Gut Ischemia/Reperfusion Induced Acute Lung Injury is an Alveolar Macrophage Dependent Event

Moraes, Luciana Borsoi; Murakami, Abel H.; Fontes, Belchor; Poggetti, Renato Sérgio; Rooijen, Nico van; Younes, Riad N.; Heimbecker, Ana Maria Cattani; Birolini, D

doi:10.1097/ta.0b013e31816c5ca6

Cited by 32 publications

(31 citation statements)

References 29 publications

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“…In the present study, protein levels in BAL were significantly increased after blunt chest trauma. Comparable to our own previous experiments on Evans blue lung-plasma ratio (26), these data indicate that lung contusion induces a breakdown of the alveolocapillary barrier as described previously (6,27). Under this condition, the transfer of mediators from the lung to the bloodstream and vice versa is facilitated and chemokines may arrive in the circulation to stimulate immune cells.…”

Section: Discussionsupporting

confidence: 84%

Blunt chest trauma induces mediator-dependent monocyte migration to the lung

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Palmer

et al. 2010

Critical Care Medicine

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Section: Discussionsupporting

confidence: 84%

Blunt chest trauma induces mediator-dependent monocyte migration to the lung

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Niesler

Palmer

et al. 2010

Critical Care Medicine

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“…I/R causes gut barrier disruption and endotoxin entry into the circulation, leading to severe systemic inflammation and eventually multiple organ failure [4-7]. Acute lung injury (ALI) is a common complication that occurs after intestinal I/R and is a major contributor to the high mortality rate [7-11]. Limited pharmacological treatment options exist for ALI, with most targeting inflammatory mediators and oxidative stress pathways [12].…”

Section: Introductionmentioning

confidence: 99%

“…After activation by proinflammatory cytokines and chemotactic factors, neutrophils are then able to penetrate the vasculature and transmigrate through the interstitium into the alveolar space [18,19]. In addition, alveolar macrophages are also essential players in the initiation of ALI [11,20]. …”

Section: Introductionmentioning

confidence: 99%

Cyclic arginine-glycine-aspartate attenuates acute lung injury in mice after intestinal ischemia/reperfusion

et al. 2013

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IntroductionIntestinal ischemia is a critical problem resulting in multiple organ failure and high mortality of 60 to 80%. Acute lung injury (ALI) is a common complication after intestinal ischemia/reperfusion (I/R) injuries and contributes to the high mortality rate. Moreover, activated neutrophil infiltration into the lungs is known to play a significant role in the progression of ALI. Integrin-mediated interaction is involved in neutrophil transmigration. Synthetic peptides containing an arginine-glycine-aspartate sequence compete with adhesive proteins and inhibit integrin-mediated interaction and signaling. Thus, we hypothesized that the administration of a cyclic arginine-glycine-aspartate peptide (cRGD) inhibited neutrophil infiltration and provided protection against ALI induced by intestinal I/R.MethodsIschemia in adult male C57BL/6 mice was induced by fastening the superior mesenteric artery with 4-0 suture. Forty-five minutes later, the vascular suture was released to allow reperfusion. cRGD (5 mg/kg body weight) or normal saline (vehicle) was administered by intraperitoneal injection 1 hour prior to ischemia. Blood, gut, and lung tissues were collected 4 hours after reperfusion for various measurements.ResultsIntestinal I/R caused severe widespread injury to the gut and lungs. Treatment with cRGD improved the integrity of microscopic structures in the gut and lungs, as judged by histological examination. Intestinal I/R induced the expression of β1, β2 and β3 integrins, intercellular adhesion molecule-1, and fibronectin. cRGD significantly inhibited myeloperoxidase activity in the gut and lungs, as well as neutrophils and macrophages infiltrating the lungs. cRGD reduced the levels of TNF-α and IL-6 in serum, in addition to IL-6 and macrophage inflammatory protein-2 in the gut and lungs. Furthermore, the number of TUNEL-staining cells and levels of cleaved caspase-3 in the lungs were significantly lowered in the cRGD-treated mice in comparison with the vehicle mice.ConclusionsTreatment with cRGD effectively protected ALI and gut injury, lowered neutrophil infiltration, suppressed inflammation, and inhibited lung apoptosis after intestinal I/R. Thus, there is potential for developing cRGD as a treatment for patients suffering from ALI caused by intestinal I/R.

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“…Kubes et al 28 showed that most of the liver I/R models (including liver transplantation) have some degree of intestinal ischemia, which enhances the liver injury by inducing the release of toxins and intestinal neutrophil recruitment 27,29 . Recently, intestinal transplantation has become the preferred therapy for patients with short bowel syndrome, with intolerance to total parenteral nutrition 14,17,19 .…”

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confidence: 99%

Ischemic preconditioning modifies mortality and inflammatory response

et al. 2016

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PURPOSE:To evaluate the effect of ischemic preconditioning on mortality, inflammatory mediators and oxidative stress after intestinal ischemia and reperfusion. METHODS:Male Wistar rats were allocated according to the period of ischemia with or without ischemic preconditioning which consist on clamping the superior mesenteric artery for 10 minutes followed by reperfusion for 10 minutes before the sustained ischemia period. Mortality was assessed in Phase 1 study, and the CINC-1, CINC-2 and MDA levels in the lungs were analyzed in Phase 2. RESULTS:Mortality was lower in the ischemic preconditioning group subjected to 90 minutes of ischemia compared to the group without ischemic preconditioning (I-90: 50% and IPC-90: 15%, p=0.018), and it was lower in the ischemic preconditioning group as a whole compared to the groups without ischemic preconditioning (IPC-14% and I=30%, p=0.006). Lower levels of MDA, CINC-1, and CINC-2 were observed in the animals that were subjected to ischemic preconditioning compared to the animals that were not (MDA: I-45=1.23 nmol/mg protein, and IPC-45=0.62 nmol/mg protein, p=0.0333; CINC-1: I-45=0.82 ng/mL and IPC-45=0.67 ng/mL, p=0.041; CINC-2: I-45=0.52 ng/mL and IPC-45=0.35 ng/mL, p=0.032). CONCLUSION:Ischemic preconditioning reduces mortality, inflammatory process and oxidative stress in rats subjected to intestinal ischemia and reperfusion.

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Gut Ischemia/Reperfusion Induced Acute Lung Injury is an Alveolar Macrophage Dependent Event

Cited by 32 publications

References 29 publications

Blunt chest trauma induces mediator-dependent monocyte migration to the lung

Blunt chest trauma induces mediator-dependent monocyte migration to the lung

Cyclic arginine-glycine-aspartate attenuates acute lung injury in mice after intestinal ischemia/reperfusion

Ischemic preconditioning modifies mortality and inflammatory response

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