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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, OBJECTIVE, METHODS, RESULTS. Meshes: Adult, Animals, Antigens, Fungal, Arylsulfonates, Aspergillus, Asthma, Cell Line, Cells, Cultured, Claudins, Humans, Immunoglobulin E, Interleukin-13, Male, Mice, Inbred C57BL, Mice, Knockout, Permeability, RNA, Messenger, RNA, Small Interfering, Respiratory Mucosa, Respiratory System, Young Adult.
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Is claudin-18 deficiency associated with airway epithelial barrier dysfunction and asthma? Context: Epithelial barrier dysfunction and increased permeability may contribute to antigen sensitization and disease progression in asthma. Claudin-18.1 is the only known lung-specific tight junction protein, but its contribution to airway barrier function or asthma is unclear. We sought to test the hypotheses that claudin-18 is a determinant of airway epithelial barrier function that is downregulated by IL-13 and that claudin-18 deficiency results in increased aeroantigen sensitization and airway hyperresponsiveness. Claudin-18.1 mRNA levels were measured in airway epithelial brushings from healthy controls and patients with asthma. In patients with asthma, claudin-18 levels were compared with a three-gene-mean marker of T Epithelial brushings from patients with asthma (n = 67) had significantly lower claudin-18 mRNA levels than did those from healthy controls (n = 42). Claudin-18 levels were lowest among T
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These data support the hypothesis that claudin-18 is an essential contributor to the airway epithelial barrier to aeroantigens. Furthermore, T Final Decision: yes