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Oxidative and antioxidative status of children with acute bronchiolitis.

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Oxidative and antioxidative status of children with acute bronchiolitis.

J Pediatr (Rio J). 2013 Jun 21;

Authors: Dundaroz R, Erenberk U, Turel O, Demir AD, Ozkaya E, Erel O

Abstract
OBJECTIVE: Oxidative stress has been shown to contribute to the pathogenesis of acute and chronic lung inflammatory diseases. This article aimed to evaluate the oxidant/antioxidant status of children with acute bronchiolitis through the measurement of plasma total antioxidant capacity, total oxidant status, and oxidative stress index.
METHODS: Children with acute bronchiolitis admitted to the pediatric emergency department of a university hospital between January and April of 2012 were compared with age-matched healthy controls. Patients with acute bronchiolitis were classified as mild and moderate bronchiolitis. Oxidative and antioxidative status were assessed by measurement of plasma total antioxidant capacity, total oxidant status, and oxidative stress index.
RESULTS: Thirty-one children with acute bronchiolitis aged between 3 months and 2 years, and 39 healthy children were included. Total oxidative status (TOS) was higher in patients with acute bronchiolitis than the control group (5.16±1.99μmol H2O2versus 3.78±1.78μmol H2O2 [p=0.004]). Total antioxidant capacity (TAC) was lower in children with bronchiolitis than the control group (2.51±0.37μmol Trolox eqv/L versus 2.75±0.39μmol Trolox eqv/L [p=0.013]). Patients with moderate bronchiolitis presented higher TOS levels than those with mild bronchiolitis and the control group (p=0.03, p<0.001, respectively). Patients with moderate bronchiolitis had higher oxidative stress index levels than the control group (p=0.015). Oxygen saturation level of bronchiolitis patients was inversely correlated with TOS (r=-0.476, p<0.05).
CONCLUSION: The balance between oxidant and antioxidant systems is disrupted in children with moderate bronchiolitis, which indicates that this stress factor may have a role in the pathogenesis of the disease.

PMID: 23796358 [PubMed - as supplied by publisher]

Diffuse lung disease in children: Summary of a scientific conference.

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A multi-disciplinary scientific conference focused on diffuse and interstitial lung diseases in children was held in La Jolla, CA in June 2012.

The conference brought together clinicians (including Pediatric and Adult Pulmonologists, Neonatologists, Pathologists, and Radiologists), clinical researchers, basic scientists, government agency representatives, patient advocates, as well as children affected by diffuse lung disease (DLD) and their families, to review recent scientific developments and emerging concepts in the pathophysiology of childhood DLD.

Invited speakers discussed translational approaches, including genetics and proteomics, epigenetics and epigenomics, models of DLD, including animal models and induced pluripotent stem cells, and regenerative medicine approaches. The presentations of the invited speakers are summarized here. Pediatr Pulmonol. © 2013 Wiley Periodicals, Inc.

Novel Inflammatory Markers, Clinical Risk Factors, and Virus Type Associated with Severe Respiratory Syncytial Virus Infection.

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Virus-induced inflammation contributes to respiratory syncytial virus (RSV) pathogenesis. We sought to determine the specific mediators that are associated with more severe illness in young children.

METHODS:: Children ≤ 5 yrs of age seen in our emergency department for respiratory symptoms from September 1998 to May 2008 were eligible for enrollment. Nasopharyngeal (NP) wash samples were collected from all eligible patients, and clinical data were recorded. Individuals were included in this study if NP wash samples were positive for RSV only. Patients enrolled in the study were stratified by disease severity, defined as mild (not hospitalized), moderate (hospitalized), or severe (requiring ICU stay). Concentrations of individual inflammatory biomarkers in NP wash fluids were determined using the Luminex human 30-plex assay.

RESULTS:: 851 patients met study criteria; 268 (31.5%) with mild, 503 (59.1%) with moderate, and 80 (9.4%) with severe illness. As expected, illness severity was directly associated with young age, prematurity, heart or lung disease, infection with RSV group A, and elevated concentrations of interleukin (IL)-2R, IL-6, CXCL8, tumor necrosis factor (TNF)-α, interferon (IFN)-α, CCL3, CCL4, and CCL2. In addition, we report several novel and mechanistically important inflammatory biomarkers of severe RSV disease, including IL-1β, IL1-RA, IL-7, epidermal growth factor (EGF), and hepatocyte growth factor (HGF).

