Nasal microbiota dominated by Moraxella spp. is associated with respiratory health in the elderly population: a case control study.

BACKGROUND: The elderly (≥65 years) are one of the populations most at risk for respiratory tract infections (RTIs). The aim of this study was to determine whether nasal and/or oropharyngeal microbiota profiles are associated with age and RTIs. METHODS: Nasal and oropharyngeal swabs of 152 controls and 152 patients with an RTI were included. The latter group consisted of 72 patients with an upper respiratory tract infection (URTI) and 80 with a lower respiratory tract infection (LRTI). Both nasal and oropharyngeal swabs were subjected to microbiota profiling using amplicon sequencing of the 16S rRNA gene. Moraxella species were determined using quantitative real-time PCR and culture. RESULTS: Based on the microbiota profiles of the controls and the patients with an RTI, eight nasal and nine oropharyngeal microbiota clusters were defined. Nasal microbiota dominated by either Moraxella catarrhalis or Moraxella nonliquefaciens was significantly more prevalent in elderly compared to mid-aged adults in the control group (p = 0.002). Dominance by M. catarrhalis/nonliquefaciens was significantly less prevalent in elderly with an LRTI (p = 0.001) compared to controls with similar age. CONCLUSIONS: Nasal microbiota dominated by M. catarrhalis/nonliquefaciens is associated with respiratory health in the elderly population.

Asymptomatic worsening of airway inflammation during low-dose allergen exposure in asthma: protection by inhaled steroids.

Asthma is a chronic inflammatory disease that persists even during adequate therapy and asymptomatic episodes. We questioned whether "silent" chronic allergen exposure can induce and maintain airway inflammation and whether this still occurs during regular treatment with inhaled steroids. Twenty-six patients with house dust mite allergy and mild asthma (dual responders) participated in a parallel, double-blind study. All patients inhaled a low-dose of allergen on 10 subsequent working days (Days 1-5, 8-12). They were treated with 400 micro g budesonide once daily (n = 13) or placebo (n = 13) from Days -3 to 19. At baseline (Day -6) and on Days 5, 12, and 19 we measured the provocative concentration of methacholine causing a 20% fall in FEV(1) (PC(20)), and percent eosinophils, interleukin (IL)-5/interferon-gamma messenger RNA ratio (in sputum cells by real-time reverse transcription-polymerase chain reaction [RT-PCR]), and eosinophilic cationic protein (ECP) in induced sputum. Symptoms, peak expiratory flow (PEF), FEV(1), and exhaled nitric oxide (NO) were recorded repeatedly during the study. In the placebo group, repeated low-dose allergen exposure resulted in a significant increase in sputum eosinophils (p = 0.043), ECP (p = 0.011), IL-5/IFN-gamma messenger RNA ratio (p = 0.04), and in exhaled NO (p = 0.001), without worsening of symptoms, PEF, or baseline FEV(1) (p > 0.07). In the budesonide group, the changes in PC(20), sputum ECP, and exhaled NO were significantly different as compared with the placebo group (p < 0.03). We conclude that repeated low-dose allergen exposure in asthma can lead to airway inflammation without worsening of symptoms, which can be prevented by inhaled steroid treatment. This suggests that antiinflammatory therapy is beneficial during allergen exposure, even during asymptomatic episodes.

Are rhinovirus-induced airway responses in asthma aggravated by chronic allergen exposure?

Airway inflammation in asthma may represent a favorable environment for respiratory viral infections, augmenting virus-induced exacerbations in asthma. We postulated that repeated low-dose allergen exposure preceding experimental rhinovirus 16 (RV16) infection increases the severity of RV-induced airway obstruction and inflammation. Thirty-six house dust mite-allergic patients with mild to moderate asthma participated in a three-arm, parallel, placebo-controlled, double-blind study. Patients inhaled a low dose of house dust mite allergen for 10 subsequent working days (Days 1-5 and 8-12) and/or were subsequently infected with RV16 (Days 15 and 16). Allergen exposure resulted in a significant fall in FEV1 (p < 0.001) and provocative concentration of histamine causing a 20% fall in FEV1 (p < 0.001) and an increase in exhaled nitric oxide (p < 0.001) and percentage of sputum eosinophils (p < 0.001). RV16 infection led to a fall in FEV1 (p = 0.02) and increases in the percentage of sputum neutrophils (p = 0.01), sputum interleukin-8 (p = 0.04), and neutrophil elastase (p = 0.04). Successive allergen exposure and RV16 infection had no synergistic or additive effect on any of the clinical or inflammatory outcomes. In conclusion, repeated low-dose allergen exposure and RV16 infection induce distinct inflammatory profiles within the airways in asthma without apparent interaction between these two environmental triggers. This suggests that preceding allergen exposure, at the used dose and duration, is not a determinant of the severity of RV-induced exacerbations in patients with mild to moderate asthma.