Circulating cytokines present in the serum of peripheral arterial disease patients induce endothelial dysfunction.

Peripheral arterial disease (PAD) is a chronic condition caused by atherosclerosis and is a severe complication of type 2 diabetes (T2D). We hypothesised that chronic condition of arterial disease engenders inflammation and endothelial damage in response to circulating cytokines released in the blood stream of PAD patients. We explored the levels of circulating cytokines in PAD patients with and without diabetes by multiplex cytokine array compared with non-PAD controls. Serum from PAD patients with or without diabetes showed high levels of VEGF, IFN-gamma, TNF-alpha, MCP-1, and EGF. VEGF levels correlated with TNF-alpha and IFN-gamma, significantly. Endothelial cells (ECs) were exposed to the different altered cytokines to evaluate changes in cell growth, migration and tubule-like formation, displaying impairment on proliferation, migration and tubule formation. Our findings demonstrate that a set of cytokines is significantly increased in the serum of PAD patients. These cytokines act to induce endothelial dysfunction synergistically. VEGF strongly correlated with TNF-alpha and IFN-gamma, opening new therapeutic perspectives.

Osteoprotegerin, RANK and RANKL are not modified by acute exercise in elite rugby players.

AIM: The OPG-RANK-RANKL system is a new family of bone metabolism biomarkers belonging to the immune system. In this study, were evaluated these biomarkers in professional rugby players after a single-bout of training session. METHODS: The study has been performed on 30 professional male rugby players during a training camp of the Italian National Team, in July, before the start of the competitive season. Blood drawings were performed before and after training in the same day. Levels of soluble OPG, RANKL RANK in serum specimens were measured by commercially available according to the manufacturers' protocols. RESULTS: All the bone markers examined displayed no significative changes after training session. CONCLUSION: Short exercise is insufficient for modifying serum concentrations of these osteoimmunologic markers, as previously indicated for commonly used bone metabolism markers. Future studies will be conducted over an entire competition season in order to define a common profile of bone markers in rugby players.

Asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA) and L-arginine in patients with arteriogenic and non-arteriogenic erectile dysfunction.

The plasma concentration of asymmetrical dimethylarginine (ADMA), an inhibitor of nitric oxide synthase, has been linked to endothelial dysfunction. We investigated the relation between ADMA, symmetric dimethylarginine (SDMA) and L-arginine concentrations and erectile dysfunction. We compared plasma levels of ADMA, SDMA and L-arginine in 61 men in good health with erectile dysfunction of arteriogenic and non-arteriogenic origin. Diagnosis of erectile dysfunction was based on the International Index of Erectile Function Score and its aetiology was classified with penile echo-colour-Doppler in basal condition and after intracavernous injection of prostaglandin E1. The ADMA and SDMA concentrations were significantly higher in men with arteriogenic erectile dysfunction compared with those with erectile dysfunction of non-arteriogenic origin (p < 0.05) and the concentrations in both subgroups were significantly higher than in controls (p < 0.001). There was a negative correlation between ADMA and International Index of Erectile Function Score only in arteriogenic erectile dysfunction subgroup. L-arginine did not differ significantly neither between the two erectile dysfunction subgroups (p > 0.05) nor between each of the two erectile dysfunction subgroups and controls (p > 0.05). The L-arginine/ADMA and the L-arginine/SDMA ratios in arteriogenic erectile dysfunction subgroups were significantly lower than both in controls (p < 0.05) and in non-arteriogenic erectile dysfunction patients (p < 0.05); the two ratios in non-arteriogenic erectile dysfunction patients did not differ from those in the controls (p > 0.05). We conclude that ADMA and SDMA concentrations are significantly higher and L-arginine/ADMA ratio lower in patients who have arteriogenic erectile dysfunction compared with both patients with non-arteriogenic erectile dysfunction and controls. The negative correlation between ADMA and severity of erectile dysfunction is present only in patients with arteriogenic erectile dysfunction. This study supports the importance to always distinguish arteriogenic from non-arteriogenic erectile dysfunction patients to study the complicate erectogenic mechanisms that lead to erectile dysfunction and also to provide potential therapeutic agents for patients with arteriogenic erectile dysfunction.

Iron status evaluation as a marker of postoperative joint infection: a pilot study.

