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Urinary Peptides As a Novel Source of T Cell Allergen Epitopes.
da Silva Antunes R, Pham J, McMurtrey C, Hildebrand WH, Phillips E, Mallal S, Sidney J, Busse P, Peters B, Schulten V, Sette A
(2018) Front Immunol 9: 886
MeSH Terms: Adult, Allergens, Animals, Asthma, Epitopes, T-Lymphocyte, Female, Humans, Immunoglobulin E, Male, Mice, Middle Aged, Peptides, Proteome, Proteomics, Rhinitis, Allergic, T-Lymphocytes
Show Abstract · Added March 30, 2020
Mouse allergy in both laboratory workers and in inner-city children is associated with allergic rhinitis and asthma, posing a serious public health concern. Urine is a major source of mouse allergens, as mice spray urine onto their surroundings, where the proteins dry up and become airborne on dust particles. Here, we tested whether oligopeptides that are abundant in mouse urine may contribute to mouse allergic T cell response. Over 1,300 distinct oligopeptides were detected by mass spectrometry analysis of the low molecular weight filtrate fraction of mouse urine (LoMo). Posttranslationally modified peptides were common, accounting for almost half of total peptides. A pool consisting of 225 unique oligopeptides of 13 residues or more in size identified within was tested for its capacity to elicit T cell reactivity in mouse allergic donors. Following 14-day stimulation of PBMCs, we detected responses in about 95% of donors tested, directed against 116 distinct peptides, predominantly associated with Th2 cytokines (IL-5). Peptides from non-urine related proteins such as epidermal growth factor, collagen, and Beta-globin accounted for the highest response (15.9, 9.1, and 8.1% of the total response, respectively). Peptides derived from major urinary proteins (MUPs), kidney androgen-regulated protein (KAP), and uromodulin were the main T cell targets from kidney or urine related sources. Further analysis of enrichment of 4-1BB expressing cells demonstrated that LoMo pool-specific T cell reactivity can be detected directly in mouse allergic but not in non-allergic donors. Further cytometric analysis of responding cells revealed a bone fide memory T cell phenotype and confirmed their Th2 polarization. Overall, these data suggest that mouse urine-derived oligopeptides are a novel target for mouse allergy-associated T cell responses, which may contribute to immunopathological mechanisms in mouse allergy.
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Unique application of awake tracheoscopy and endobronchial ultrasound in the management of tracheal mucoepidermoid carcinoma.
Rehman S, Lovvorn HN, Rickman OB, Wootten CT, Chinnadurai S
(2018) Head Neck 40: E58-E61
MeSH Terms: Adolescent, Asthma, Bronchoscopy, Carcinoma, Mucoepidermoid, Deglutition Disorders, Dyspnea, Emergency Service, Hospital, Endosonography, Female, Humans, Minimally Invasive Surgical Procedures, Rare Diseases, Risk Assessment, Tracheal Neoplasms, Treatment Outcome
Show Abstract · Added November 30, 2020
BACKGROUND - Mucoepidermoid carcinoma of the trachea is a rare pediatric malignancy that presents unique challenges in diagnosis, operative management, and surveillance.
METHODS AND RESULTS - We present a 17-year-old girl with primary tracheal mucoepidermoid carcinoma presenting in acute respiratory distress due to near-total occlusion of the tracheal airway. An algorithmic approach to preoperative planning was developed to evaluate and remove the tumor endoscopically without compromising oxygenation. After initial palliative resection, endobronchial ultrasound was uniquely applied to evaluate depth of tumor invasion, and subsequent tracheal resection with primary anastomosis was performed as curative treatment.
CONCLUSION - Removal of distal tracheal masses can be performed safely with the implementation of an algorithmic approach to tumor visualization and resection. Endobronchial ultrasound can be used to evaluate the extent of tumor invasion and plan for definitive resection.
© 2018 Wiley Periodicals, Inc.
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Glucagon-like peptide 1 signaling inhibits allergen-induced lung IL-33 release and reduces group 2 innate lymphoid cell cytokine production in vivo.
