Amine oxidases (AOs) are ubiquitous enzymes involved in the metabolism of biogenic amines. Copper AOs (Cu-AOs) catalyze the oxidative deamination of primary amine groups of several biogenic amines, such as putrescine, cadaverine, and histamine. In the present review, the effects of a plant amine oxidase (Cu-AO, histaminase, EC1.4.3.6) purified from pea seedlings in the modulation of IgE-mediated allergic reactions, and in the prevention of cardiac and splachnic postischemic reperfusion damage are reported.

Emanuela Masini

Danielle Bani

Cosimo Marzocca

Mircea Alexandru Mateescu

Pier Francesco Mannaioni

Rodolfo Federico

Bruno Mondovì

Pea Seedling Histaminase as a Novel Therapeutic Approach to Anaphylactic and Inflammatory Disorders

Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily of ligand-activated transcription factors that are related to retinoid, steroid, and thyroid hormone receptors. Three isotypes of PPARs have been identified: alpha, beta/delta, and gamma, encoded by different genes and distributed in various tissues. PPARs are implicated in the control of inflammatory responses and in energy homeostasis and, thus, can be defined as metabolic and anti-inflammatory transcription factors. They exert anti-inflammatory effects by inhibiting the induction of proinflammatory cytokines, adhesion molecules, and extracellular matrix proteins, or by stimulating the production of anti-inflammatory molecules. Moreover, PPARs modulate the proliferation, differentiation, and survival of immune cells. This review presents the current state of knowledge regarding the involvement of PPARs in the control of inflammatory response, and their potential therapeutic applications in several types of shock, as well as hemorrhagic, septic, and nonseptic shock.

Emanuela Esposito

Salvatore Cuzzocrea

Rosaria Meli

Peroxisome Proliferator-Activated Receptors and Shock State

Several studies have recognized the strong impact that the acute myocardial infarctions (AMI) have on the morbidity and mortality of patients affected by cardiovascular diseases. Still open, however, is the field concerning the mediators and the pathways involved in the etiology of this cardiovascular event. The present review would support the relatively new discovered role that the polymorphonuclear leukocytes (PMNs) have in the pathogenesis of the AMI, through a brief analysis of past and ongoing research. Particularly, it is reviewed here the possibility that inhibition of the activity of PMNs and inhibition of the signaling pathways related to their activity may result useful in AMI and may improve the prognosis of this pathology. This review, indeed, presents and discusses new data on one of the lipid kinase, the phosphoinositide 3-kinase gamma (PI3Kγ), and its role in neutrophil recruitment during AMI.

Clara Di Filippo

Francesco Rossi

Michele D'Amico

Targeting Polymorphonuclear Leukocytes in Acute Myocardial Infarction

The leukotrienes (LTs) are metabolic products of arachidonic acid via the 5-lipoxygenase (5-LO) pathway. The biological activities of LTs suggest that they are mediators of acute inflammatory and immediate hypersensitivity responses. In particular, the 5-LO activation has been proposed to be an important regulator for pathogenesis in multicellular organisms. The role of LTs in tissue damage, associated with septic and nonseptic shock and ischemia-reperfusion, has been extensively studied by the use of 5-LO inhibitors, receptor antagonists, and mice with a targeted disruption of the 5-LO gene (5-LOKO). In particular, several data indicate that LTs regulate neutrophil trafficking in damaged tissue in shock and ischemia-reperfusion, mainly through the modulation of adhesion molecule expression. This concept may provide new insights into the interpretation of the protective effect of 5-LO inhibition, which may be useful in the therapy of pathological conditions associated with septic and nonseptic shock and ischemia-reperfusion injury.

Antonietta Rossi

Carlo Pergola

Lidia Sautebin

The Role of 5-Lipoxygenase and Leukotrienes in Shock and Ischemia-Reperfusion Injury

A considerable body of experimental evidence suggests that tumor necrosis factor (TNF)-α plays a major role in several aspects of inflammation and shock. In particular, it is pivotal in many detrimental effects of acute pancreatitis, and it represents a major determinant of the systemic progression and end-organ damage (such as acute lung injury and liver failure) of this pathologic condition. Given the importance of TNF-α in the pathogenesis of acute pancreatitis, investigators have regarded blocking the action of this mediator as an attractive treatment option. Different specific and nonspecific inhibitors have been developed with promising results in animal models, but, on the other hand, no clinical trials have been designed so far. Difficulties in clinical applications may be multifactorial; experimental models are not fully reliable and reproduce at least some aspects of human disease, timing of intervention should be related to changes in TNF-α serum levels, and inclusion criteria should be accurately selected to better define the population most likely to benefit.

Giuseppe Malleo

Emanuela Mazzon

Ajith K. Siriwardena

TNF-α  as a Therapeutic Target in Acute Pancreatitis — Lessons from Experimental Models

Glucocorticoid-induced TNFR-Related (GITR) protein is a member of the tumor necrosis factor receptor superfamily that modulates acquired and natural immune response. It is expressed in several cells and tissues, including T cells, natural killer cells, and, at lower levels, in cells of innate immunity. GITR is activated by its ligand, GITRL, mainly expressed on antigen presenting and endothelial cells. Recent evidence suggests that the GITR/GITRL system participates in the development of inflammatory responses, including shock, either due to early response of neutrophils and macrophages, or together with autoimmune/allergic pathogenesis. The pro-inflammatory role of the GITR/GITRL system is due to: 1) modulation of the extravasation process, 2) activation of innate immunity cells, 3) activation of effector T cells also favored by partial inhibition of suppressor T cells and modulation of dendritic function. This review summarizes the in vivo role of the GITR/GITRL system in inflammation and shock, explaining the mechanisms responsible for their effects, considering the interplay among the different cells of the immune system and transduction pathways activated by GITR and GITRL triggering. The hidden aspects about GITR/GITRL function, crucial for treatment planning of inflammatory diseases and shock by modulation of this system is stressed.

Ludovic Tibor Krausz

Rodolfo Bianchini

Simona Ronchetti

Katia Fettucciari

Giuseppe Nocentini

Carlo Riccardi

GITR-GITRL System, A Novel Player in Shock and Inflammation

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