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Bronchiectasis patients are susceptible to infection with Pseudomonas aeruginosa. Isolation is associated with increased severity of disease, greater airflow obstruction and poorer quality of life. It is not known whether infection by P. aeruginosa is a marker of disease severity or contributes to disease progression.Consecutive non-cystic fibrosis adult bronchiectasis outpatients (n5163) with multiple sputum cultures and follow-up pulmonary function tests were designated, according to isolation of P. aeruginosa, as ''never infected'' (group 1; n567), ''intermittently isolated'' (group 2; n582) and ''chronically infected'' (group 3; n514). Based upon change in forced expiratory volume in one second (FEV1) % predicted levels at o2 yrs after presentation, longitudinal behaviour was characterised as ''improvement'' (o10% rise), ''decline'' (o10% fall) or ''stability''. Baseline pulmonary-function tests and longitudinal behaviour were examined in relation to pseudomonas status.There was no difference between the groups in age, sex, smoking habit or length of follow-up. Baseline FEV1 levels were highest in group 1 (mean¡SD: 77.4¡24.3) and higher in group 2 (67.3¡25.7) than in group 3 (55.2¡18.5). The same significant trends were seen for baseline FEV1/forced vital capacity ratios and diffusing capacity of the lung for carbon monoxide levels. Subsequent longitudinal behaviour was linked to baseline FEV1 levels, which were lowest in patients with improvement and lower in association with decline than with stability. However, longitudinal behaviour did not differ between groups 1, 2 and 3, either before or after adjustment for baseline FEV1 levels.Infection by Pseudomonas aeruginosa occurs in bronchiectasis patients with more severe impairment of pulmonary function but does not influence rate of decline in pulmonary function either before or after adjustment for baseline disease severity. Thus, Pseudomonas aeruginosa is a marker of bronchiectasis severity but is not linked to an accelerated decline in pulmonary function.

Orexins are synthesized by neurons in the hypothalamus and contribute to multiple physiological functions. Orexin fibers innervate many regions of the CNS, which include areas involved in descending control of pain. We examined the role orexins may play in endogenous modulation of pain transmission using prepro-orexin (precursor of orexin A and B) knockout mice. Baseline pain thresholds of knockout and wild type mice were not different. Knockout mice presented greater degree of hyperalgesia induced by peripheral inflammation and less stress-induced analgesia than wild type mice. Double staining of orexin and c-Fos in wild type mice revealed activation of orexin neurons under both conditions. These results suggest that persistent pain and stress activate orexin neurons, which act to inhibit pain transmission.

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