Toki S, Goleniewska K, Reiss S, Zhang J, Bloodworth MH, Stier MT, Zhou W, Newcomb DC, Ware LB, Stanwood GD, Galli A, Boyd KL, Niswender KD, Peebles RS
(2018) J Allergy Clin Immunol 142: 1515-1528.e8
MeSH Terms: Allergens, Alternaria, Animals, Asthma, Cytokines, Dermatophagoides pteronyssinus, Eosinophilia, Female, Glucagon-Like Peptide 1, Glucagon-Like Peptide-1 Receptor, Immunity, Innate, Interleukin-33, Lung, Lymphocytes, Mice, Inbred BALB C, Mice, Transgenic, Mucus, Signal Transduction
Show Abstract · Added April 10, 2018
BACKGROUND - IL-33 is one of the most consistently associated gene candidates for asthma identified by using a genome-wide association study. Studies in mice and in human cells have confirmed the importance of IL-33 in inducing type 2 cytokine production from both group 2 innate lymphoid cells (ILC2s) and T2 cells. However, there are no pharmacologic agents known to inhibit IL-33 release from airway cells.
OBJECTIVE - We sought to determine the effect of glucagon-like peptide 1 receptor (GLP-1R) signaling on aeroallergen-induced airway IL-33 production and release and on innate type 2 airway inflammation.
METHODS - BALB/c mice were challenged intranasally with Alternaria extract for 4 consecutive days. GLP-1R agonist or vehicle was administered starting either 2 days before the first Alternaria extract challenge or 1 day after the first Alternaria extract challenge.
RESULTS - GLP-1R agonist treatment starting 2 days before the first Alternaria extract challenge decreased IL-33 release in the bronchoalveolar lavage fluid and dual oxidase 1 (Duox1) mRNA expression 1 hour after the first Alternaria extract challenge and IL-33 expression in lung epithelial cells 24 hours after the last Alternaria extract challenge. Furthermore, GLP-1R agonist significantly decreased the number of ILC2s expressing IL-5 and IL-13, lung protein expression of type 2 cytokines and chemokines, the number of perivascular eosinophils, mucus production, and airway responsiveness compared with vehicle treatment. GLP-1R agonist treatment starting 1 day after the first Alternaria extract challenge also significantly decreased eosinophilia and type 2 cytokine and chemokine expression in the airway after 4 days of Alternaria extract challenge.
CONCLUSION - These results reveal that GLP-1R signaling might be a therapy to reduce IL-33 release and inhibit the ILC2 response to protease-containing aeroallergens, such as Alternaria.
Copyright © 2018 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
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A survey of drug allergy training opportunities in the United States.
Derrick MI, Williams KB, Shade LMP, Phillips EJ
(2018) J Allergy Clin Immunol Pract 6: 302-304
MeSH Terms: Allergens, Aspirin, Asthma, Aspirin-Induced, Desensitization, Immunologic, Drug Hypersensitivity, Education, Fellowships and Scholarships, Humans, Preceptorship, Surveys and Questionnaires, United States
Added March 30, 2020
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Seasonal patterns of Asthma medication fills among diverse populations of the United States.
Turi KN, Gebretsadik T, Lee RL, Hartert TV, Evans AM, Stone C, Sicignano NM, Wu AC, Iribarren C, Butler MG, Mitchel E, Morrow J, Larkin EK, Wu P
(2018) J Asthma 55: 764-770
MeSH Terms: Administration, Inhalation, Administration, Oral, Adolescent, Adrenergic beta-Agonists, Adult, Anti-Asthmatic Agents, Asthma, Child, Child, Preschool, Drug Prescriptions, Drug Therapy, Combination, Female, Glucocorticoids, Humans, Male, Medication Adherence, Middle Aged, Retrospective Studies, Seasons, United States, Young Adult
Show Abstract · Added March 14, 2018
OBJECTIVE - Nonadherence to controller and overuse of reliever asthma medications are associated with exacerbations. We aimed to determine patterns of seasonal asthma medication use and to identify time period(s) during which interventions to improve medication adherence could reduce asthma morbidity.
