Levels of Interleukin-8 in Patients with Adult Respiratory Distress Syndrome

Torre, Donato; Zeroli, Claudia; Giola, Massimo; Gp, Fiori; Minoja, Giulio; Maraggia, D; Chiaranda, Maurizio

doi:10.1093/infdis/167.2.505

Cited by 15 publications

(11 citation statements)

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“…In agreement with others [66,[78][79][80][81], we have found an increased BAL:plasma ratio for all measured cytokines [49,50]. Increased BAL levels indicate increased intrapulmonary production and not leakage into the lung from increased vascular permeability [79].…”

Section: The Host Defence Response In Ardssupporting

confidence: 92%

The role of the host defence response in the progression and outcome of ARDS: pathophysiological correlations and response to glucocorticoid treatment

Gu¹

1996

Eur Respir J

114

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T Th he e r ro ol le e o of f t th he e h ho os st t d de ef fe en nc ce e r re es sp po on ns se e i in n t th he e p pr ro og gr re es ss si io on n a an nd d o ou ut tc co om me e o of f A AR RD DS S: : p pa at th ho op ph hy ys si io ol lo og gi ic ca al l c co or rr re el la at ti io on ns s a an nd d r re es sp po on ns se e t to o g gl lu uc co oc co or rt ti ic co oi id d t tr re ea at tm me en nt t

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Section: The Host Defence Response In Ardssupporting

confidence: 92%

The role of the host defence response in the progression and outcome of ARDS: pathophysiological correlations and response to glucocorticoid treatment

Gu¹

1996

Eur Respir J

114

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“…Alveolar space IL-8 concentrations were substantially higher than circulating IL-8 levels, which is in accordance with predominant local generation of this cytokine. The data on BAL IL-8 support previous studies demonstrating consistently increased lavage IL-8 concentrations in ARDS patients [3,4,39], and in patients at risk for this disease [2]. This inflammatory cytokine allowed a clear separation of ARDS/PN from cardiogenic pulmonary oedema, in which only moderately elevated levels were noted; previous data for the latter group are not known to the authors.…”

Section: Interleukin-8supporting

confidence: 84%

“…As anticipated from the previously described features of IL-8, elevations of serum concentrations of this cytokine were less marked than the rise in the levels in the alveolar space in all groups of patients [1,4]. This finding does not refute the hypothesis that under conditions of a predominance of sepsis and septic shock, substantial IL-8 concentrations may appear in the vascular compartment [5,7,42].…”

Section: Interleukin-8mentioning

confidence: 67%

“…Interleukin-8 (IL-8) is important for the recruitment of inflammatory cells into the alveolar space, which is a hallmark of the acute respiratory distress syndrome (ARDS) and severe pneumonia (PN). Elevated levels of IL-8 have been shown in bronchoalveolar lavage (BAL) fluids of ARDS patients [1][2][3][4], as well as under general conditions of sepsis and multiorgan failure [5][6][7]. Tumour necrosis factor-α (TNF-α) is secreted by monocytes or macrophages, including those of the alveolar space, after exposure to bacterial lipopolysaccharides and a variety of proinflammatory mediators [8,9].…”

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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“…IL-8, a cytokine produced by many cell types, including endothelial cells, fibroblasts, respiratory epithelial cells, macrophages, and PMNs, is a potent chemoattractant for PMNs and binds to a subfamily of related G-protein-coupled receptors (17). It is found in high concentrations in the bronchoalveolar lavage fluid of ARDS patients and in the circulation during clinical and experimental human sepsis (18,19). In PMNs, IL-8 also increases surface expression of adhesion molecules, transendothelial migration, degranulation, and superoxide anion formation (17).…”

mentioning

confidence: 99%

Recruitment of Murine Neutrophils in Vivothrough Endogenous Sialidase Activity

Cross¹,

Sakarya²,

Rifat³

et al. 2003

Journal of Biological Chemistry

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Upon activation with various noncytokine stimuli, polymorphonuclear leukocytes (PMNs) mobilize intracellular sialidase to the plasma membrane, where the sialidase releases sialic acid from the cell surface. This desialylation enhances PMN adherence, spreading, deformability, and motility, functions critical to diapedesis. We now have examined the role of sialidase activity in PMN adhesion to and migration across the endothelium in vivo. A polyclonal antibody prepared against Clostridium perfringens neuraminidase 1) detected surface expression of sialidase on human PMNs stimulated with IL-8 in vitro and on murine PMNs stimulated in vivo, but not on that of unstimulated cells, 2) recognized proteins in human PMN lysates and granule preparations that were not detected by preimmune antibody, 3) inhibited bacterial neuraminidase and human PMN sialidase activities in vitro, and 4) inhibited both pulmonary leukostasis in mice systemically infused with cobra venom factor and intrapulmonary transendothelial migration of PMNs into the bronchoalveolar compartment of mice intranasally challenged with interleukin-8. We conclude that the chemokine interleukin-8, like other PMN agonists, induces the translocation of sialidase to the PMN surface and that surface expression of this sialidase is a prerequisite to PMN recruitment in vivo. The ability of antibodies raised against a prokaryotic neuraminidase to recognize eukaryotic sialidase extends the concept of the neuraminidase superfamily to mammalian enzymes. Inhibition of mobilized endogenous sialidase may provide a novel strategy for limiting the inflammatory response.

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Levels of Interleukin-8 in Patients with Adult Respiratory Distress Syndrome

Cited by 15 publications

References 0 publications

The role of the host defence response in the progression and outcome of ARDS: pathophysiological correlations and response to glucocorticoid treatment

The role of the host defence response in the progression and outcome of ARDS: pathophysiological correlations and response to glucocorticoid treatment

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

Recruitment of Murine Neutrophils in Vivothrough Endogenous Sialidase Activity

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