SummaryChronic obstructive pulmonary disease (COPD) is characterized by an abnormal innate immune response. We have investigated the changes in the innate immune response of COPD alveolar macrophages exposed to both cigarette smoke and Toll-like receptor (TLR) stimulation. COPD and control alveolar macrophages were exposed to cigarette smoke extract (CSE) followed by TLR-2, -4 and -5 ligands [Pam3CSK4, lipopolysaccharide (LPS) and phase I flagellin (FliC), respectively] or non-typeable Haemophilus influenzae (NTHi). CSE exposure suppressed TLR-induced tumour necrosis factor (TNF)-α, interleukin (IL)-6, IL-10 and regulated on activation, normal T cell expressed and secreted (RANTES) production in both COPD and control alveolar macrophages, but had no effect on interleukin 8 (CXCL8) production. Similarly, CSE suppressed NTHi-induced TNF-α but not NTHiinduced CXCL8 production in COPD alveolar macrophages. Gene expression analysis showed that CSE suppressed LPS-induced TNF-α transcription but not CXCL8 transcription in COPD alveolar macrophages. The dampening effect of CSE on LPS-induced cytokine production was associated with a reduction in p38, extracellular signal regulated kinase (ERK) and p65 activation. In conclusion, CSE caused a reduced innate immune response in COPD alveolar macrophages, with the exception of persistent CXCL8 production. This could be a mechanism by which alveolar macrophages promote neutrophil chemotaxis under conditions of oxidative stress and bacterial exposure.
Background -Patients with non-tuberculous mycobacteria are usually started on conventional antituberculous triple therapy once acid fast bacilli are detected, before the exact type of mycobacteria has been identified. The ability to identify the characteristics of patients with tuberculous and non-tuberculous mycobacteria may be helpful in identifying before treatment those patients more likely to have non-tuberculous infection. Methods -A retrospective study was conducted of all patients in one unit in whom non-tuberculous mycobacteria were identified in sputum or bronchoalveolar washings in the period 1987-93.
Bilateral renal artery occlusion caused by malposition of a stent-graft is probably underreported. If revascularization of the kidneys by endovascular techniques fails, there is no consensus as to the optimal approach. Delayed revascularization should be considered if the kidneys show concentration of imaging contrast. Hepato-spleno-renal bypass, which has not heretofore been indicated for renal salvage post EVAR, can provide a good functional result in this situation.
Non-tuberculous mycobacteria (NTM) are an emerging pathogen worldwide in both cystic fibrosis (CF) and non-CF pulmonary disease (PD), with reports suggesting an increasing prevalence [1,2]. It is an opportunistic infection acquired from the environment [3], though conflicting evidence remains around person-to-person transmission [4,5]. Recent evidence suggests that Mycobacterium abscessus complex (MABSC) may be the most detrimental airway infection to lung function in CF [6], yet its treatment remains poorly evidenced.The paediatric CF service at the Royal Brompton Hospital (RBH) has had standardised diagnostic and treatment guidelines since 2011, which follow the American Thoracic Society (ATS) guidelines for the diagnosis of NTM-PD [7] and latterly CF-specific consensus guidelines [8,9]. In CF, the two most commonly encountered species are MABSC and Mycobacterium avium complex (MAC), with the former more prevalent in the UK and the latter in the USA [1,10]. A recent consensus statement on treatment outcome definitions could not reach consensus on a definition of cure, but a microbiological cure was agreed as the end of anti-microbial treatment after culture conversion [11].
SUMMARY An antigen capture immunoassay was developed for the detection of mycobacterial antigens in sera from patients with tuberculosis. The assay was evaluated together with an antibody measuring enzyme immunoassay in a clinical trial for serodiagnosis of tuberculosis.Sensitivity of the antibody assay for active pulmonary tuberculosis, including relapsed infections, was 75%, and specificity with other lung diseases was 97%. Sensitivity for extrapulmonary tuberculosis was 84-5% and specificity 84%. Sensitivity of the antigen assay for active tuberculosis was 45% with no false positive reactions. Combination of the results from the two assays increased total sensitivity to 96-5% with a positive predictive value of 0-81 and a negative predictive value of 0-98.The two assay test was relatively simple to perform and offered improved serological diagnosis of tuberculosis over a single antibody test.
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