can induce structural remodeling. Reciprocally, collagen accumulation can affect the local immunity. We have shown that the colonization of germ-free (GF) mice colon by conventional mice (CV) intestinal microflora quickly modifies the local and systemic immunity. Contemporarily, it induces a fast remodeling of the collagen scaffold in the intestinal mucosa. Using a rat model of chronic colitis (dextran sodium sulphate — DSS — induced colitis) and of carcinogenesis (using azoxymethane — AOM - carcinogen for the colon) we have shown that, in both models, inflammation activates remodeling of the collagen scaffold organization even when the mucosa appears recovered from the acute induction. Multi-photon confocal microscopy of CV and GF animal mucosa resulted with higher complexity in structure in the CV rats (with microbiome). The immunological data suggest that the response to the microbiota presence elicit effective homeostatic regulation in the healthy CV rats, to avoiding inflammation and maintaining cytokine levels near the spontaneous production found in the GF animals. These conditions establish what we define as "inflammatory threshold" of the mucosa, allowing a range of tolerance to the continuous immune activation. The results also indicated that the collagen scaffold adapts to the immune microenvironment conditions, and quickly it can be altered if the immune threshold is overcome.

Název v anglickém jazyce

Smouldering inflammation: from tissue remodeling to cancer niche

Popis výsledku anglicky

Long lasting chronic inflammation induces progressive fibrosis of the involved tissues. Chronic inflammation, a leading factor in many pathological processes, can address cancer establishment and evolution. Local changes of immune activation inside a tissue, if maintained and supported by the environment, can induce structural remodeling. Reciprocally, collagen accumulation can affect the local immunity. We have shown that the colonization of germ-free (GF) mice colon by conventional mice (CV) intestinal microflora quickly modifies the local and systemic immunity. Contemporarily, it induces a fast remodeling of the collagen scaffold in the intestinal mucosa. Using a rat model of chronic colitis (dextran sodium sulphate — DSS — induced colitis) and of carcinogenesis (using azoxymethane — AOM - carcinogen for the colon) we have shown that, in both models, inflammation activates remodeling of the collagen scaffold organization even when the mucosa appears recovered from the acute induction. Multi-photon confocal microscopy of CV and GF animal mucosa resulted with higher complexity in structure in the CV rats (with microbiome). The immunological data suggest that the response to the microbiota presence elicit effective homeostatic regulation in the healthy CV rats, to avoiding inflammation and maintaining cytokine levels near the spontaneous production found in the GF animals. These conditions establish what we define as "inflammatory threshold" of the mucosa, allowing a range of tolerance to the continuous immune activation. The results also indicated that the collagen scaffold adapts to the immune microenvironment conditions, and quickly it can be altered if the immune threshold is overcome.

Druh

D - Stať ve sborníku

CEP obor

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OECD FORD obor

30102 - Immunology

Projekt

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Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2023

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název statě ve sborníku

EUR J IMMUNOL

ISBN

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ISSN

0014-2980

e-ISSN

1521-4141

Počet stran výsledku

2

Strana od-do

24-25

Název nakladatele

WILEY

Místo vydání

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Místo konání akce

Prague

Datum konání akce

22. 11. 2022

Typ akce podle státní příslušnosti

EUR - Evropská akce

Kód UT WoS článku

001058863800022