Abstract <p>Irritable bowel syndrome (IBS) is a common disease affectingup to 20% of the global population. It is characterized by a highfrequency of recurrent pain and alterations in gastrointestinalfunction in the absence of a definite organic cause. Research confirmsthe close coexistence of emotional, cognitive, and gastrointestinalsymptoms of IBS. The aim of the study was to identify the relationshipbetween visceral and somatic pain, behavioral responses in micewith a post-inflammatory IBS model, and the level of oxidative stress,neuroinflammation, as well as the permeability of the blood–brainand intestinal barriers. In our study, IBS mice exhibited increased anxietylevels (as assessed in the Open Field and Light-Dark Box tests,and by the integral anxiety index) without changes in locomotoractivity or motor coordination. Moreover, we demonstrated the developmentnot only of visceral hypersensitivity but also of somatic pain syndrome.In the novel object recognition test, IBS mice spent less time exploringthe new object than their control counterparts. Spatial short-termmemory, as assessed by spontaneous alternation behavior in the T-maze, wasalso impaired. IBS mice showed increased brain levels of malondialdehydeand interleukin-6, along with decreased levels of total glutathione,sulfide ions, and the synthesis of these antioxidants. One of themechanisms underlying neuroinflammation in IBS may be the increasedpermeability of the blood–brain and intestinal barriers that weobserved. Our work demonstrated that central nervous system dysfunction,increased oxidative stress, and inflammation in mouse brain tissuesmay be associated with increased permeability to toxins, first ofthe intestinal barrier and then of the blood–brain barrier, whenmodeling IBS.</p>