We evaluated the effect of different inflammatory conditions on iron status and, as a consequence, the possible use of iron markers as indicators of infection in the diagnosis of postoperative prosthetic orthopaedic joint infections. The study population was consisted of 26 patients undergoing revision of total hip or total knee joint arthroplasty and subdivided into three groups according to the cause of prosthesis implant failure: 10 as having had previous infection (Group A), 10 patients were categorized as having infection (Group B); and the remaining 6 (Group C) as not having infection. These patients were assayed for mean corpuscular haemoglobin concentration (MCHC) and serum values of iron (Fe), ferritin (Fer), transferrin (Tf), soluble transferrin receptor (sTfR), and transferrin saturation (sat Tf). Septic patients display statistically significant lower serum iron concentration, higher sTfR and ferritin levels, lower, but not statistically significant, MCHC compared to non septic ones. Little differences were observed for Tf, sat Tf, tibc, TfR index, among the three groups of patients. Our study suggests that iron status parameters, in particular serum iron, ferritin, sTfR and TfR index, could be useful tools for the early detection and the diagnosis of orthopaedic prosthetic joint infections.

Receptor binding mode and pharmacological characterization of a potent and selective dual CXCR1/CXCR2 non-competitive allosteric inhibitor.

BACKGROUND AND PURPOSE: DF 2156A is a new dual inhibitor of IL-8 receptors CXCR1 and CXCR2 with an optimal pharmacokinetic profile. We characterized its binding mode, molecular mechanism of action and selectivity, and evaluated its therapeutic potential. EXPERIMENTAL APPROACH: The binding mode, molecular mechanism of action and selectivity were investigated using chemotaxis of L1.2 transfectants and human leucocytes, in addition to radioligand and [(35) S]-GTPγS binding approaches. The therapeutic potential of DF 2156A was evaluated in acute (liver ischaemia and reperfusion) and chronic (sponge-induced angiogenesis) experimental models of inflammation. KEY RESULTS: A network of polar interactions stabilized by a direct ionic bond between DF 2156A and Lys(99) on CXCR1 and the non-conserved residue Asp(293) on CXCR2 are the key determinants of DF 2156A binding. DF 2156A acted as a non-competitive allosteric inhibitor blocking the signal transduction leading to chemotaxis without altering the binding affinity of natural ligands. DF 2156A effectively and selectively inhibited CXCR1/CXCR2-mediated chemotaxis of L1.2 transfectants and leucocytes. In a murine model of sponge-induced angiogenesis, DF 2156A reduced leucocyte influx, TNF-α production and neovessel formation. In vitro, DF 2156A prevented proliferation, migration and capillary-like organization of HUVECs in response to human IL-8. In a rat model of liver ischaemia and reperfusion (I/R) injury, DF 2156A decreased PMN and monocyte-macrophage infiltration and associated hepatocellular injury. CONCLUSION AND IMPLICATIONS: DF 2156A is a non-competitive allosteric inhibitor of both IL-8 receptors CXCR1 and CXCR2. It prevented experimental angiogenesis and hepatic I/R injury in vivo and, therefore, has therapeutic potential for acute and chronic inflammatory diseases.

Platelet rich plasma therapy: inflammatory molecules involved in tissue healing.

Inflammation represents a fundamental aspect of the healing process. Besides their primary role in hemostasis, platelets play an active role in the immunological and inflammatory aspect of tissue healing. Indeed , they can be directly involved in the inflammatory response by the production and release of several inflammatory mediators, including a variety of cytokines, such as TGF-beta, IL-1 beta, CD40L, and chemokines, such as CXCL7, CXCL4, CXCL4L1, CCl5, CXCL1, CXCL8, CXCL5, CXCL12, CCL2, CCL3. Platelet are not only a source of several chemokine involved in the inflammatory response and tissue healing, but they also express chemokine receptors, in particular CCR1 CCR3 CCR4 and CXCR4, thus being able to being able to regulate the inflammatory response associated to the healing process. However, this local inflammation must be taken under control, and platelets can prevent the excess of leukocytes recruitment by anti-inflammatory cytokines, such as TGF-beta. For this biological properties of platelets, platelet rich plasma therapy (PRP) is considered an innovative and promising approach that has been extended to many field of medicine, ranging from non-union defects, bone fractures, spinal fusion, bone implant and osteointegration, joint arthroplasty, to the treatment of several traumatic or degenerative pathologies of tendons, cartilage and ligaments.

Procalcitonin, C-reactive protein, interleukin-6, and soluble intercellular adhesion molecule-1 as markers of postoperative orthopaedic joint prosthesis infections.

