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YMAI12515 Proof 1..15 All abstracts are strictly embargoed until the date of presentation at the 2017 Annual Meeting. J ALLERGY CLIN IMMUNOL Abstracts AB1 VOLUME 139, NUMBER 2 Staphylococcus Aureus Colonization Is Associated with of Club cell aberration to IPF was confirmed by marked pleomorphism and 1 Increased Atopy and Inhaled Steroid Use in Patients wide distribution of Cldn10-positive Club cells in IPF lungs. with Atopic Dermatitis and Asthma CONCLUSIONS: Oxidative stress induces aberrant fibrotic reactions in Atp8b1 mutant mice. This model can be a new format to unravel the role of Peter Uong, MD1, Douglas Curran-Everett, PhD1, and Donald Y. M. Club cells in the development of IPF. Leung, MD, PhD, FAAAAI2; 1National Jewish Health, Denver, CO, 2K926i, National Jewish Health, Denver, CO. Chronic Rhinitis Is A Strong Clinical Predictor for Early RATIONALE: Staphylococcus aureus (S. aureus) colonization has been 3 Hospital Readmission Of Chronic Obstructive Lung associated with severe atopic dermatitis (AD), and in experimental models, Disease Patients has been shown to increase IgE and corticosteroid insensitivity. We tested Umesh Singh, MD, PhD1, Victoria Wangia-Anderson, PhD2, Linda the hypothesis that S. aureus colonization may also contribute to increased 1 1,3 1 environmental allergen sensitization and severity of asthma. Levin, PhD , and Jonathan A. Bernstein, MD, FAAAAI ; University of Cincinnati College of Medicine, Cincinnati, OH, 2University of Cincin- METHODS: We reviewed the patient research database at National 3 Jewish Health and found 557 patients (less than or equal to 18 years of age) nati, College of Allied Health Sciences, Cincinnati, OH, Bernstein Al- SATURDAY with a concurrent diagnosis of AD and asthma who had been cultured for S lergy Group, Inc, Cincinnati, OH. aureus. We queried for total and allergen specific serum IgE levels, positive RATIONALE: Hospital performance measures are determined by 30-day prick skin tests to inhalant allergens, exhaled nitric oxide (eNO), asthma readmission rates (30d-RR) for specific medical conditions. Purpose of control test (ACT) scores, and medications prescribed. this study was to assess the 30d-RR for chronic obstructive lung disease RESULTS: Of the 557 patients with AD and asthma who were cultured for (COLD) using a large university hospital patient database. S aureus, 459 subjects had positive S aureus cultures (average age 6.4 years METHODS: De-identified patient records of hospital encounters, de- old; 60% males) and 98 subjects had negative S. aureus cultures (average mographics and comorbidities admitted with a primary diagnosis of age 5.3 years old; 62% males). asthma or chronic obstructive pulmonary disease (i.e., COLD) from Subjects with S aureus colonization, as compared to S. aureus negative the University of Cincinnati Hospitals (UCH) between October, 2012 subjects, had significantly higher total serum IgE (P<.001), percent posi- and July, 2016 were analyzed to determine the 30d-RR compared to the na- tive skin prick tests for aeroallergens (P5.003), and higher eNO tional average of 22.1%. Age and mortality-adjusted comorbidities as risk (P5.05). Importantly, asthmatics colonized with S. aureus required a factors for 30d-RR were determined in multivariate logistic regression higher daily dose of inhaled corticosteroids (P 5.02) despite similar analysis. Adjustment for medical complexity and social vulnerability ACT scores (P5.92). was not performed due to missing data. CONCLUSIONS: Our data suggests that S. aureus colonization in asth- RESULTS: Of the 11,311 hospital encounters for 5,735 COLD patients, matics with concomitant AD is associated with increased IgE responses 2,104 (18.6%) were readmitted within 30d. The mean age of readmitted 5 5 to environmental allergens, increased eNO, and increased inhaled cortico- (n 2,087) and non-readmitted (n 3,648) patients were 53.2 vs. 50.6 p steroid use. We postulate that S aureus colonization contributes to systemic years, respectively ( <.001). No difference in average length of stay was allergy and corticosteroid insensitivity. observed between these two groups (1.74 vs. 1.68 days), however, a signif- icantly greater percentage of readmitted (4.1%) versus non-readmitted Oxidative stress induces fibrotic reactions in Atp8b1 (2.7%) patients died over this period. Logistic regression analysis 2 mutant mice through abnormal behavior of Club cells identified chronic rhinitis (OR52.7; p<.0001), diabetes mellitus (OR51.3; p<.0014), cardiac arrhythmia (OR51.7; p<.0001), anemia Jutaro Fukumoto, MD, PhD, Andrew J. Cooke, MD, Ramani (OR51.5; p<.0001), tobacco use (OR51.5; p<.0001), or obesity Soundararajan, PhD, Richard F. Lockey, MD, FAAAAI, and Narasaiah (OR51.6; p<.0001) significantly increased the 30d-RR. Kolliputi, PhD; Division