METHODS - We conducted a retrospective cohort study of asthmatics 4-50 years of age and enrolled in three diverse health insurance plans. Seasonal patterns of medications were reported by monthly prescription fill rates per 1000 individuals with asthma from 1998 to 2013, and stratified by healthcare plan, sex, and age.
RESULTS - There was a distinct and consistent seasonal fill pattern for all asthma medications. The lowest fill rate was observed in the month of July. Fills increased in the autumn and remained high throughout the winter and spring. Compared with the month of May with high medication fills, July represented a relative decrease of fills ranging from 13% (rate ratio, RR: 0.87, 95% confidence interval, 95%CI: 0.72-1.04) for the combination of inhaled corticosteroids (ICS) + long acting beta agonists (LABA) to 45% (RR: 0.55, 95%CI: 0.49-0.61) for oral corticosteroids. Such a seasonal pattern was observed each year across the 16-year study period, among healthcare plans, sexes, and ages. LABA containing control medication (ICS+LABA and LABA) fill rates were more prevalent in older asthmatics, while leukotriene receptor antagonists were more prevalent in the younger population.
CONCLUSIONS - A seasonal pattern of asthma medication fill rates likely represents a reactive response to a loss of disease control and increased symptoms. Adherence to and consistent use of asthma medications among individuals who use medications in reaction to seasonal exacerbations might be a key component in reducing the risk of asthma exacerbations.
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Relationship Between Body Mass Index and Outcomes Among Hospitalized Patients With Community-Acquired Pneumonia.
Bramley AM, Reed C, Finelli L, Self WH, Ampofo K, Arnold SR, Williams DJ, Grijalva CG, Anderson EJ, Stockmann C, Trabue C, Fakhran S, Balk R, McCullers JA, Pavia AT, Edwards KM, Wunderink RG, Jain S, Centers for Disease Control and Prevention Etiology of Pneumonia in the Community (EPIC) Study Team
(2017) J Infect Dis 215: 1873-1882
MeSH Terms: Adolescent, Adult, Aged, Asthma, Body Mass Index, Child, Child, Preschool, Community-Acquired Infections, Comorbidity, Female, Hospitalization, Humans, Intensive Care Units, Length of Stay, Male, Middle Aged, Obesity, Odds Ratio, Pneumonia, Prospective Studies, Respiration, Artificial, Treatment Outcome, Young Adult
Show Abstract · Added July 27, 2018
Background - The effect of body mass index (BMI) on community-acquired pneumonia (CAP) severity is unclear.
Methods - We investigated the relationship between BMI and CAP outcomes (hospital length of stay [LOS], intensive care unit [ICU] admission, and invasive mechanical ventilation) in hospitalized CAP patients from the Centers for Disease Control and Prevention Etiology of Pneumonia in the Community (EPIC) study, adjusting for age, demographics, underlying conditions, and smoking status (adults only).
Results - Compared with normal-weight children, odds of ICU admission were higher in children who were overweight (adjusted odds ratio [aOR], 1.7; 95% confidence interval [CI], 1.1-2.8) or obese (aOR, 2.1; 95% CI, 1.4-3.2), and odds of mechanical ventilation were higher in children with obesity (aOR, 2.7; 95% CI, 1.3-5.6). When stratified by asthma (presence/absence), these findings remained significant only in children with asthma. Compared with normal-weight adults, odds of LOS >3 days were higher in adults who were underweight (aOR, 1.6; 95% CI, 1.1-2.4), and odds of mechanical ventilation were lowest in adults who were overweight (aOR, 0.5; 95% CI, .3-.9).
Conclusions - Children who were overweight or obese, particularly those with asthma, had higher odds of ICU admission or mechanical ventilation. In contrast, adults who were underweight had longer LOS. These results underscore the complex relationship between BMI and CAP outcomes.
Published by Oxford University Press for the Infectious Diseases Society of America 2017. This work is written by (a) US Government employee(s) and is in the public domain in the US.
