Chemokines in acute respiratory distress syndrome

Puneet, Padmam; Moochhala, Shabbir; Bhatia, Madhav

doi:10.1152/ajplung.00405.2003

Cited by 280 publications

(255 citation statements)

References 124 publications

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“…Although critical for innate immunity and pathogen clearance, they also cause tissue destruction by releasing proteases such as neutrophil elastase, MMP8, MMP9, MMP25, cathepsin G and protease 3, and reactive oxygen intermediates (ROIs), such as hydrogen peroxide (H 2 O 2 ), hypohalous acids, chloramines and hydroxyl radicals [63]. Their tissue recruitment is mediated by the ELR and CXC chemokines, growth-related oncogene (GRO), epithelial neutrophil-activating protein-78, granulocyte chemotactic protein-2 and IL-8 (or the murine homologs, GRO/ macrophage inflammatory protein-2/KC and granulocyte chemotactic protein-2/LIX), and both alveolar macrophages and alveolar type II cells can highly express many of these chemokines in response to proinflammatory cytokines or bacterial products [64].…”

Section: Release Of Chemokines Cytokines and Other Inflammatory Modulamentioning

confidence: 99%

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Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Manicone¹

2009

Expert Review of Clinical Immunology

109

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Acute lung injury (ALI) is a clinical disease marked by respiratory failure due to disruption of the epithelial and endothelial barrier, flooding of the alveolar compartment with protein-rich fluid and recruitment of neutrophils into the alveolar space. ALI affects approximately 200,000 patients annually in the USA and results in approximately 75,000 deaths. It is associated with prolonged mechanical ventilation, intensive medical care, high morbidity and mortality, and rising healthcare costs. Owing to its impact on public health, great strides have been made towards understanding the pathobiology of ALI to affect outcome. This review will focus on the role of the epithelial cell in the pathogenesis and resolution of ALI and the role of various inflammatory mediators in ALI. Keywordsβ2-agonist; acute lung injury; acute respiratory distress syndrome; chemokine; cytokine; epithelial cell; inflammation; methylprednisolone; neutrophil; salbutamol; steroid; ventilator-induced lung injuryAcute lung injury/acute respiratory distress syndrome (ALI/ARDS) was first described in 1967 by Ashbaugh and colleagues in a group of 12 patients who shared a constellation of clinical symptoms including acute respiratory distress, hypoxemia refractory to supplemental oxygen, decreased lung compliance and diffuse pulmonary infiltrates [1]. Since this first description, the clinical criteria have evolved to include acute onset of respiratory distress, bilateral pulmonary infiltrates seen on chest radiographs, absence of left-sided heart failure and hypoxemia, with the severity of hypoxemia distinguishing ALI and ARDS (Box 1) [2]. Extrapolating from recent epidemiologic studies using these criteria, ALI affects about 200,000 patients annually in the USA and results in approximately 75,000 deaths [3]. This disease, which can be caused by common events such as pneumonia, sepsis and trauma, results in high morbidity, mortality and healthcare expenditures associated with prolonged mechanical ventilation and intensive care. Because of its impact on public health and patient outcomes, great strides have been made towards understanding the pathobiology of ALI.When defined broadly to include all processes related to defense against microbes, other environmental insults and injury, a wide variety of cell types and proteins participate in inflammation and immunity. Leukocytes are the paradigmatic inflammatory cell type, but they are not the only cells that function in defense and immunity. The epithelial lining of all tissues forms a continuous barrier to the environment and is the first line of defense against infectious agents and toxins. Though specialized to serve distinct functions among tissues, epithelial cells respond similarly to injury and infection, and regulate leukocyte influx through the production of proinflammatory cytokines, chemokines and other factors that modulate chemokine gradients and effect leukocyte migration. This review will focus on the role of the pulmonary epithelium and inflammatory mediators in ALI. More s...

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Section: Release Of Chemokines Cytokines and Other Inflammatory Modulamentioning

confidence: 99%

“…Indeed, small-molecule antagonists to chemokine receptors, such as CXCR2, have been developed [64]. As new therapeutic approaches are considered and developed, attention needs to be paid to potential outcomes that arise due to altering one process that impacts on others.…”

Section: Five-year Viewmentioning

confidence: 99%

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Manicone¹

2009

Expert Review of Clinical Immunology

109

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“…Various medications directed at key stages of the pathophysiology are not clinically efficacious as indicated in the preceding experimental trials [23] . Therefore, therapies for preventing or reversing lung injury would be ideal for the treatment of AP [1,2,21,[24][25][26] .…”

Section: A B C Dmentioning

confidence: 99%

Protective effects of erythropoietin against acute lung injury in a rat model of acute necrotizing pancreatitis

