OBJECTIVES: Kudoa septempunctata has been identified as the causative agent of food poisoning following the consumption of raw farmed Paralichthys olivaceus. However, cohort studies providing robust evidence for an association between K. septempunctata and gastrointestinal symptoms remain limited. This prospective cohort study investigated the association between the consumption of K. septempunctata–infected farmed P. olivaceus and the occurrence of gastrointestinal symptoms. METHODS: Individuals who purchased raw farmed P. olivaceus between 2020 and 2021 were selected as the study population. Study data included 2 rounds of questionnaire surveys administered before and after consumption, 2 muscle specimens obtained from each purchased fish, and human biological specimens collected from individuals who developed gastrointestinal symptoms within 24 hours after consumption. Data were analyzed using the chi-square test and t-test, and the association between consumption of K. septempunctata–infected farmed P. olivaceus and gastrointestinal symptoms was evaluated using relative risk estimates between exposure groups. RESULTS: The relative risk of gastrointestinal symptoms associated with exposure to K. septempunctata–infected P. olivaceus ranged from 71.2 (95% confidence interval [CI], 27.0 to 178.6) to 124.5 (95% CI, 43.5 to 355.0) across the 2 case definitions. A strong and statistically significant association was observed between exposure to K. septempunctata–infected P. olivaceus and the development of acute gastrointestinal symptoms. CONCLUSIONS These findings indicate both an association and a causal relationship between consumption of K. septempunctata–infected farmed P. olivaceus and the onset of gastrointestinal symptoms.

Infiltration and activation of peripheral immune cells are critical in the progression of multiple sclerosis and its experimental animal model, experimental autoimmune encephalomyelitis (EAE). This study investigates the role of high mobility group box 1 (HMGB1) in oligodendrocyte precursor cells (OPCs) in modulating pathogenic T cells infiltrating the central nervous system through the blood-brain barrier (BBB) by using OPC-specific HMGB1 knockout (KO) mice. We found that HMGB1 released from OPCs promotes BBB disruption, subsequently allowing increased immune cell infiltration. The migration of CD4+ T cells isolated from EAE-induced mice was enhanced when co-cultured with OPCs compared to oligodendrocytes (OLs). OPC-specific HMGB1 KO mice exhibited lower BBB permeability and reduced immune cell infiltration into the CNS, leading to less damage to the myelin sheath and mitigated EAE progression. CD4+ T cell migration was also reduced when co-cultured with HMGB1 knock-out OPCs. Our findings reveal that HMGB1 secretion from OPCs is crucial for regulating immune cell infiltration and provides insights into the immunomodulatory function of OPCs in autoimmune diseases.
Animals ; Encephalomyelitis, Autoimmune, Experimental/metabolism* ; HMGB1 Protein/deficiency* ; Mice, Knockout ; Oligodendrocyte Precursor Cells/immunology* ; Mice, Inbred C57BL ; CD4-Positive T-Lymphocytes/immunology* ; Cell Movement ; Blood-Brain Barrier/immunology* ; Mice ; Myelin Sheath/pathology* ; Disease Models, Animal ; Coculture Techniques ; Oligodendroglia/metabolism* ; Female ; Cells, Cultured

Jugular foramen syndrome (JFS) results from a dysfunction of the lower cranial nerves (CN IX–XII) traversing the jugular foramen and presents with diverse clinical manifestations depending on the nerves involved. Surgical resection is the primary treatment for benign jugular foramen tumors, but postoperative neurological deterioration remains a significant concern. This paper reports a case of worsened dysphagia following the surgical treatment of JFS despite anatomical preservation of the lower cranial nerves. A 68-year-old man presented with long-standing left-sided hearing loss, tongue atrophy, and a recent onset of dysphagia. Imaging revealed a left jugular foramen mass that was initially suspected of being a schwannoma. The patient underwent tumor removal via a combined transcochlear and transcervical approach, with intraoperative preservation of CN IX–XII. Histopathology confirmed paraganglioma. Postoperatively, the patient experienced aggravated dysphagia, with video fluoroscopic swallowing studies showing persistent residue in the left pyriform sinus. Although the subjective swallowing function gradually improved, the neurological deficits did not fully recover. This case shows that even when a preexisting cranial nerve dysfunction is present and the nerves are preserved intraoperatively, the swallowing function can deteriorate after surgery. Therefore, a thorough preoperative functional assessment and careful consideration of potential postoperative functional decline are essential in the surgical management of jugular foramen tumors.