CONCLUSIONS:: In a large, longitudinal study (10 years, 851 enrolled patients) limited to RSV infection only, in which well-known risk factors are confirmed, we identified five novel biomarkers specifically of severe disease. These markers may ultimately serve to elucidate disease mechanisms.

Depletion of Alveolar Macrophages during Influenza Infection Facilitates Bacterial Superinfections.

Viruses such as influenza suppress host immune function by a variety of methods. This may result in significant morbidity through several pathways, including facilitation of secondary bacterial pneumonia from pathogens such as Streptococcus pneumoniae.

PKH26-phagocytic cell labeling dye was administered intranasally to label resident alveolar macrophages (AMs) in a well-established murine model before influenza infection to determine turnover kinetics during the course of infection. More than 90% of resident AMs were lost in the first week after influenza, whereas the remaining cells had a necrotic phenotype.

To establish the impact of this innate immune defect, influenza-infected mice were challenged with S. pneumoniae. Early AM-mediated bacterial clearance was significantly impaired in influenza-infected mice: ∼50% of the initial bacterial inoculum could be harvested from the alveolar airspace 3 h later. In mock-infected mice, by contrast, >95% of inocula up to 50-fold higher was efficiently cleared. Coinfection during the AM depletion phase caused significant body weight loss and mortality. Two weeks after influenza, the AM population was fully replenished with successful re-establishment of early innate host protection. Local GM-CSF treatment partially restored the impaired early bacterial clearance with efficient protection against secondary pneumococcal pneumonia.

We conclude that resident AM depletion occurs during influenza infection. Among other potential effects, this establishes a niche for secondary pneumococcal infection by altering early cellular innate immunity in the lungs, resulting in pneumococcal outgrowth and lethal pneumonia. This novel mechanism will inform development of novel therapeutic approaches to restore lung innate immunity against bacterial superinfections.

Adult-Onset Asthma Becomes the Dominant Phenotype among Women by Age 40 Years. The Longitudinal CARDIA Study.

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Adult-Onset Asthma Becomes the Dominant Phenotype among Women by Age 40 Years. The Longitudinal CARDIA Study.

Ann Am Thorac Soc. 2013 Jun;10(3):188-97

Authors: Sood A, Qualls C, Schuyler M, Arynchyn A, Alvarado JH, Smith LJ, Jacobs DR

Abstract
Rationale: Although asthma is usually considered to originate in childhood, adult-onset disease is being increasingly reported. Objectives: To contrast the proportion and natural history of adult-onset versus pediatric-onset asthma in a community-based cohort. We hypothesized that asthma in women is predominantly of adult onset rather than of pediatric onset. Methods: This study used data from the Coronary Artery Risk Development in Young Adults (CARDIA) cohort in the United States over a 25-year period. Adult- and pediatric-onset asthma phenotypes were studied, as defined by age at onset of 18 years or older. Subjects with asthma were categorized by sex, obesity, atopy, smoking, and race by mean age/examination year, using a three-way analysis of covariance model. Natural history of disease was examined using probabilities derived from a Markov chain model. Measurements and Main Results: Asthma of adult onset became the dominant (i.e., exceeded 50%) phenotype in women by age 40 years. The age by which adult-onset asthma became the dominant phenotype was further lowered for obese, nonatopic, ever-smoking, or white women. The prevalence trend with increasing time for adult-onset disease was greater among subjects with nonatopic than atopic asthma among both sexes. Furthermore, adult-onset asthma had remarkable sex-related differences in risk factors. In both sexes, the quiescent state for adult-onset asthma was less frequent and also "less stable" over time than for pediatric-onset asthma. Conclusions: Using a large national cohort, this study challenges the dictum that most asthma in adults originates in childhood. Studies of the differences between pediatric- and adult-onset asthma may provide greater insight into the phenotypic heterogeneity of asthma.

PMID: 23802814 [PubMed - in process]

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