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Prostaglandin I2 Suppresses Proinflammatory Chemokine Expression, CD4 T Cell Activation, and STAT6-Independent Allergic Lung Inflammation.
Zhou W, Zhang J, Goleniewska K, Dulek DE, Toki S, Newcomb DC, Cephus JY, Collins RD, Wu P, Boothby MR, Peebles RS
(2016) J Immunol 197: 1577-86
MeSH Terms: Allergens, Animals, Antihypertensive Agents, Asthma, CD4-Positive T-Lymphocytes, Cell Proliferation, Chemokines, Epoprostenol, Hypersensitivity, Indomethacin, Inflammation, Interleukin-13, Interleukin-5, Lung, Lymphocyte Activation, Mice, Mice, Inbred BALB C, Mice, Knockout, Ovalbumin, Receptors, Epoprostenol, STAT6 Transcription Factor, Signal Transduction, Th2 Cells
Show Abstract · Added March 14, 2018
Allergic airway diseases are immune disorders associated with heightened type 2 immune responses and IL-5 and IL-13 production at the site of inflammation. We have previously reported that cyclooxygenase (COX) inhibition by indomethacin augmented allergic airway inflammation in a STAT6-independent manner. However, the key COX product(s) responsible for restraining indomethacin-mediated STAT6-independent allergic inflammation is unknown. In this study, using the mouse model of OVA-induced allergic airway inflammation, we identified that PGI2 receptor (IP) signaling was critical for indomethacin-induced, STAT6-independent proallergic effects. We demonstrated that IP deficiency increased inflammatory cell infiltration, eosinophilia, and IL-5 and IL-13 expression in the lung in a STAT6-independent manner. The augmented STAT6-independent allergic inflammation correlated with enhanced primary immune responses to allergic sensitization and elevated production of multiple inflammatory chemokines (CCL11, CCL17, CCL22, and CXCL12) in the lung after allergen challenge. We also showed that the PGI2 analogue cicaprost inhibited CD4 T cell proliferation and IL-5 and IL-13 expression in vitro, and IP deficiency diminished the stimulatory effect of indomethacin on STAT6-independent IL-5 and IL-13 responses in vivo. The inhibitory effects of PGI2 and the IP signaling pathway on CD4 T cell activation, inflammatory chemokine production, and allergic sensitization and airway inflammation suggest that PGI2 and its analogue iloprost, both Food and Drug Administration-approved drugs, may be useful in treating allergic diseases and asthma. In addition, inhibiting PGI2 signaling by drugs that either block PGI2 production or restrain IP signaling may augment STAT6-independent pathways of allergic inflammation.
Copyright © 2016 by The American Association of Immunologists, Inc.
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The intersection between asthma and acute chest syndrome in children with sickle-cell anaemia.
DeBaun MR, Strunk RC
(2016) Lancet 387: 2545-53
MeSH Terms: Acute Chest Syndrome, Adolescent, Age Distribution, Anemia, Sickle Cell, Anti-Bacterial Agents, Asthma, Bronchial Hyperreactivity, Child, Child, Preschool, Female, Humans, Infant, Infant, Newborn, Male, Risk Factors, Young Adult
Show Abstract · Added July 20, 2016
Acute chest syndrome is a frequent cause of acute lung disease in children with sickle-cell disease. Asthma is common in children with sickle-cell disease and is associated with increased incidence of vaso-occlusive pain events, acute chest syndrome episodes, and earlier death. Risk factors for asthma exacerbation and an acute chest syndrome episode are similar, and both can present with shortness of breath, chest pain, cough, and wheezing. Despite overlapping risk factors and symptoms, an acute exacerbation of asthma or an episode of acute chest syndrome are two distinct entities that need disease-specific management strategies. Although understanding has increased about asthma as a comorbidity in sickle-cell disease and its effects on morbidity, substantial gaps remain in knowledge about best management.
Copyright © 2016 Elsevier Ltd. All rights reserved.
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Improved Guideline Adherence With Integrated Sickle Cell Disease and Asthma Care.