of Allergy and Immunology, Department of In- CONCLUSIONS: The 30d-RR for COLD at UCH was 18.6% which ternal Medicine, Morsani College of Medicine, University of South Flor- is better than the national average. Interestingly, the comorbidities ida, Tampa, FL. identified, most notably chronic rhinitis, are novel and suggest that their RATIONALE: Atp8b1 is a cardiolipin transporter in the apical membrane treatment should be prioritized in these high risk patients to further reduce of lung epithelial cells. While the role of Atp8b1 in pneumonia-induced 30d-RR. acute lung injury (ALI) has been well studied, its potential role in oxidative stress (hyperoxia)-induced ALI and recovery from it are poorly understood. METHODS: WT mice and Atp8b1G308V/G308V mutants (functionally defi- cient; referred to as Atp8b1 mutant mice hereinafter) were exposed to 100% O2. A portion of mice were euthanized 48 hrs after exposure for sam- ple collection (acute inflammatory phase). The remaining mice were eutha- nized after an additional 12 days under normoxia (post-inflammatory recovery phase). Cell apoptosis, proliferation, inflammatory response, and tissue fibrosis were evaluated using bronchoalveolar lavage (BAL) fluid and lung tissue samples. Human lung samples from patients with idio- pathic pulmonary fibrosis (IPF) and COPD were subjected to immunohis- tochemical labeling for Club cell markers, CCSP and Claudin-10 (Cldn10). RESULTS: H&E-stained and TUNEL-stained lung sections from WTand Atp8b1 mutant mice revealed that Atp8b1 mutant mice under hyperoxia display accelerated alveolar cell death and patchy proliferation of bronchiolar epithelial cells. BAL analysis and immunohistochemical labeling for Ki-67 revealed that TUNEL-negative Club cells proliferate in Atp8b1 mutant lungs under inflammatory conditions, which was followed by fibrotic reactions during the recovery phase. Clinical relevance All abstracts are strictly embargoed until the date of presentation at the 2017 Annual Meeting. AB2 Abstracts J ALLERGY CLIN IMMUNOL SATURDAY FEBRUARY 2017 IL-22 Generated in Response to Cutaneous Sensitization inflammatory cytokines. TRPM8 protein expression was significantly 4 Drives Neutrophilic Airway Inflammation Following increased in patients with asthma compared with healthy controls using Antigen Inhalation in a Mouse Model of Atopic ELISA of sputum supernatants. There were positive correlations between Dermatitis TRPM8 mRNA level and TSLP, IL-25, and -33 in the sputum of asthmatics. Juan-Manuel Leyva-Castillo, Juhan Yoon, and Raif Geha; Division of CONCLUSIONS: Activation of TRPM8 receptor of bronchial epithelial Immunology, Children’s Hospital and Department of Pediatrics, Harvard cells induces airway inflammatory cytokines, suggesting the TRPM8 Medical School, Boston, MA. receptor may involve in cold induced asthma exacerbations. RATIONALE: Asthma is a heterogeneous chronic pulmonary inflamma- tory disease, commonly preceded by atopic dermatitis (AD). We have A composite of exhaled eicosanoids is associated with recently shown that systemic IL-22 is induced by epicutaneous (EC) 6 childhood asthma and its convalescence sensitization in a mouse model of AD. We examined whether this IL-22 1 2 3 response contributes to airway inflammation triggered by antigen inhala- Li-Chen Chen, MD , H. M. Tseng, PhD , M. L. Kuo, PhD , Ai-Hsuan Wu4, Kuo-Wei Yeh, MD, FAAAAI5, Jing-Long Huang, MD6, and Shau- tion in EC sensitized mice. 7 1 METHODS: Wild type (WT) and Il22-/- mice were subjected to EC sensi- Ku Huang, PhD ; Chang Gung Memorial Hospital, Taiwan, Taoyuan, Taiwan, 2Department of Healthcare Management, Chang Gung Univer- tization with ovalbumin (OVA) or saline followed by intranasal (i.n.) OVA 3 challenge. WT mice were adoptively transferred with OVA TCR-specific sity, Taoyuan, Taoyuan, Taiwan, Department of Microbiology and Immu- -/- nology, Graduate Institute of Basic Medical Research, Chang Gung Th22 from WT or Il22 mice and i.n. challenged with OVA. rIL-22, rIL- 4 17A and rTNFa, alone or in combination were instilled intranasally in University, Taoyuan, Taiwan, Chang-Gung Memorial Hospital, Taoyuan, Taiwan, 5Chang Gung Memorial Hospital, Taoyuan, Taiwan, 6Chang WT mice. Airway inflammation, mRNA levels in the lungs and airway hy- 7 perresponsiveness (AHR) were examined. Gung Memorial Hospital, Taoyuan, Taiwan, Division of Environmental RESULTS: EC OVAsensitization promoted IL-22 production in the lungs Health and Occupational Medicine, National Health Research Institutes, after i.n. challenge. EC OVA sensitized Il22-/- mice exhibited diminished Miaoli, Taiwan. eosinophil and neutrophil airway infiltration and decreased AHR following RATIONALE: Aberrant generation of eicosanoids is associated with i.n. OVA challenge. Moreover, Il22-/- mice exhibited
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