Tumour Necrosis Factor in Bronchopulmonary Secretions of Patients With Adult Respiratory Distress Syndrome

Millar, Ann; Singer, Mervyn; Meager, Anthony; Foley, Noeleen; Johnson, N.; Rook, G.A.W.

doi:10.1016/s0140-6736(89)90772-1

Cited by 187 publications

(66 citation statements)

References 11 publications

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“…We may, thus, have missed early peaks of TNF-α generation due to our lavage protocol dictated by clinical necessities. Dilution of the alveolar space concentrations by the lavage fluid may be another important factor to explain the discrepancy between the current and preceding studies, in which TNF-α was directly quantified in bronchoalveolar aspirates [20,24].…”

Section: Tumour Necrosis Factorcontrasting

confidence: 72%

“…In previous investigations, elevated alveolar space TNF-α levels were found in patients with ARDS [19,20,24]. In contrast, TNF-α was very rarely detected in the BAL fluids either in ARDS or in severe PN in the current study.…”

Section: Tumour Necrosis Factorcontrasting

confidence: 65%

“…Together with other cytokines, it appears to orchestrate the response to an inflammatory stimulus. Many features of septic shock [10][11][12][13] and ARDS [14,15] have been ascribed to TNF-α, but measurements of this cytokine under such clinical conditions (serum and lavage fluid) have produced inconsistent results [16][17][18][19][20][21][22][23][24]. Interleukin-6 (IL-6) is produced by a variety of inflammatory cells in response to other cytokines or bacterial agents.…”

mentioning

confidence: 99%

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Bronchoalveolar and systemic cytokine profiles in patients with ARDS, severe pneumonia and cardiogenic pulmonary oedema

Schütte¹,

Lohmeyer²,

Rosseau³

et al. 1996

Eur Respir J

207

130

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B Br ro on nc ch ho oa al lv ve eo ol la ar r a an nd d s sy ys st te em mi ic c c cy yt to ok ki in ne e p pr ro of fi il le es s i in n p pa at ti ie en nt ts s w wi it th h A AR RD DS S, ,s se ev ve er re e p pn ne eu um mo on ni ia a a an nd d c ca ar rd di io og ge en ni ic c p pu ul lm mo on na ar ry y o oe ed de em ma a (PN) and a combined group (PN+ARDS).In all patients with ARDS and/or PN, markedly elevated BAL levels of IL-6 and IL-8 were detected, which were significantly greater than levels in CPO and healthy controls. Absolute quantities and time-course of these cytokines did not differentiate between the absence and presence of lung infection, or different categories of PN. Similarly, circulating IL-6 levels were comparably elevated in patients with ARDS and/or PN, whereas circulating IL-8 concentrations were inconsistently increased. TNF-α was rarely detected in BAL samples, but increased serum concentrations were measured in ARDS and/or PN patients.Bronchoalveolar lavage levels of interleukin-6 and interleukin-8, but not tumour necrosis factor-α, and serum concentrations of interleukin-6 are consistently elevated in acute respiratory distress syndrome and/or severe pneumonia, discriminating these entities from cardiogenic pulmonary oedema. Alveolar and systemic cytokine profiles do not differentiate between acute respiratory distress syndrome in the absence of lung infection and states of severe primary or secondary pneumonia, which evidently present with comparable local and systemic inflammatory sequelae.

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Section: Tumour Necrosis Factorcontrasting

confidence: 72%

Section: Tumour Necrosis Factorcontrasting

confidence: 65%

mentioning

confidence: 99%

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Bronchoalveolar and systemic cytokine profiles in patients with ARDS, severe pneumonia and cardiogenic pulmonary oedema

Schütte¹,

Lohmeyer²,

Rosseau³

et al. 1996

Eur Respir J

207

130

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“…For instance, RATG has been shown to induce proinflammatory mediators, such as tumour necrosis factor-α (TNF-α) [26] which itself is recognized as having specific effects on endothelial cells in the lungs [27]. TNF-α has also been reported to be a potentially important mediator in the development of adult respiratory distress syndrome [28].…”

Section: Discussionmentioning

confidence: 99%

Pulmonary diffusion impairment following heart transplantation: a prospective study

Egan

Lowe²,

Yonan³

et al. 1996

Eur Respir J

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The aim of this prospective study was to confirm whether and when a fall in gas transfer occurs following heart transplantation (HT); and to examine the potential relationship between gas transfer and haemodynamic change, immunosuppression, and cytomegalovirus (CMV) infection.The lung physiology of 34 heart transplant recipients (HTR) and 14 control patients undergoing coronary artery bypass grafting (CABG) were studied. The absolute and standardized residual values of forced expiratory volume in one second (FEV1), forced vital capacity (FVC), residual volume (RV), forced residual volume (FRC), total lung capacity (TLC), transfer factor of the lungs for carbon monoxide (TL,CO) and carbon monoxide transfer coefficient (KCO) were measured before and at 30, 60, 90, 120 and 150 days after HT. These data were compared to haemodynamic status, graft rejection, cyclosporin levels and episodes of CMV infection. Lung function was studied in a group of patients before and 4 weeks after CABG.There was a significant fall in mean KCO after HT (pre-HT=1.29 and post-HT= 1.06 mmol·min -1 ·kPa·L -1 ) but not after CABG (pre-CABG=1.49, post-CABG=1.5 mmol·min -1 ·kPa·L -1 . No relationship was observed between gas transfer and CMV.At the latest stage following HT (150 days) there was a positive correlation between TL,CO (absolute value and standardized residual) and mean cyclosporin level (r=0.48 and r=0.44, respectively) and also between the absolute KCO and actual (r=0.56) and mean (r=0.55) cyclosporin levels. Following HT, there is an early fall in gas transfer, which is independent of the effects of surgery and bypass, implicating early immunosuppression (e.g. antithymocyte globulin/cyclosporin).

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“…These effects include pulmonary edema, left ventricular dysfunction, left ventricular remodeling, cardiomyopathy and abnormalities in myocardial metabolism [3][4][5][6][7][8]. It is the particular balance of pro-inflammatory and anti-inflammatory cytokines that influence cardiac homeostasis.…”

Section: Introductionmentioning

confidence: 99%

The Immunoregulatory Role of Cytokines in Congestive Heart Failure

Chen¹,

Patel²,

Mohamed³

2014

Interdiscip J Microinflammation

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Background: Cytokines have been shown to be associated with heart failure and to have multiple biological effects that can lead to left ventricular dysfunction, pulmonaryedema, and left ventricular remodeling. However, the effects of different cytokines, separately and in combination have not been fully determined. We aim to evaluate the levels of both pro-inflammatory and anti-inflammatory cytokines in patients with congestive heart failure (CHF), as well as in patients with coronary artery disease (CAD) and compare them to levels in normal controls (individuals without CHF or CAD) as to suggest their possible etiologic role.

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Tumour Necrosis Factor in Bronchopulmonary Secretions of Patients With Adult Respiratory Distress Syndrome

Cited by 187 publications

References 11 publications

Bronchoalveolar and systemic cytokine profiles in patients with ARDS, severe pneumonia and cardiogenic pulmonary oedema

Bronchoalveolar and systemic cytokine profiles in patients with ARDS, severe pneumonia and cardiogenic pulmonary oedema

Pulmonary diffusion impairment following heart transplantation: a prospective study

The Immunoregulatory Role of Cytokines in Congestive Heart Failure

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