McClain BL, Ivy ZK, Bryant V, Rodeghier M, DeBaun MR
(2016) Am J Prev Med 51: S62-8
MeSH Terms: Anemia, Sickle Cell, Asthma, Child, Delivery of Health Care, Integrated, Female, Guideline Adherence, Humans, Male, Patient Care Team, Prospective Studies, Respiratory Function Tests, Respiratory Therapy, Spirometry
Show Abstract · Added July 20, 2016
INTRODUCTION - In children with sickle cell disease (SCD), concomitant asthma is associated with increased morbidity and mortality when compared with children with SCD without asthma. Despite the well-established burden of asthma in children with SCD, no paradigm of care exists for the co-management of these two diseases.
METHODS - To address this gap, an integrated SCD and asthma clinic was created in a community health center that included (1) a dual respiratory therapist/asthma case manager; (2) an SCD nurse practitioner with asthma educator certification; (3) an onsite pulmonary function test laboratory; (4) a pediatric hematologist with expertise in managing SCD and asthma; and (5) application of the National Asthma Education and Prevention Program guidelines. A before (2010-2012) and after (2013-2014) study design was used to assess for improved quality of care with implementation of an integrative care model among 61 children with SCD and asthma followed from 2010 to 2014.
RESULTS - Asthma action plan utilization after initial diagnosis increased with the integrative care model (n=16, 56% before, 100% after, p=0.003), as did the use of spirometry in children aged ≥5 years (n=41, 65% before, 95% after, p<0.001) and correction of lower airway obstruction (n=10, 30% before, 80% after, p=0.03).
CONCLUSIONS - Although the use of an integrative care model for SCD and asthma improved evidence-based asthma care, longer follow-up and evaluation will be needed to determine the impact on SCD-related morbidity.
Copyright © 2016 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.
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Pattern of Lung Function Is Not Associated with Prior or Future Morbidity in Children with Sickle Cell Anemia.
Cohen RT, Strunk RC, Rodeghier M, Rosen CL, Kirkham FJ, Kirkby J, DeBaun MR
(2016) Ann Am Thorac Soc 13: 1314-23
MeSH Terms: Acute Chest Syndrome, Adolescent, Anemia, Sickle Cell, Asthma, Child, Comorbidity, Female, Humans, Logistic Models, Lung, Male, Multivariate Analysis, Pain, Prospective Studies, Respiratory Function Tests, Respiratory Physiological Phenomena, Risk Factors, Spirometry, Surveys and Questionnaires, United States, Young Adult
Show Abstract · Added July 20, 2016
RATIONALE - Patient factors associated with development of abnormal lung function in children with sickle cell anemia (SCA) have not been fully characterized.
OBJECTIVES - To characterize lung function abnormalities among children with SCA and to determine whether these steady-state lung function results were associated with morbidity before or after testing among children with SCA.
METHODS - This study was part of the prospective National Institutes of Health-funded Sleep and Asthma Cohort Study. Children with HbSS or Hb Sβ(o) (SCA) were enrolled without regard for sickle cell-related comorbidities or diagnosis of asthma. Lung function was measured by spirometry and plethysmography on the same day, when free of acute disease. Standardized asthma symptom questionnaires and review of the medical records were also performed.
MEASUREMENTS AND MAIN RESULTS - A total of 149 children aged 6 to 19 years completed lung function testing, of whom 139 participants had retrospective morbidity data from birth to the test date, and 136 participants were followed prospectively for a median of 4.3 years from the test date. At baseline, percentages with normal, obstructive, restrictive, nonspecific, and mixed lung function patterns were 70, 16, 7, 6, and 1, respectively. Neither retrospective rates of pain nor acute chest syndrome was associated with lung function patterns. Furthermore, baseline lung function pattern was not predictive of future pain or acute chest syndrome episodes.
CONCLUSIONS - The majority of children with SCA have lung function that is within the normal range. Abnormal lung function patterns were not associated with prior vasoocclusive pain or acute chest syndrome episodes, and baseline lung function patterns did not predict future vasoocclusive pain or chest syndrome episodes.
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21 MeSH Terms