There is a universally recognized need to identify new, reliable markers of inflammation that can aid in the rapid diagnosis of orthopaedic joint prosthesis infections (OJP-Is). Since prompt diagnosis is key to timely intervention in the course of infection, different molecules have been studied. In this study, we examined three groups of patients: those with prosthesis infection, those without infection, and a third group with previous infection in whom the infection had been cleared. Four presumed markers of infection were tested: procalcitonin (PCT); C-reactive protein (CRP); interleukin-6 (IL-6); and soluble intercellular adhesion molecule-1 (sICAM-1). The results showed that PCT cannot be considered as a good marker of periprosthetic infection as no statistically significant difference in serum PCT levels emerged between patients with infection and controls or patients without infection. In contrast, both sICAM-1 and CRP may be considered as good markers of infection, as measurement of their levels allowed us to distinguish between patients with and without infection, and between patients with infection and those with previous infection, since marker levels quickly returned to baseline values after clearance of the infection. IL-6 was found to be a good marker for inflammation, as it distinguished between patients with infection and the other groups. In the patients with previous infection, the IL-6 values remained high versus the controls but lower and with a statistically significant difference versus the patients with infection. Further studies are needed to determine the cut-off value of IL-6 between patients with infection and those with previous infection.

High articular levels of the angiogenetic factors VEGF and VEGF-receptor 2 as tissue healing biomarkers after single bundle anterior cruciate ligament reconstruction.

Various factors may account for the positive association between meniscal repair and anterior cruciate ligament reconstruction, one being the modulation of healing response of meniscal fibrochondrocytes by growth factors released with intra-articular bleeding and fibrin clot formation. Analysis of vascular endothelial growth factor (VEGF) and its receptors, VEGFR1 and VEGFR2, may be useful in the clinical assessment of bone and soft-tissue remodeling. We measured systemic and local levels of VEGF (VEGF165), VEGFR1 and VEGFR2 after either arthroscopic partial meniscectomy (APM) or single-bundle anterior cruciate ligament reconstruction (ACLR) in order to determine the local effect of bone tunnelling and notchplasty on the release of these growth factors. The study population included 40 patients: 20 consecutive patients had undergone ACLR with hamstring grafts and 20 had undergone APM. Thirty minutes after the end of the operation, knee joint fluid samples were collected via the drainage tube and at the same time venous blood samples were drawn. In both sets of samples, VEGF, VEGFR1 and VEGFR2 concentrations were determined by enzyme-linked immunosorbent assay (ELISA). No significant differences in VEGF, VEGFR1 or VEGFR2 concentrations in the venous blood were observed between the two treatment groups. In contrast, VEGF and VEGFR2 levels were significantly higher in the knee joint fluid of the ACLR group; furthermore, VEGF and VEGFR1 were significantly higher in the knee joint fluid than in the venous blood, whereas VEGFR2 was lower in the knee joint fluid than in the venous blood. Local release of VEGF and its angiogenetic receptor VEGFR2, but not the negative regulator VEGFR1, was significantly higher after ACLR than after APM, indicating a better vasculogenic potential for enhanced bone-graft and meniscus healing. These results could suggest that VEGF and VEGFRs could be considered as good biomarkers of tissue healing after knee joint surgery.

Effect of immersion in CO2-enriched water on free radical release and total antioxidant status in peripheral arterial occlusive disease.

AIM: The aim of this paper was to investigate the release of oxygen free radicals in patients with peripheral occlusive arterial disease and the effects of immersion of the legs and feet in carbon dioxide (CO(2))-enriched water. METHODS: Twenty-five patients with peripheral occlusive arterial disease (Fontaine stage II) and 15 healthy controls were treated by immersing the lower legs in either CO(2)-enriched or normal spa water. Blood samples were collected in heparinized tubes and total antioxidant status (TAS) and reactive oxygen metabolites (ROMs) were measured after five treatments a week for two weeks. RESULTS: d-ROM plasma levels decreased in patients with peripheral occlusive disease after immersion in CO(2)-enriched water (P<0.001), and in healthy controls (P<0.01), in line with a significant increase in TAS (P<0.001). CONCLUSION: CO(2)-enriched water immersion had a positive effect, reducing free radical plasma levels and raising the levels of antioxidants, suggesting an improvement in the microcirculation.

Circulating cytokines and growth factors in professional soccer players: correlation with in vitro-induced motor neuron death.

