scispace - formally typeset
P

Peter J. Barnes

Researcher at National Institutes of Health

Publications -  1554
Citations -  177909

Peter J. Barnes is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Asthma & COPD. The author has an hindex of 194, co-authored 1530 publications receiving 166618 citations. Previous affiliations of Peter J. Barnes include University of Nebraska Medical Center & Novartis.

Papers
More filters
Journal ArticleDOI

A molecular mechanism of action of theophylline: Induction of histone deacetylase activity to decrease inflammatory gene expression

TL;DR: It is shown that low-dose theophylline exerts an anti-asthma effect through increasing activation of HDAC which is subsequently recruited by corticosteroids to suppress inflammatory genes.
Journal ArticleDOI

Cigarette smoking reduces histone deacetylase 2 expression, enhances cytokine expression, and inhibits glucocorticoid actions in alveolar macrophages.

TL;DR: It is shown that cigarette smoke, an oxidative stress, decreased HDAC activity in human biopsies and macrophages in vivo and this reduced activity correlated with enhanced induction of inflammatory cytokines and a reduction in glucocorticoid responsiveness in vitro.
Journal ArticleDOI

Effects of inhaled platelet activating factor on pulmonary function and bronchial responsiveness in man

TL;DR: PAF may contribute to the pathogenesis of bronchial hyperresponsiveness, which is the most characteristic abnormality in asthma, and has a greater effect in raising responsiveness.
Journal ArticleDOI

New concepts in the pathogenesis of bronchial hyperresponsiveness and asthma

TL;DR: PAF antagonists will reveal whether PAF plays an important role in the eosinophilic inflammation of asthma, which may lead to epithelial damage, a key feature of asthmatic airways.
Journal ArticleDOI

Chronic obstructive pulmonary disease.

TL;DR: In this paper, the authors investigated the mechanisms underlying chronic obstructive pulmonary disease (COPD), which is associated with chronic inflammation that is usually corticosteroid resistant, and accelerated ageing of the lungs and an abnormal repair mechanism driven by oxidative stress.