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J N Kline

Publications and source records attributed to J N Kline.

23 records · Page 2Linked to original sources
PubMed1993

Relative release of interleukin-1 beta and interleukin-1 receptor antagonist by alveolar macrophages. A study in asbestos-induced lung disease, sarcoidosis, and idiopathic pulmonary fibrosis.

We examined the influence of untreated interstitial lung disease (ILD) on the in vitro release of interleukin-1 beta (IL-1 beta) and interleukin-1 receptor antagonist (IL-Ira) from alveolar macrophages (AM); AM were harvested from normal volunteers, ILD patients, and patients with asbestos-related pleural disease but no ILD. AM were cultured for 24 h and assays for IL-1 beta and IL-1ra were done using sensitive and specific enzyme-linked immunosorbent assay. A greater amount of IL-1 beta was detected in AM supernatants from asbestosis, sarcoidosis, and IPF patients than in those from normal subjects. The IL-1 beta:IL-1ra ratio (IL-1 beta activity index [IL-1AI]) was significantly lower in supernatants of normal macrophages compared with macrophage supernatants from individuals with ILD. The IL-1AI correlated with bronchoalveolar lavage cellularity, a marker of disease activity. Current smoking was associated with lower IL-1 beta and IL-1ra release in ILD. The IL-1AI is a convenient method for comparison of IL-1 beta activity between patient populations.

Adult↗
PubMed1992

IL-1 receptor antagonist release is regulated differently in human alveolar macrophages than in monocytes.

These studies compared the release of interleukin-1 receptor antagonist (IL-1 RA) from alveolar macrophages and peripheral blood monocytes. The cells were cultured in medium containing various amounts of heat-inactivated fetal calf serum (FCS), granulocyte-macrophage colony-stimulating factor (GM-CSF), lipopolysaccharide (LPS), and immunoglobulin G (IgG). In serum-free medium alone, IL-1 RA release was similar from macrophages and monocytes. Increasing FCS concentration caused a significant upregulation of IL-1 RA release in macrophages but not in monocytes. GM-CSF caused a small increase in both cell types. LPS caused downregulation of IL-1 RA release from monocytes but not from macrophages. IgG did not affect IL-1 RA release in either cell group. These studies demonstrate that regulation of IL-1 RA release is different in monocytes and macrophages.

Autoradiography↗
PubMedDate not supplied

Psychiatric disorders and survival after lung transplantation.

The 30 patients who underwent lung transplantation between 1990 and 1996 were included in this study, and data were analyzed to find predictors of 1-year survival posttransplantation. All patients were followed throughout the posttransplantation period. Fifteen patients had a pretransplantation diagnosis of an anxiety and/or depressive disorders. Of the 30 patients transplanted, 19 survived 12 months or more, and 11 died less than 12 months posttransplantation. The > 12-month survival group had a mean age of 45.2 years at transplantation, compared with a mean age of 43.0 years in the < 12-month group (NS). The mean Psychosocial Assessment of Candidates for Transplant score and premorbid history of smoking did not differ between the groups. The > 12-month survival group had more psychiatric illness pretransplantation than the < 12-month survival group (56% vs. 27%, P < 0.05). The recipients with a psychiatric history (N = 15) were more likely to survive 1 year posttransplantation than the recipients without a psychiatric history (80% vs. 47%, P < 0.05) and were not significantly different from the recipients without a psychiatric history in terms of episodes of rejection, bronchiolitis obliterans, or noncompliance with treatment. Depression and anxiety are treatable disorders that occur frequently in patients with end-stage lung disease, and a premorbid history of either did not predict a worse outcome posttransplantation in this study of lung transplantation recipients.

Adult↗
PubMedDate not supplied

Synergistic activation of the human cytomegalovirus major immediate early promoter by prostaglandin E2 and cytokines.

Human cytomegalovirus (HCMV) is a common cause of morbidity and mortality in immunosuppressed patients, especially transplant recipients. In this population, infection is frequently due to reactivation of latent virus. The major immediate early promoter of HCMV controls production of immediate early gene products, which are both trans- and cis-active and are responsible for reactivation. Activation of this promoter is therefore a crucial step in regulation of reactivation infection. It is known that there are cAMP-response elements in the HCMV major immediate early promoter. We hypothesized that prostaglandins (PG), like PGE2, which are known to increase cAMP, as well as cytokines known to be released during acute inflammation, may be important in the regulation of this promoter and thus in reactivation of HCMV. To examine this, we transfected pCAT760, a plasmid containing the major immediate early promoter of HCMV upstream of a chloramphenicol acetyltransferase (CAT) gene, into THP-1 cells. These cells were subsequently stimulated with PGE2 and/or one of a variety of cytokines. We found that PGE2, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1 beta each upregulated the HCMV major immediate early promoter. TNF-alpha, IL-1 beta, IL-6, and IL-10 were each synergistic or additive with PGE2 in upregulating the promoter. Since PGE2 and the cytokines are all products of activated macrophages, we suggest that acute inflammation and macrophage activation may predispose to reactivation of latent HCMV.

Cytokines↗