Neutrophil-activating peptide-1/interleukin 8, a novel cytokine that activates neutrophils.

Baggiolini, Marco; Walz, Alfred; Kunkel, Steven L.

doi:10.1172/jci114265

Cited by 1,833 publications

(1,062 citation statements)

References 60 publications

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“…The chemokine IL-8, corresponding to the rodent homolog macrophage inflammatory protein-2 (MIP-2), was originally described as a chemotactic and activating factor for neutrophils, [74][75][76] but has also been implicated in the activation of basophils, T cells, and monocytes. 77 Aloisi et al 77 reported that IL-8 is released by cytokinestimulated human astrocytes, suggesting that these cells promote the recruitment of circulating blood cells into brain inflammatory sites.…”

Section: Interleukin-8/macrophage Inflammatory Protein-2mentioning

confidence: 99%

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

2010

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Summary:Despite dramatic improvements in the management of traumatic brain injury (TBI), to date there is no effective treatment available to patients, and morbidity and mortality remain high. The damage to the brain occurs in two phases, the initial primary phase being the injury itself, which is irreversible and amenable only to preventive measures to minimize the extent of damage, followed by an ongoing secondary phase, which begins at the time of injury and continues in the ensuing days to weeks. This delayed phase leads to a variety of physiological, cellular, and molecular responses aimed at restoring the homeostasis of the damaged tissue, which, if not controlled, will lead to secondary insults. The development of secondary brain injury represents a window of opportunity in which pharmaceutical compounds with neuroprotective properties could be administered. To establish effective treatments for TBI victims, it is imperative that the complex molecular cascades contributing to secondary injury be fully elucidated. One pathway known to be activated in response to TBI is cellular and humoral inflammation. Neuroinflammation within the injured brain has long been considered to intensify the damage sustained following TBI. However, the accumulated findings from years of clinical and experimental research support the notion that the action of inflammation may differ in the acute and delayed phase after TBI, and that maintaining limited inflammation is essential for repair. This review addresses the role of several cytokines and chemokines following focal and diffuse TBI, as well as the controversies around the use of therapeutic anti-inflammatory treatments versus genetic deletion of cytokine expression.

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Section: Interleukin-8/macrophage Inflammatory Protein-2mentioning

confidence: 99%

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

2010

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“…Differences were considered significant at P<.05. metabolites. 6 The activation of PMN by TNF-α, IL-lß, and IL-8 may lead to adherence of PMN to endothelial cells with induction of vessel wall injury due to the release of toxic oxygen species and lysosomal proteinases. 15 " 17 N EUTROPHIL ELASTASE, a powerful neutral serine proteinase released from the azurophil granules, is thought to play a central role in PMN-mediated endothelial injury.…”

Section: Statisticsmentioning

confidence: 99%

“…Because inflammatory cytokines have been found to activate PMN, 6 " 16 it could be hypothesized that these cytokines may also be involved in the increased release of proteolytic enzymes by PMN during sepsis, in asmuch elevated serum levels of the PMN-activating cyto kines TNF-α, IL-lß, and IL-8 were described after injection of endotoxin or Ε coli in experimental and clinical models. 1 " 4 However, in contrast to the marked increase of released elastase observed in human whole blood from pa tients with sepsis, the release of the PMN-activating cyto kines TNF-α and IL-1 β was significantly depressed during the entire observation period.…”

Section: Commentmentioning

confidence: 99%

Enhanced Release of Elastase Is Not Concomitant With Increased Secretion of Granulocyte-Activating Cytokines in Whole Blood From Patients With Sepsis

Ertel

Jarrar²,

Jochum³

et al. 1994

Arch Surg

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“…We sought to identify molecular mechanisms by which DC-mediated chronic inflammation induced by cigarette smoke constituents not only predisposes to chronic airway inflammation, but may additionally promote lung cancer development though epithelial cell transformation. We postulated that cigarette smoke induces the generation of the neutrophilic chemokine CXCL8 / IL-8, a central mediator of neutrophil recruitment in human airways (Baggiolini et al, 1989). We also postulated that cigarette smoke constituents induce the production of prostaglandin-E2 (PgE 2 ), an arachidonic acid metabolite that profoundly influences DC function, and has been associated with epithelial cell transformation, an important step in new cancer formation (Yoshimatsu et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Nicotine and oxidative cigarette smoke constituents induce immune-modulatory and pro-inflammatory dendritic cell responses

Vassallo

Kroening

Parambil

et al. 2008

Molecular Immunology

100

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Chronic airway inflammation is a cardinal feature of chronic obstructive pulmonary disease (COPD), a destructive cigarette smoke-induced lung disease. Although it is apparent that dendritic cells (DCs) are an important constituent of the chronic inflammatory cell influx found in airways of COPD patients, the functional roles of DCs in the pathogenesis of smoking-induced emphysema are unknown. We postulated that DCs activated by cigarette smoke constituents directly participate in the chronic inflammation that characterizes COPD airways. Concordant with this hypothesis, we observed that incubation of DCs with cigarette smoke extract (CSE), and chronic exposure of mice to cigarette smoke, both augmented the generation of neutrophilic chemokines by immature and lipopolysaccharide (LPS) or CD40L-matured DCs. The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the antioxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation. Cigarette smoke extract and nicotine also augment the production of secreted prostaglandin E 2 and intracellular cyclooxygenase-2 (COX-2) in maturing DCs. Whereas NAC suppressed production of CXCL8 by CSEconditioned DCs, it augmented production of PGE 2 and cellular COX-2 levels in maturing DCs. These studies indicate that the stimulation of DCs by cigarette smoke-induced oxidative stress and nicotine promote the generation of pro-inflammatory responses that promote chronic inflammation in smokers. Certain pharmacologic strategies such as anti-oxidant therapy may be only partially effective in mitigating cigarette smoke-induced pro-inflammatory DC-mediated responses in smokers.

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Neutrophil-activating peptide-1/interleukin 8, a novel cytokine that activates neutrophils.

Cited by 1,833 publications

References 60 publications

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

Enhanced Release of Elastase Is Not Concomitant With Increased Secretion of Granulocyte-Activating Cytokines in Whole Blood From Patients With Sepsis

Nicotine and oxidative cigarette smoke constituents induce immune-modulatory and pro-inflammatory dendritic cell responses

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