Treatment with antileukinate, a CXCR2 chemokine receptor antagonist, protects mice against acute pancreatitis and associated lung injury

Bhatia, Madhav; Hegde, Akhil

doi:10.1016/j.regpep.2006.08.006

Cited by 57 publications

(53 citation statements)

References 25 publications

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“…In a cerulein model of AP, platelet depletion via an antibody (anti-GP1b ) reduced many markers of severe AP including serum amylase levels, acinar cell necrosis, interstitial pancreatic hemorrhage, inflammatory infiltration by neutrophils, pancreatic MPO, pancreatic macrophage inflammatory protein-2 (MIP-2), and circulating leukocytes and neutrophils (Abdulla et al, 2011a). This study along with others showed that platelets exert a proinflammatory response by invoking MIP-2 chemokine synthesis in pancreatic cells (macrophage and acinar cells) (Ramnath & Bhatia, 2006;Sun & Bhatia, 2007), a major signal for neutrophil infiltration and chemotaxis (Bhatia & Hegde, 2007;Li et al, 2004). Therefore targeting the inflammatory nature of platelets may have therapeutic potential in reducing pancreatic tissue injury and the severity of acute pancreatitis (Abdulla et al, 2011 2009;²Radenkovic et al 2004;³Mavrommatis et al 2000;Kinasewitz et al 2004;Collins et al 2006;Maeda et al 2006;Stief et al 2007;Lindstrom et al 2006;Sawa et al 2006;¹⁰Gando et al 1998;¹¹Powell et al 2001;¹²Ogura et al 2001;¹³Osmanovic et al 2000;¹ Lu et al 2007;¹ Yasuda et al 2009;¹ Uehara et al 2009;¹ Vinazzer et al 1988;¹ Ida et al 2009; †Denotes a non-significant value compared with normal controls.…”

Section: Targeting Platelet Activating Factor (Paf) and Platelets In Apsupporting

confidence: 56%

Coagulation Abnormalities in Acute Pancreatitis

Gould¹,

Mai²,

Liaw³

2012

Pancreatitis - Treatment and Complications

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Section: Targeting Platelet Activating Factor (Paf) and Platelets In Apsupporting

confidence: 56%

Coagulation Abnormalities in Acute Pancreatitis

Gould¹,

Mai²,

Liaw³

2012

Pancreatitis - Treatment and Complications

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“…Only CXCL1/KC and CXCL2/MIP-2 release were measured. Although other molecules can recruit neutrophils to inflamed tissue, we chose to focus on CXCL1/KC and CXCL2/MIP-2 because both signal via CXCR2, which has been shown to play a central role in neutrophil recruitment and tissue injury in a variety of disease models [35][36][37][38][39] and because both are known to be transcriptionally regulated by NF-κB, which is activated following Fas stimulation [15,16]. This study did not address whether the Fas-MyD88 interaction is direct or indirect.…”

Section: Discussionmentioning

confidence: 99%

Fas (CD95) induces macrophage proinflammatory chemokine production via a MyD88-dependent, caspase-independent pathway

Altemeier

Zhu

Berrington

et al. 2007

Journal of Leukocyte Biology

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Activation of the prototypical death receptor, Fas (CD95), can induce both caspase-dependent cell death and production of pro-inflammatory chemokines, leading to neutrophil recruitment and endorgan injury. The precise mechanism(s), by which Fas upregulates chemokine production and release, is currently unclear. We hypothesized that Fas-induced chemokine release by macrophages is dependent on the MyD88 adapter molecule and independent of caspase activity. To test this hypothesis, we measured chemokine response to Fas activation both in RAW 264.7 cells with RNAi-attenuated MyD88 expression and in MyD88-deficient primary macrophages. We found that Fas-induced chemokine release was abrogated in the absence of MyD88. In vivo, MyD88 −/− mice had impaired CXCL1/KC release and polymorphonuclear cell recruitment in response to intratracheal treatment with the Fas-activating monoclonal antibody, Jo-2. Furthermore, Fas-induced chemokine release was not dependent on either IL-1 receptor signaling or on caspase activity. We conclude that MyD88 plays an integral role in Fas-induced macrophage-mediated inflammation.

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“…Similar to IL-8, CXCL1, CXCL2, lipopolysaccharide-induced CXC chemokine (LIX, also named CXCL5) and lungkine (CXCL15) bind to CXCR2. Inhibition or knockout of CXCR2 receptor diminishes neutrophil influx into the lung (75)(76)(77)(78)(79)(80)(81)(82). In contrast to the multiple CXC chemokines only two CXC chemokines receptors, CXCR1 and CXCR2, have been shown to mediate the response to CXC chemokines in human neutrophils.…”

Section: Chemokinesmentioning

confidence: 99%

Contribution of Neutrophils to Acute Lung Injury

Grommes

Soehnlein

2010

Mol Med

1,117

897

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Treatment of acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), remain unsolved problems of intensive care medicine. ALI/ARDS are characterized by lung edema due to increased permeability of the alveolar-capillary barrier and subsequent impairment of arterial oxygenation. Lung edema, endothelial and epithelial injury are accompanied by an influx of neutrophils into the interstitium and broncheoalveolar space. Hence, activation and recruitment of neutrophils are regarded to play a key role in progression of ALI/ARDS. Neutrophils are the first cells to be recruited to the site of inflammation and have a potent antimicrobial armour that includes oxidants, proteinases and cationic peptides. Under pathological circumstances, however, unregulated release of these microbicidal compounds into the extracellular space paradoxically can damage host tissues. This review focuses on the mechanisms of neutrophil recruitment into the lung and on the contribution of neutrophils to tissue damage in ALI.

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Treatment with antileukinate, a CXCR2 chemokine receptor antagonist, protects mice against acute pancreatitis and associated lung injury

Cited by 57 publications

References 25 publications

Coagulation Abnormalities in Acute Pancreatitis

Coagulation Abnormalities in Acute Pancreatitis

Fas (CD95) induces macrophage proinflammatory chemokine production via a MyD88-dependent, caspase-independent pathway

Contribution of Neutrophils to Acute Lung Injury

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