Po-Yu Chu1, Hai-Lun Sun2, Jiunn-Liang Ko3, Min-Sho Ku4, Ling-Jun Lin5, Yu-Tzu Lee3, Pei-Fen Liao4, Hui-Hsien Pan4, Hsueh-Lin Lu4, Ko-Huang Lue6. 1. Department of Pediatrics, Chung-Shan Medical University Hospital, Taichung, Taiwan, ROC; Department of Pediatrics, Ministry of Health and Welfare Feng-Yuan Hospital, Taichung, Taiwan, ROC. 2. Department of Pediatrics, Chung-Shan Medical University Hospital, Taichung, Taiwan, ROC; Institute of Medicine, Chung-Shan Medical University, Taichung, Taiwan, ROC. 3. Institute of Medicine, Chung-Shan Medical University, Taichung, Taiwan, ROC. 4. Department of Pediatrics, Chung-Shan Medical University Hospital, Taichung, Taiwan, ROC. 5. Institute of Microbiology and Immunology, Chung-Shan Medical University, Taichung, Taiwan, ROC. 6. Department of Pediatrics, Chung-Shan Medical University Hospital, Taichung, Taiwan, ROC; Institute of Medicine, Chung-Shan Medical University, Taichung, Taiwan, ROC; School of Medicine, Chung-Shan Medical University, Taichung, Taiwan, ROC. Electronic address: cshy095@csh.org.tw.
Abstract
BACKGROUND/ PURPOSE: House dust mite (HDM) is well known as one of the major indoor allergens that trigger allergic inflammation, especially asthma, and accounts for 85% of all cases. So far, asthma has been thought of as a condition of imbalance between T helper (Th)1 and Th2. Fungal immunomodulatory protein-Flammulina velutipes (FIP-fve) has been seemingly demonstrated to modulate the response to Th1 cytokine production. The aim of this study was to investigate if the oral administration of FIP-fve can inhibit HDM-induced asthma inflammation in the mouse model. METHODS: We divided the mice (female BALB/c, 4-6 weeks) into four groups: the prevention group, which consisted of mice sensitized by HDM (intraperitoneally on Day 1, Day 7, and Day 14, and intranasally on Day 14, Day 17, Day 21, Day 24, and Day 27) fed with FIP-fve from Day 1 to Day 14; the treatment group, which comprised mice that received treatment from Day 14 to Day 28; the positive control (PC, sensitized by HDM fed without FIP-fve) group; and the negative control group (NC, nonsensitized). Airway hyperresponsiveness induced by methacholine challenge was determined using whole-body barometric plethysmography. In addition, cytokines were analyzed from bronchoalveolar lavage fluid and serum. Histopathological studies and Liu's staining method in mice lungs were also performed. RESULTS: The results showed that both pre- and posttreated FIP-fve groups had significantly reduced airway hyperresponsiveness compared with the PC group after methacholine challenge. In addition, a significantly decreased level of HDM-specific immunoglobulin E in serum and decreased production of Th2 cytokines in bronchoalveolar lavage fluid and serum were observed in these two FIP-fve fed groups. Moreover, more decreased amounts of infiltrating inflammatory cells were present in the lungs of FIP-fve fed groups than those of the PC group. CONCLUSION: Oral FIP-fve had an anti-inflammatory effect on the acute phase of the airway inflammatory process induced by HDM in the mouse model and might have a potentially therapeutic role for allergic airway diseases.
BACKGROUND/ PURPOSE: House dust mite (HDM) is well known as one of the major indoor allergens that trigger allergic inflammation, especially asthma, and accounts for 85% of all cases. So far, asthma has been thought of as a condition of imbalance between T helper (Th)1 and Th2. Fungal immunomodulatory protein-Flammulina velutipes (FIP-fve) has been seemingly demonstrated to modulate the response to Th1 cytokine production. The aim of this study was to investigate if the oral administration of FIP-fve can inhibit HDM-induced asthma inflammation in the mouse model. METHODS: We divided the mice (female BALB/c, 4-6 weeks) into four groups: the prevention group, which consisted of mice sensitized by HDM (intraperitoneally on Day 1, Day 7, and Day 14, and intranasally on Day 14, Day 17, Day 21, Day 24, and Day 27) fed with FIP-fve from Day 1 to Day 14; the treatment group, which comprised mice that received treatment from Day 14 to Day 28; the positive control (PC, sensitized by HDM fed without FIP-fve) group; and the negative control group (NC, nonsensitized). Airway hyperresponsiveness induced by methacholine challenge was determined using whole-body barometric plethysmography. In addition, cytokines were analyzed from bronchoalveolar lavage fluid and serum. Histopathological studies and Liu's staining method in mice lungs were also performed. RESULTS: The results showed that both pre- and posttreated FIP-fve groups had significantly reduced airway hyperresponsiveness compared with the PC group after methacholine challenge. In addition, a significantly decreased level of HDM-specific immunoglobulin E in serum and decreased production of Th2 cytokines in bronchoalveolar lavage fluid and serum were observed in these two FIP-fve fed groups. Moreover, more decreased amounts of infiltrating inflammatory cells were present in the lungs of FIP-fve fed groups than those of the PC group. CONCLUSION: Oral FIP-fve had an anti-inflammatory effect on the acute phase of the airway inflammatory process induced by HDM in the mouse model and might have a potentially therapeutic role for allergic airway diseases.