IL-10 administration attenuates pulmonary neutrophil infiltration and alters pulmonary iNOS activation following hemorrhagic shock

Kobbe, Philipp; Schmidt, Joachim; Stoffels, Burkhard; Chanthaphavong, R. Savanh; Bauer, Anthony J.; Pape, Hans-Christian

doi:10.1007/s00011-009-8116-z

Cited by 30 publications

(25 citation statements)

References 40 publications

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“…In addition, recent studies have shown the protective role of IL-10 in hemorrhagic shock induced lung inflammation and injury [29,30]. Our results together with these data raise the possibility that one of the mechanisms of action of adenosine in protecting against lung injury is through augmenting IL-10 expression.…”

Section: Discussionsupporting

confidence: 75%

Stimulation of A2B adenosine receptors protects against trauma–hemorrhagic shock-induced lung injury

Koscsó¹,

Trepakov²,

Csóka³

et al. 2013

Purinergic Signalling

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Inflammation is responsible for secondary organ failure after trauma and hemorrhagic shock (T/HS). Adenosine, acting through four G protein-coupled cell surface receptors, A 1 , A 2A , A 2B , and A 3 , exerts a number of tissue protective and anti-inflammatory effects. The goal of the present study was to test the effect of A 2B adenosine receptor stimulation on T/HS-induced organ injury and inflammation in rats. Rats after T/HS were resuscitated with Ringer's lactate containing the A 2B receptor agonist BAY 60-6583 or its vehicle. We found that BAY 60-6583 decreased T/HS-induced lung permeability and plasma creatine kinase levels but failed to affect T/HS-induced lung neutrophil infiltration and IκBα expression and plasma alanine aminotransferase levels. Thus, we conclude that stimulation of A 2B receptors protects against T/HS-induced lung and muscle injury.

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Section: Discussionsupporting

confidence: 75%

Stimulation of A2B adenosine receptors protects against trauma–hemorrhagic shock-induced lung injury

Koscsó¹,

Trepakov²,

Csóka³

et al. 2013

Purinergic Signalling

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“…It should be noted in this context that administration of exogenous IL-10 or introduction of the IL-10 gene conferred protection against Pseudomonas aeruginosainduced (22) and bleomycin-induced lung injuries (23) in mice, as well as against immune complex-induced lung injury following intrapulmonary deposition of IgG or IgA in rats (24). Exogenous IL-10 administration was also found to attenuate lung injury following hemorrhagic shock (25).…”

Section: Discussionmentioning

confidence: 97%

“…These cells infiltrate to the tissue early after exposure, accumulate over time (17,26), and actively secrete damage mediators, such as neutrophil elastase, metalloproteinases, defensins, and reactive oxygen species (ROS), all of which induce and enhance tissue injury (27). Increased IL-10 levels were suggested to reduce lung neutrophil content (23,25). In the present study, a dramatic reduction in lung neutrophil content, almost by one-half at 72 h postexposure, was indeed observed in the ricinintoxicated group of mice treated with ciprofloxacin.…”

Section: Discussionmentioning

confidence: 99%

Potent Antiedematous and Protective Effects of Ciprofloxacin in Pulmonary Ricinosis

Gal

Sapoznikov

Falach

et al. 2016

Antimicrob Agents Chemother

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The plant toxin ricin is considered a biological threat agent of concern and is most toxic when inhaled. Pulmonary exposure to a lethal dose of ricin can be redressed by treatment with antiricin antibodies; however, late antitoxin intervention is of limited efficacy. This limitation is associated with overt lung damage, clinically manifested as severe pulmonary inflammation, which develops over time. Increased evidence indicates that ciprofloxacin, a broad-spectrum antimicrobial agent, possesses immunomodulatory properties. Here we demonstrate that while antiricin antibody administration at late hours after intranasal exposure to ricin confers limited protection to mice, highly efficient protection can be achieved by adding ciprofloxacin to the antibody treatment. We further demonstrate that parameters associated with lung injury, in particular, pulmonary proinflammatory cytokine production, neutrophil migration, and edema, are sharply reduced in ricin-intoxicated mice that were treated with ciprofloxacin. The presented data highlight the potential clinical application of ciprofloxacin as a beneficial immunomodulatory agent in the course of ricin intoxication. Ricin, a type II ribosome-inactivating protein, is a plant toxin derived from the seeds of Ricinus communis (castor beans). The holotoxin consists of two polypeptide chains (A and B) linked by a disulfide bond. The B chain is a lectin, which binds to galactose residues on the cell surface. The A chain possesses RNA Nglycosidase activity that irreversibly inactivates the 28S rRNA of the mammalian 60S ribosome subunit, subsequently arresting cell protein synthesis (1). Due to its high availability and relative ease of production, ricin is considered a biological threat agent (2). The toxicity of ricin depends on the route of exposure, inhalatory exposure being considered the most severe (3). Pathological studies of pulmonary ricin intoxication have demonstrated that injury is confined mostly to the lungs (4) and characterized by a local cytokine storm, massive neutrophil recruitment, increased prooxidant enzyme activity, and development of proteinaceous pulmonary edema, subsequently resulting in respiratory failure and death (4, 5).Prophylactic antiricin vaccines are being developed (6), yet postexposure medical countermeasures are needed for treatment of unvaccinated victims after pulmonary exposure to lethal doses of the toxin. Previous studies have examined the possibility of protecting animals against pulmonary ricinosis by passive immunization with polyclonal antiricin antibodies; nevertheless, under this mode of protection, survival rates declined sharply in correlation with antitoxin administration timing following intoxication, so that antiricin antibodies administered 24 h after exposure gave rise to limited rates of survival (5, 7). At this late time point, the pathophysiological condition of some of the intoxicated mice may have deteriorated so that the loss of function of the lungs is irreversible. Conversely, we previously showed that higher sur...

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“…2 Cell counts in the BAL of mice treated for 4 h. Total cell counts in the BAL were obtained from pelleted cells after lysis of red cells and staining with trypan blue and counting using a manual hemocytometer. The figure shows box-whisker graph with individual data points, boxes (25th to 75th percentiles of the data), whisker bars (5th to 95th percentiles), and mean (±1 SEM) of airway inflammation show that cytokines such as IL-10 and IL-12 can inhibit bronchial and alveolar inflammation [43,44] and neutrophil infiltration [45,46], and that high levels of RANTES decrease the activity of its receptor CCR5 and reduce inflammatory cell migration into inflammatory loci [47]. In the current study we found that AAT strongly enhances LPS-induced IL-10, IL-12, and RANTES levels in mice.…”

Section: Discussionmentioning

confidence: 99%

Effects of alpha 1-antitrypsin on endotoxin-induced lung inflammation in vivo

et al. 2010

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IL-10 administration attenuates pulmonary neutrophil infiltration and alters pulmonary iNOS activation following hemorrhagic shock

Abstract: These findings suggest that administration of IL-10 modulates the degree of hemorrhage-induced systemic and pulmonary inflammation and support the notion of a central role for iNOS in acute lung injury.

Cited by 30 publications

References 40 publications

Stimulation of A2B adenosine receptors protects against trauma–hemorrhagic shock-induced lung injury

Stimulation of A2B adenosine receptors protects against trauma–hemorrhagic shock-induced lung injury

Potent Antiedematous and Protective Effects of Ciprofloxacin in Pulmonary Ricinosis

Effects of alpha 1-antitrypsin on endotoxin-induced lung inflammation in vivo

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