Takehito Kobayashi1, Kazuyuki Nakagome2, Toru Noguchi1, Kiyoko Kobayashi3, Yutaka Ueda4, Tomoyuki Soma5, Kenji Ikebuchi3, Hidetomo Nakamoto6, Makoto Nagata5. 1. Department of Respiratory Medicine, Saitama Medical University, Saitama, Japan; Allergy Center, Saitama Medical University, Saitama, Japan; Department of General Internal Medicine, Saitama Medical University, Saitama, Japan. 2. Department of Respiratory Medicine, Saitama Medical University, Saitama, Japan; Allergy Center, Saitama Medical University, Saitama, Japan. Electronic address: nakagomek-tky@umin.ac.jp. 3. Department of Laboratory Medicine, Saitama Medical University, Saitama, Japan. 4. Department of Respiratory Medicine, Saitama Medical University, Saitama, Japan; Allergy Center, Saitama Medical University, Saitama, Japan; Department of Pediatrics, Saitama Medical University, Saitama, Japan. 5. Department of Respiratory Medicine, Saitama Medical University, Saitama, Japan; Allergy Center, Saitama Medical University, Saitama, Japan. 6. Department of General Internal Medicine, Saitama Medical University, Saitama, Japan.
Abstract
BACKGROUND: Recent evidence has suggested that the innate immune response may play a role in the development of eosinophilic airway inflammation. We previously reported that uric acid (UA) and adenosine triphosphate (ATP), two important damage-associated molecular pattern molecules (DAMPs), activate eosinophil functions, suggesting that these molecules may be involved in the development of eosinophilic airway inflammation. The objective of this study was to measure the concentrations of DAMPs including UA and ATP in the bronchoalveolar lavage fluid (BALF) of patients with eosinophilic pneumonia (EP). METHODS: BAL was performed in patients with EP including acute and chronic eosinophilic pneumonia, and in patients with hypersensitivity pneumonia, and sarcoidosis. UA, ATP, and cytokine concentrations in the BALF were then measured. RESULTS: The UA concentration was increased in the BALF of EP patients. UA concentrations correlated with eosinophil numbers, and with eosinophil-derived neurotoxin and interleukin (IL)-5 concentrations. Furthermore, the ATP concentration was increased in the BALF of EP patients and ATP concentrations correlated with UA concentrations. Moreover, IL-33 was increased in EP patients and IL-33 concentrations correlated with UA and ATP concentrations. CONCLUSIONS: The UA and ATP concentration was increased in the BALF of EP patients. UA concentrations correlated with eosinophil numbers, and with ATP and IL-33 concentrations. Our findings suggest that DAMPs such as UA and ATP play a role in the pathogenesis of EP.
BACKGROUND: Recent evidence has suggested that the innate immune response may play a role in the development of eosinophilic airway inflammation. We previously reported that uric acid (UA) and adenosine triphosphate (ATP), two important damage-associated molecular pattern molecules (DAMPs), activate eosinophil functions, suggesting that these molecules may be involved in the development of eosinophilic airway inflammation. The objective of this study was to measure the concentrations of DAMPs including UA and ATP in the bronchoalveolar lavage fluid (BALF) of patients with eosinophilic pneumonia (EP). METHODS: BAL was performed in patients with EP including acute and chronic eosinophilic pneumonia, and in patients with hypersensitivity pneumonia, and sarcoidosis. UA, ATP, and cytokine concentrations in the BALF were then measured. RESULTS: The UA concentration was increased in the BALF of EP patients. UA concentrations correlated with eosinophil numbers, and with eosinophil-derived neurotoxin and interleukin (IL)-5 concentrations. Furthermore, the ATP concentration was increased in the BALF of EP patients and ATP concentrations correlated with UA concentrations. Moreover, IL-33 was increased in EP patients and IL-33 concentrations correlated with UA and ATP concentrations. CONCLUSIONS: The UA and ATP concentration was increased in the BALF of EP patients. UA concentrations correlated with eosinophil numbers, and with ATP and IL-33 concentrations. Our findings suggest that DAMPs such as UA and ATP play a role in the pathogenesis of EP.