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Rycina z artykułu: Wpływ zanieczyszczeń...
 
SŁOWA KLUCZOWE
DZIEDZINY
STRESZCZENIE
Wprowadzenie i cel:
Celiakia to przewlekła choroba autoimmunologiczna jelita cienkiego, rozwijająca się u osób z predyspozycją genetyczną (HLA-DQ2/DQ8) po ekspozycji na gluten. Mimo że czynniki genetyczne odgrywają kluczową rolę w jej patogenezie, obserwowany w ostatnich dekadach wzrost liczby zachorowań sugeruje wpływ także czynników środowiskowych. Celem pracy było przeanalizowanie najnowszych danych dotyczących wpływu zanieczyszczeń powietrza oraz ekspozycji na metale ciężkie na ryzyko rozwoju i przebieg choroby trzewnej u dzieci i młodzieży.

Opis stanu wiedzy:
Coraz więcej badań wskazuje, że metale ciężkie mogą odgrywać rolę w powstaniu i nasileniu celiakii. Nanocząstki srebra, tlenku tytanu i złota zaburzają mikrobiom jelitowy, uszkadzają barierę śluzówkową i aktywują układ odpornościowy, zwiększając poziom cytokin prozapalnych (m.in. IL-15, IFNγ, IL-8). U chorych obserwuje się nadmiar bakterii z rodzaju Bacteroides i Firmicutes, co może być skutkiem ekspozycji na metale. Dodatkowo związki te upośledzają integralność połączeń między komórkami nabłonka i zaburzają autofagię w enterocytach, sprzyjając destrukcji jelita cienkiego. Osoby na diecie bezglutenowej są też bardziej narażone na akumulację metali (np. z ryżu), co może nasilać uszkodzenia. Zanieczyszczenia powietrza, takie jak NO₂, pyły PM i ozon, także uszkadzają barierę jelitową, wpływają na odporność i zwiększają ryzyko celiakii. Wśród dzieci choroba trzewna częściej diagnozowana jest u tych, które mieszkają w rejonach o większym zanieczyszczeniu.

Podsumowanie:
Metale ciężkie i zanieczyszczenia powietrza mogą wpływać na mikrośrodowisko jelitowe, barierę nabłonkową i odpowiedź immunologiczną, stanowiąc potencjalne czynniki ryzyka rozwoju celiakii. Ich rola w patogenezie tej choroby wymaga dalszych, wieloośrodkowych badań.

Introduction and objective:
Coeliac disease is a chronic autoimmune disorder of the small intestine that develops in genetically predisposed individuals (HLA-DQ2/DQ8) following gluten exposure. Although genetic factors play a pivotal role in its pathogenesis, the rising incidence observed over recent decades suggests that environmental factors also contribute. The aim of the review is to analyze recent data regarding the influence of air pollution and heavy metal exposure on the risk and course of coeliac disease in children and adolescents.

Brief description of the state of knowledge:
An increasing number of studies indicate that heavy metals and air pollutants may contribute to the development and progression of coeliac disease. Nanoparticles of silver, titanium dioxide, and gold disrupt the gut microbiota, damage the intestinal barrier, and activate the immune system, elevating pro-inflammatory cytokines such as IL-15, IFN-γ, and IL-8. Exposure to heavy metals is associated with over-representation of Bacteroides and Firmicutes, impaired tight junctions, and disrupted autophagy in enterocytes, all promoting intestinal injury. Individuals on gluten-free diets, especially those rich in rice-based products, may accumulate more heavy metals, exacerbating mucosal damage. Likewise, pollutants like nitrogen dioxide, particulate matter, and ozone weaken gut integrity, alter immune responses, and are linked to increased coeliac disease prevalence, particularly in children in polluted areas.

Summary:
Heavy metals and air pollution may alter the intestinal microenvironment, epithelial barrier function, and immune response, representing potential risk factors for the development of coeliac disease. Their role in the disease’s pathogenesis warrants further multicentre, multidisciplinary research.
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