Klaudini i upalne bolesti crijeva

Biljana Knežević, Sanda Mustapić, Marko Banić, Lidija Požgaj, Vesna Eraković Haber

Upalne bolesti crijeva kronične su upalne bolesti čija točna etiologija još uvijek nije poznata. Imunološki, genetski i okolišni čimbenici uz promjene crijevne mikrobiote i intestinalne barijere najvjerojatniji su patogenetski mehanizmi nastanka bolesti. Crijevna propusnost jedan je od bitnih čimbenika u nastanku crijevne upale, a povezana je s disbiozom, upalnim odgovorom i promjenama međustaničnih uskih spojeva crijevne epitelne barijere. Klaudini koji su dio obitelji proteina koji čine uske spojeve ključni su za održavanje integriteta crijevne barijere i sudjeluju u regulaciji paracelularne propusnosti. Sagledavajući multifaktorijalnu prirodu bolesti, uloga klaudina u nastanku upalne bolesti crijeva postaje predmet brojnih istraživanja s obzirom na novija saznanja koja upućuju na to da klaudini nemaju samo ulogu transmembranskih proteina, već da imaju i brojne druge funkcije te da promjene u izražaju, prostornoj i vremenskoj raspodjeli određenih klaudina mogu implicirati dosada neprepoznate patofiziološke mehanizme odgovorne za nastanak upalnih bolesti crijeva.

Inflammatory bowel diseases are chronic disorders of the digestive system, the exact etiology of which is still unknown. Immunological, genetic, and environmental factors, along with changes in the gut microbiota and intestinal barrier, are the most likely pathogenetic mechanisms of disease development. Intestinal permeability is one of the essential factors in the onset of inflammation and is associated with dysbiosis, inflammatory response, and changes in the tight junctions of the intestinal epithelial barrier. Claudins, which are part of the family of proteins that form tight junctions, are crucial for maintaining the integrity of the intestinal barrier and participate in the
regulation of paracellular permeability. Considering the multifactorial nature of the disease, the role of claudins in the development of inflammatory bowel disease has become the subject of numerous studies in light of recent findings suggesting that claudins not only serve as transmembrane proteins but also have various other functions, and that changes in the expression, spatial, and temporal distribution of certain claudins may imply previously unrecognized pathophysiological mechanisms responsible for the onset of inflammatory bowel diseases.