Pleurisy

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Kazuhiko Yamamoto - One of the best experts on this subject based on the ideXlab platform.

Yasuo Nagafuchi - One of the best experts on this subject based on the ideXlab platform.

Peter J Barnes - One of the best experts on this subject based on the ideXlab platform.

  • immune response to mycobacterium tuberculosis infection in the parietal pleura of patients with tuberculous Pleurisy
    PLOS ONE, 2011
    Co-Authors: Gaetano Caramori, Lisa Lasagna, Angelo G Casalini, Ian M Adcock, Paolo Casolari, Marco Contoli, Federica Tafuro, Anna Padovani, Kian Fan Chung, Peter J Barnes
    Abstract:

    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.

Fumitaka Ogushi - One of the best experts on this subject based on the ideXlab platform.

Michelle Petri - One of the best experts on this subject based on the ideXlab platform.

  • associates and predictors of Pleurisy or pericarditis in sle
    Lupus science & medicine, 2017
    Co-Authors: Wei Fu, Michelle Petri
    Abstract:

    Background/Purpose Serositis is one of both ACR and SLICC classification criteria for systemic lupus erythematosus (SLE) and a common type of extra renal flare. However, little is known about clinical or immunological associations of Pleurisy or pericarditis. The aim of this study is to analyze associates and predictors of Pleurisy versus pericarditis in Caucasians and African Americans with SLE. Methods 2,390 SLE patients in the Hopkins Lupus Cohort were analyzed for demographic, clinical and serologic associates of Pleurisy or pericarditis, defined using the SELENA revision of the SLE Disease Activity Index (SLEDAI). The cross-sectional and prospective study using either univariate or multivariate analysis were performed to evaluate the associates of serositis in SLE. We reported associates with a p-value of less than 0.05 for Pleurisy or pericarditis. Results 43% had Pleurisy and 22% had pericarditis. African-American ethnicity was a predictive factor for new pericarditis. Hemolytic anemia, proteinuria, lymphadenopathy and anti-Sm were predictive only of pericarditis, whereas pulmonary fibrosis and GI infarction were predictive only of Pleurisy. Fever, Raynaud’s syndrome, and anti-DNA were predictors for both pericarditis and Pleurisy. Conclusion Our study provides further insights into the associates of Pleurisy and pericarditis in SLE. Predictors of Pleurisy and pericarditis are shown for the first time. The long term consequences from the cross-sectional analysis gives a lesson that serositis in SLE should not be considered benign.