Login to your account

Username *
Password *
Remember Me

Blog With Right Sidebar

    Vous êtes ici :  
  1. Accueil
  2. Blog With Right Sidebar

The Infant Nasopharyngeal Microbiome Impacts Severity of Lower Respiratory Infection and Risk of Asthma Development.

The nasopharynx (NP) is a reservoir for microbes associated with acute respiratory infections (ARIs). Lung inflammation resulting from ARIs during infancy is linked to asthma development. We examined the NP microbiome during the critical first year of life in a prospective cohort of 234 children, capturing both the viral and bacterial communities and documenting all incidents of ARIs.

Most infants were initially colonized with Staphylococcus or Corynebacterium before stable colonization with Alloiococcus or Moraxella. Transient incursions of Streptococcus, Moraxella, or Haemophilus marked virus-associated ARIs. Our data identify the NP microbiome as a determinant for infection spread to the lower airways, severity of accompanying inflammatory symptoms, and risk for future asthma development. Early asymptomatic colonization with Streptococcus was a strong asthma predictor, and antibiotic usage disrupted asymptomatic colonization patterns.

In the absence of effective anti-viral therapies, targeting pathogenic bacteria within the NP microbiome could represent a prophylactic approach to asthma.

Molecular allergy diagnosis for the clinical characterization of asthma.

Defining the allergen sensitization of a patient with asthma at the molecular level by measuring specific IgE to purified natural or recombinant allergens can improve diagnostic accuracy and improve asthma phenotyping.

Molecular diagnosis is possible thanks to the specificity of some markers of species-specific sensitization and resolve cross-reactivity phenomena from a true co-sensitization. None of this precision is possible with conventional allergy tests, and such information will eventually give clinicians the possibility to individualize the actions taken, including indications on reducing targeted-allergen exposure or selection of suitable allergens for specific immunotherapy, thereby increasing the safety and efficacy of immunotherapy. Nevertheless, all in vitro tests should be assessed alongside clinical history, as allergen sensitization does not necessarily imply clinical responsiveness.

The VCDQ - a Questionnaire for Symptom Monitoring in Vocal Cord Dysfunction.

Vocal Cord Dysfunction (VCD) typically involves abnormal adduction of the vocal cords during inspiration, mimics the symptoms of asthma and leads to the prescription of ineffective medications.

OBJECTIVE: We aimed to develop a clinical tool to monitor symptoms and response to treatment in confirmed VCD.

METHODS: We collated symptoms of VCD from focus groups comprising patients and healthcare-professionals; phrases describing these symptoms were assessed for face validity and internal correlation, and rated for importance. The resultant 12 item questionnaire (VCDQ) rated the impact of each on a 5-point Likert scale (total score range 12 to 60), and was tested for reliability, concurrent validity and performance in 31 patients with endoscopically confirmed VCD (± asthma), 29 asthmatics with no history of VCD, and 14 healthy controls. We assessed response to speech and language therapy and the minimal important difference by measuring the VCDQ pre- and post- therapy in a 20 new patients.

RESULTS: The VCDQ had excellent test-retest reliability, and differentiated VCD versus healthy (Mann-Whitney test: z = -5.390, P < 0.001) and asthma (z = -5.730, p < 0.001). All patients improved post-therapy, assessed both by a global rating of change score (GRCS) and by the VCDQ [median (IQR) score pre-therapy 50.5 (48.0 - 54.8), post therapy 35.0 (29.3 - 41.8), p < 0.001]. The minimal important difference in the VCDQ associated with a rating of "minimally better" on the GRCS was 4 points.

CONCLUSIONS AND CLINICAL RELEVANCE: The VCDQ is a valid and responsive tool suitable for measuring changes in symptoms in patients with VCD. It also gives insight into which symptoms are important to patients, and could guide future therapy refinements. Future assessments of novel therapies for this condition should use an appropriately validated tool such as the VCDQ to measure response. This article is protected by copyright. All rights reserved.

In utero Vitamin D Deficiency Increases Airway Smooth Muscle Mass and Impairs Lung Function.

We have previously demonstrated increased airway smooth muscle (ASM) mass and airway hyperresponsiveness (AHR) in whole-life vitamin D-deficient female mice.

In this study we aimed to uncover the molecular mechanisms contributing to altered lung structure and function. RNA was extracted from lung tissue of whole-life vitamin D-deficient and -replete female mice, and gene expression patterns were profiled by RNA-Seq. The data showed that genes involved in embryonic organ development, pattern formation, branching morphogenesis, Wnt signalling, and inflammation were differentially expressed in vitamin D-deficient mice. Network analysis suggested that differentially expressed genes were connected by the hubs MMP9, NFKBIA, EGFR and EP300. Given our findings that developmental pathways may be altered, we investigated if the timing of vitamin D exposure (in utero versus postnatal) had an impact on lung health outcomes. Gene expression was measured in in utero or postnatal vitamin D-deficient mice, as well as whole-life vitamin D-deficient and -replete mice at 8-weeks of age. Baseline lung function, AHR and airway inflammation were measured and lungs fixed for lung structure assessment using stereological methods, and quantification of ASM mass.

In utero vitamin D deficiency was sufficient to increase ASM mass, baseline airway resistance, and alter lung structure. There were increased neutrophils but decreased lymphocytes in bronchoalveolar lavage. Expression of inflammatory molecules S100A9 and S100A8 was mainly increased in postnatal vitamin D-deficient mice.

These observations suggest that in utero vitamin D deficiency can alter lung structure and function, and increase inflammation, contributing to symptoms in chronic diseases such as asthma.

Connective Tissue Disease–related Thoracic Disease

Pulmonary involvement is a frequent manifestation of connective tissue disease (CTD)–related thoracic disease. It is important to characterize the underlying pattern when pulmonary involvement occurs in a patient with CTD, and to exclude other causes. A systematic approach, evaluating each compartment of the lung (airway, interstitium, pleura, pulmonary vasculature) may be helpful. In complex cases, a multidisciplinary approach should be considered, potentially including the pulmonologist, rheumatologist, radiologist, pathologist, and sometimes the infectious disease specialist or oncologist. New techniques, such as quantitative computed tomography and MRI, are expected to be helpful for evaluation and management of CTD-associated thoracic disease. (Source: Clinics in Chest Medicine)

Search

Search