Altered chemokine response in an animal model of multiple organ dysfunction syndrome induced by zymosan

Thomas, Neal J.; Umstead, Todd M.; Phelps, David S.

doi:10.1016/j.jpedsurg.2004.11.042

Cited by 3 publications

(1 citation statement)

References 22 publications

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“…A number of studies have shown that in general tyrphostins express their anti-inflammatory activity by modulation of pro-inflammatory gene expression, such as cyclooxygenase-2 (COX2), inducible nitric oxide synthase (iNOS) and several pivotal cytokines ( Figure 1). The activation of macrophages by different stimulilike lypopolisaccharide 20 , resulted in tumour necrosis factor-α (TNF-α), interleukine-1β (IL-1β) and eicosanoid production via phosphorylation of TYKs 11,21 . In turn, targeted cell activation by these mediators happens through TYK signalling pathways.…”

Section: Introductionmentioning

confidence: 99%

Tyrphostins as a promising therapeutic tool in inflammation-related conditions

Dimitrova¹,

Ivanovska²

2013

OA Inflammation

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IntroductionProtein kinases regulate the expression of many genes that are pivotal for inflammation. This review aims to summarise data on a group of small molecules capable to inhibit tyrosine kinases (TYKs), named tyrphostins. They are derivatives of benzylidenemalonitrile that decrease tyrosine phosphorylation, thereby affecting not a single mediator, but cell signalling transduction is affected. No single animal model fully represents the human disease, but these models provide valuable tools to understand particular pathways. In this review, we describe some of the recent investigations on tyrphostins as anti-inflammatory agents in vivo in animal models, and in vitro in cell culture systems. ConclusionIt is anticipated that tyrphostins are suitable for the treatment of inflammation-related diseases. Future research is required to understand the mechanisms of their action to pave way for gaining pharmacological benefits in clinical practice.

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Section: Introductionmentioning

confidence: 99%

Tyrphostins as a promising therapeutic tool in inflammation-related conditions

Dimitrova¹,

Ivanovska²

2013

OA Inflammation

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Ulinastatin-mediated protection against zymosan-induced multiple organ dysfunction in rats

Yang

Liu

et al. 2010

Biologicals

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Pathophysiology of Pediatric Multiple Organ Dysfunction Syndrome

Carcillo

Podd

Aneja

et al. 2017

Pediatric Critical Care Medicine

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Objective To describe the pathophysiology associated with multiple organ dysfunction syndrome (MODS) in children. Data Sources Literature review, research data, and expert opinion Study Selection Not applicable Data Extraction Moderated by an experienced expert from the field, pathophysiological processes associated with MODS in children were described, discussed and debated with a focus on identifying knowledge gaps and research priorities. Data Synthesis Summary of presentations and discussion supported and supplemented by relevant literature. Conclusions Experiment modeling suggests that persistent macrophage activation may be a pathophysiologic basis for MODS. Children with MODS have 1) reduced cytochrome P450 metabolism inversely proportional to inflammation, 2) increased circulating damage associated molecular pattern molecules (DAMPS) from injured tissues, 3) increased circulating pathogen associated molecular pattern molecules (PAMPS) from infection or endogenous microbiome, and 4) cytokine driven epithelial, endothelial, mitochondrial, and immune cell dysfunction. Cytochrome P450s metabolize endogenous compounds and xenobiotics, many of which ameliorate inflammation, whereas DAMPS and PAMPS alone and together amplify the cytokine production leading to the inflammatory MODS response. Genetic and environmental factors can impede inflammation resolution in children with a spectrum of MODS pathobiology phenotypes. Thrombocytopenia associated MODS patients have extensive endothelial activation and thrombotic microangiopathy with associated oligogenic deficiencies in inhibitory complement and ADAMTS13. Sequential MODS patients have sfasL-fas mediated hepatic failure with associated oligogenic deficiencies in perforin and granzyme signaling. Immune paralysis associated MODS patients have impaired ability to resolve infection, and have associated environmental causes of lymphocyte apoptosis. These inflammation phenotypes can lead to macrophage activation syndrome. Resolution of MODS requires elimination of the source of inflammation. Full recovery of organ functions is noted six to eighteen weeks later when epithelial, endothelial, mitochondrial, and immune cell regeneration and reprogramming is completed.

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Altered chemokine response in an animal model of multiple organ dysfunction syndrome induced by zymosan

Cited by 3 publications

References 22 publications

Tyrphostins as a promising therapeutic tool in inflammation-related conditions

Tyrphostins as a promising therapeutic tool in inflammation-related conditions

Ulinastatin-mediated protection against zymosan-induced multiple organ dysfunction in rats

Pathophysiology of Pediatric Multiple Organ Dysfunction Syndrome

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