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Immune Response to Mycobacterium tuberculosis Infection in the Parietal Pleura of Patients with Tuberculous Pleurisy.

The T lymphocyte-mediated immune response to Mycobacterium tuberculosis infection in the parietal pleura of patients with tuberculous pleurisy is unknown. The aim of this study was to investigate the immune response in the parietal pleura of tuberculous pleurisy compared with nonspecific pleuritis.

We have measured the numbers of inflammatory cells particularly T-cell subsets (Th1/Th2/Th17/Treg cells) in biopsies of parietal pleura obtained from 14 subjects with proven tuberculous pleurisy compared with a control group of 12 subjects with nonspecific pleuritis.

The number of CD3+, CD4+ and CCR4+ cells and the expression of RORC2 mRNA were significantly increased in the tuberculous pleurisy patients compared with the nonspecific pleuritis subjects. The number of toluidine blue+ cells, tryptase+ cells and GATA-3+ cells was significantly decreased in the parietal pleura of patients with tuberculous pleurisy compared with the control group of nonspecific pleuritis subjects. Logistic regression with receiver operator characteristic (ROC) analysis for the three single markers was performed and showed a better performance for GATA-3 with a sensitivity of 75%, a specificity of 100% and an AUC of 0.88. There was no significant difference between the two groups of subjects in the number of CD8, CD68, neutrophil elastase, interferon (IFN)-γ, STAT4, T-bet, CCR5, CXCR3, CRTH2, STAT6 and FOXP3 positive cells.

Elevated CD3, CD4, CCR4 and Th17 cells and decreased mast cells and GATA-3+ cells in the parietal pleura distinguish patients with untreated tuberculous pleurisy from those with nonspecific pleuritis.

Lipid and smoker's inclusions in sputum macrophages in patients with airway diseases.

We studied the effect of tobacco smoking on macrophage lipid index and macrophage smokers inclusions in induced sputum in 256 patients (143 non-smokers, 81 ex-smokers and 32 current smokers).

Lipid index was, using the Oil red O stain, the sum of the lipid staining droplet score (range 0-4) in 100 macrophages. Smokers inclusions were assessed using Wright's stain and graded as "none", "few", "moderate" or "many". Lipid index was significantly higher in current smokers (112.5, SD 58.5 units) than ex-smokers (29.2, SD 42.8 units) or non-smokers (13.4, SD 121.7). Smokers inclusions were present in all current smokers but only in 2 non-smokers. The mean smoking history of current smokers with few macrophage inclusions was 15.0 (SD 11.2), moderate 21.6 (SD 15.7), and many 30.0 (SD 21.9) pack years. There was a significant difference between the length of time ex-smokers had quit smoking if they had no or few smokers inclusions (mean 17.6 (SD 11.2) years) compared to those with moderate or many smokers inclusions (mean 2.8 (SD 5.8) years) (p = 0.01). Lipid index was significantly correlated with smokers inclusions (r = 0.72, p < 0.01).

We conclude that smoker's inclusions within sputum macrophages is a reliable indicator of cigarette smoking and that the sputum lipid index cannot be used as an assessment of oropharyngeal reflux in cigarette smokers.

Community‐acquired methicillin‐resistant Staphylococcus aureus pneumonia: A clinical audit

Conclusions:  Community‐acquired MRSA pneumonia is increasing and should be suspected in patients with severe community‐acquired pneumonia. There was a delay in initiation of appropriate antimicrobial treatment that could have lead to increased morbidity. (Source: Respirology)

Performance characteristics and predictors of yield from transbronchial needle aspiration in the diagnosis of peripheral pulmonary lesions

Conclusions:  TBNA contributes to successful bronchoscopy for the diagnosis of PPLs, especially for lesions lacking the bronchus sign, lesion size >2 cm, location in the middle lobe, and in patients with malignancy. (Source: Respirology)

The importance of epigenetics in the development of chronic obstructive pulmonary disease

AbstractIt is generally accepted that genetic predisposition plays a role in COPD development in susceptible individuals. Therefore, many candidate genes that could be linked to the development of disease have been examined in COPD. However, inconsistent results in different study populations often limit this approach, suggesting that not only genetics, but also other factors, may be contributed to the susceptibility to COPD.Epigenetic mechanisms can affect the transcriptional activity of specific genes, at different points in time, and in different organs. Moreover, these mechanisms can have an effect on people's health. Recently, there is emerging evidence supporting a role of epigenetics for the regulation of inflammatory genes in diseases such as asthma and COPD. Moreover, recent studi...

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