BACKGROUND: professional soccer players are susceptible to amyotrophic lateral sclerosis. Strenuous physical activity has been associated with persistent inflammatory conditions and elevation of systemic cytokine levels, which could contribute to the vulnerability of these athletes. To investigate changes induced by playing soccer in the systemic profiles of growth factors and of the principal cytokines involved in the inflammatory response, we compared the serum concentrations of these factors in Italian professional soccer players and sedentary subjects. We also investigated the effects of the sera on primary cultured motor neurons in relation to their cytokine and growth factor content. METHODS: serum concentrations of cytokines and growth factors were measured by a biochip array analyzer. Neurotoxicity of sera was assessed by immunocytochemical assays in primary motor neuron cultures from mouse embryos. RESULTS: circulating levels of interleukin-8, tumor necrosis factor-alpha and interleukin-4 were lower in soccer players than controls. However, the viability of primary cultured mouse motor neurons treated with sera from the two groups did not differ significantly. Vascular endothelial growth factor (VEGF) independently emerged as a systemic protective factor for motor neurons. CONCLUSIONS: we found significant alterations in circulating pro-inflammatory cytokines in Italian professional soccer players, showing an unbalanced inflammatory condition in these subjects. VEGF was a protective serum factor affecting motor neuron survival.

Growth factors in the management of sport-induced tendinopathies: results after 24 months from treatment. A pilot study.

AIM: The efficacy of PRP in the treatment of tendinopathies has been already studied both in in vitro and in clinical studies. This paper describes the local and the systemic effects of US-guided autologous PRP (Platelet Rich Plasma) injections in chronic tendinopathies in sportspersons. METHODS: Fifteen patients (13 male, 2 female) between 17 and 68 years old, affected by chronic tendinopathies at different sites were treated with an echographically guided injection of autologous PRP within the pathological area of the tendons. VISA score and MRI data were collected pre interventions and after 90 days and 24 months from treatment. Changes in different inteleukins (ILs), tumour necrosis factor α (TNF α), interferon γ, vascular endothelial growth factor (VEGF), endothelial growth factor (EGF), chemokine (C-C motif) ligand 2 (CCL2), were analysed at four time points in the peripheral blood of five patients. RESULTS: After 90 days the VISA score significantly improved from 36±12 (range 21-64) to 74±17 (range 40-92). Reduction of irregularities was found in 80% of the tendons. After 24 months patients reported an average VISA score of 73±16 (range 42-100). No changes in IL, TNF α and interferon γ were observed. VEGF, EGF and CCL2 decreased progressively from 30m to 3 h after the treatment and returned to near the baselines after 24 h. CONCLUSION: PRP injection allow an improvement of the clinical symptomatology, which is well maintained at least for two years from treatment. The PRP-based local therapy could influence systems homeostasis and antidoping evaluations, but, in our opinion, it doesn't represent a doping substance in itself.

Matrix metalloproteases MMP-2 and MMP-9: are they early biomarkers of bone remodelling and healing after arthroscopic acromioplasty?

Arthroscopic acromioplasty, one of the most frequent procedures in shoulder surgery, can promote tissue healing process by the release of growth/angiogenic factors from the acromion. Matrix metalloproteinases MMP-2 and MMP-9 are involved in such process. The purpose of this study was to measure MMP-2 and MMP-9 levels in the articular fluid and in the peripheral blood of patients undergoing arthroscopic acromioplasty in order to better understand the local involvement of such factors in the healing process after surgical procedures. Concentrations of MMP-2 and MMP-9 in the subacromial space and peripheral blood collected shortly after surgery were determined by ELISA. MMP-2 and MMP-9 concentrations were measured in the subacromial fluid of 23 patients. In subacromial fluid, the levels between MMP-2 and MMP-9 did not reach statistical significance (127.15±45.56 vs 149.41±53.61 pg/ml, respectively, p>0.05). Peripheral blood levels of MMP-2 (130.75±47.48 pg/ml) were comparable to the subacromial fluid ones (127.15±45.56 pg/ml) whereas MMP-9 level was higher in the subacromial space (149.41±53.61 pg/ml) than in the peripheral blood (67.61±12.62 pg/ml, p<0.001). This work suggests that the measurement of bone specific MMPs (MMP-2 and MMP-9) can be an useful tool to be monitored in parallel with growth factor levels and other bone turnover markers in order to evaluate the bone remodelling and tissue healing processes. This study suggests that the measurement of bone specific MMPs levels, in particular MMP-9, may evaluate the bone remodelling and healing after arthroscopic shoulder acromioplasty.

Molecular aspects of adipokine-bone interactions.