Oge¹,

Tascilar²,

Güldeniz³

et al. 2007

WJG

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RESULTS:The mean pleural effusion volume, calculated LW/BW ratio, serum IL-6 and lung tissue MDA levels were significantly lower in EPO groups than in ANP groups. No statistically significant difference was observed in either serum or tissue values of IL-2 among the groups. The level of tumor necrosis factor-α (TNF-α) and IL-6 and accumulation of ox-LDL were evident in the lung tissues of ANP groups when compared to EPO groups, particularly at 72 h. Histopathological evaluation confirmed the improvement in lung injury parameters after exogenous EPO administration, particularly at 48 h and 72 h. C O N C L U S I O N : E P O a d m i n i s t r a t i o n l e a d s t o asignificant decrease in ALI parameters by inhibiting polymorphonuclear leukocyte (PMNL) accumulation, decreasing the levels of proinflammatory cytokines in circulation, preserving microvascular endothelial cell integrity and reducing oxidative stress-associated lipid peroxidation and therefore, can be regarded as a cytoprotective agent in ANP-induced ALI. INTRODUCTIONAcute pancreatitis (AP) is a life-threatening necroinflammatory disease with significant morbidity and mortality rates, especially when complicated by systemic inflammatory response syndrome (SIRS) and multiple organ failure (MODS) [1,2] . Death occurs in 60% of the patients within the first 6 d of disease onset and pulmonary complications including acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) Abstract AIM: To investigate the effect of exogenous erythropoietin (EPO) administration on acute lung injury (ALI) in an experimental model of sodium taurodeoxycholateinduced acute necrotizing pancreatitis (ANP). BASIC RESEARCH METHODS:Forty-seven male Wistar albino rats were randomly divided into 7 groups: sham group (n = 5), 3 ANP groups (n = 7 each) and 3 EPO groups (n = 7 each). ANP was induced by retrograde infusion of 5% sodium taurodeoxycholate into the common bile duct. Rats in EPO groups received 1000 U/kg intramuscular EPO immediately after induction of ANP. Rats in ANP groups were given 1 mL normal saline instead. All animals were sacrificed at postoperative 24 h, 48 h and 72 h. Serum amilase, IL-2, IL-6 and lung tissue malondialdehyde (MDA) were measured. Pleural effusion volume and lung/body weight (LW/BW) ratios were calculated. Tissue levels of TNF-α, IL-2 and IL-6 were screened immunohistochemically. Additionally, ox-LDL accumulation was assessed with immune-fluorescent staining. Histopathological alterations in the lungs were also scored.

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“…ALI or ARDS (4,6,25) and plasma cytokine levels are known to correlate with postoperative morbidity and mortality rates (12,13). To address this issue, we investigated the impact of the thoracic approach in thoracoabdominal esophagectomy on plasma cytokine levels.…”

Section: Introductionmentioning

confidence: 99%

Thoracotomy procedures effect cytokine levels after thoracoabdominal esophagectomy

Frick

Justinger²,

Rubie³

et al. 2011

Oncol Rep

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Abstract. Pulmonary complications together with surgical complications are the most frequent causes for morbidity and mortality after thoracoabdominal esophagectomy. The con tinuous improvement of surgical techniques has led to a decrease in surgical complications, whereas up to 30% of the patients develop postoperative pulmonary complications such as acute lung injury (ALI) or even the more severe acute respiratory distress syndrome (ARDS), which are characterized by an acute inflammation in the lung parenchyma and the airspace. Evidence from several studies indicates that a complex network of inflammatory cytokines and mediators play a key role in mediation, amplification, and perpetuation of the process of lung injury and that the thoracotomy itself is a risk factor for developing ALI or ARDS. In this trial, the cytokine levels of IL6, IL8 and IL10 were measured and compared in 30 patients who had undergone an extended radical thoracoabdominal esophagectomy for esophageal cancer, via anterolateral thoracotomy (n=17) or posterolateral thoracotomy (n=13). Patients of both groups were similar in terms of age, sex and preoperative pulmonary function as well as in the anesthetic procedures they have undergone. All patients displayed significantly increased serum levels of IL6 and IL8 after thoracoabdominal esophagectomy. However, patients who were subjected to an anterolateral thoracotomy were reported with significantly higher serum levels of IL6 and IL8 compared to patients who had received a posterolateral thoracotomy. Thus, the choice of the thoracotomy method during the thoracoabdominal esophagectomy and the resultant cytokine levels may contribute to the occurrence of postoperative pulmonary complications and may have an impact on the extent and severity of the surgical stress.

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Chemokines in acute respiratory distress syndrome

Cited by 280 publications

References 124 publications

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Role of the pulmonary epithelium and inflammatory signals in acute lung injury

Protective effects of erythropoietin against acute lung injury in a rat model of acute necrotizing pancreatitis

Thoracotomy procedures effect cytokine levels after thoracoabdominal esophagectomy

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