Members of the genus Anisakis comprise a group of parasitic nematodes with indirect life cycle, that utilize marine mammals as definitive hosts, planktonic crustaceans as intermediate hosts and fish and cephalopods as paratenic hosts. Following ingestion of raw or undercooked seafood contaminated with live third stage larvae, humans can become accidental hosts, thus contracting a disease termed anisakiasis, being recognized as an emerging public health concern. In the first part of the research histopathological and immunofluorescence analysis of gastrointestinal tract lesions of the final host was performed. Anisakis spp.-induced lesions included severe ulcerative gastritis with mixed inflammatory infiltrate often associated with colonies of bacteria, mild to moderate granulomatous gastritis and severe pyogranulomatous inflammation. Immunofluorescent staining did not yield positive signals for the applied antibodies. In the second part of the research we characterized early inflammatory response in rat model of anisakiasis by means of histopathological analysis, immunofluorescence (CD3, CD4, CD68, iNOS, S100A8/A9) and transmission electron microscopy, in addition to measuring inflammatory markers (Il1b, Il6, Il18, Ccl2, Icam1, Mmp9) and microRNA expression, as well as global DNA methylation status. Anisakis larval migration caused moderate to extensive haemorrhages in submucosal and epimysial/perimysial connective tissue of the muscles. In stomach and muscle, moderate to abundant mixed inflammatory infiltrate was present, dominated by neutrophils and macrophages, while only mild infiltration was seen in intestine. Lesions were characterized by the presence of CD3+, CD4+, CD68+, iNOS+ i S100A8/A9+ cells. Il6, Il1b and Ccl3 showed particularly strong expression in stomach and visceral adipose tissue. In total, three miRNAs were differentially expressed; two in stomach (miRNA-451-5p and miRNA-223-3p) and two in intestine (miRNA-451-5p and miRNA-672-5p). No changes in global DNA methylation were observed between infected and uninfected tissues. This study shows, that Anisakis infection induces strong inflammatory response in accidental host with marked induction of specific proinflammatory cytokines and miRNA expression.