Adipose tissue is an endocrine organ able to produce a wide series of pleiotropic molecules, defined "adipokines". In addition to the regulation of food intake and energy metabolism, adipokines are also implicated in the complex control of bone biology and specifically of bone remodeling. Leptin, the most studied adipokine, promotes satiety and energy expenditure and its circulating levels are proportional to fat mass. Some paradoxical findings originally suggested the involvement of leptin in controlling bone mass. For example, obese postmenopausal women, with elevated circulating leptin and leptin resistance, appear protected against the development of osteoporosis. Moreover, genetically leptin-deficient mice, which are hypogonadal and obese, display a decreased trabecular volume in long bones, but an increased vertebral bone mass, which is reduced by leptin administration. The complex mechanisms of leptin regulation of bone mass appear to involve selected hypothalamic neuronal populations and the sympathetic outflow, with an important role of osteoblastic beta2-adrenergic receptors. Adiponectin is another adipokine, which promotes insulin sensitivity and is reduced in obese and diabetic subjects. Adiponectin appears to exert a negative effect on bone mass and seems to be an independent predictor of lower bone mass. Although the adipokines resistin and visfatin do not seem to significantly affect bone metabolism, the potential impact of them and other adipokines is still to be determined. Moreover, the molecular adipokine-bone interactions should also be considered in the context of the adipokine changes observed in diseases such as obesity and the metabolic syndrome.

Human bone disorders: pathological role and diagnostic potential of matrix metalloproteinases.

Bone undergoes continuous remodeling under physiological and pathological conditions. Failure of the regulation of this process leads to several disorders involving bone erosion. This series of events is mainly based on the action of proteinases, particularly matrix metalloproteinases (MMPs). MMPs have been recently suggested as potential bone resorption markers which could be added to the commonly used ones, in order to predict outcome of disease processes and healing, and to monitor disease response to treatment. As for classical biochemical bone markers, MMPs are far from being applied in primary clinical diagnosis, but they could be promising in some cases for disease prognosis. MMPs as bone remodeling biomarkers could provide information that boosts our understanding of the prognosis, disease activity and pathogenesis of bone disorders. Clarifying the MMPs' role in bone remodeling and healing could potentially help predict disease progression and the effects of direct specific therapy.

Plasma adiponectin and leptin concentrations in professional rugby players.

Adipose tissue synthesizes and secretes a number of cytokine hormones, defined adipokines, which have emerged as critical regulators of several metabolic functions, including energy homeostasis, insulin action and lipid metabolism. The present study is aimed at assessing the relationship between plasma concentrations of leptin and adiponectin and body composition in a cohort of 38 male professional rugby players (age: 22-35 years). Anthropometric evaluation included body mass index (BMI, range: 23.4-35.1 kg/m2) and whole body bioelectric impedance to determine absolute fat-free mass (FFM), absolute fat mass (FAT), relative percentage of fat mass (FAT percent) and fat-free mass (FFM percent). FAT percent ranged from 15 to 34 percent, corresponding to a FAT of 11.5-38.7 kg, whereas FFM range was 62.1-83.5 kg. Plasma leptin range was 1.2-4.3 ng/mL and adiponectin range was 2.0-16.6 microg/mL. Plasma leptin and adiponectin concentrations and their ratio did not correlate with BMI, nor with FAT, FAT percent, FFM and FFM percent, even after correction for BMI. The findings of this study suggest that in professional rugby players some additional factors, like neuroendocrine adaptations, other than adipose mass play a relevant role in the determination of adipokine levels, which in this group appear to be rather independent of body composition.

Okadaic acid induces apoptosis in Down syndrome fibroblasts.

Down's syndrome (DS) is characterized by several pathological aspects leading to an increased susceptibility to cardiovascular diseases, infections, leukemia, endocrine alterations. DS patients display some of the physiopathological characteristics of aging, observed also in Alzheimer disease (AD), such as abnormalities in lipids metabolism, diabetes, high cholesterol fraction, senile plaques and neurofibrillary tangles. For this reason DS is considered a precocious and accelerated model of senescence, in which increased apoptosis is the main cornerstone. In order to better understand the apoptotic process in pathological cellular aspects of DS, the aim of this study was to investigate the apoptotic response of DS fibroblasts to OA, a toxin that induces malformations and inhibits growth in different cell lines. We focused specifically on the mitochondrial response by investigating changes in mitochondrial membrane potential (evaluate by flow cytometry and fluorescence microscopy using JC-1 probe) and alterations of mitochondrial outer membrane (evaluated by flow cytometry using annexin V/propidium iodide). Results indicates that DS Fibroblasts have a baseline of apoptosis higher than normal fibroblasts and are more susceptible to the pro-apoptotic effect of OA. Understanding the mechanism of apoptosis in DS fibroblasts could provide new insight in the pathogenic mechanism of this pathology and suggest potential therapeutical targets to the clinical treatment at complex diseases associated to this pathology.

Leptin, ciliary neurotrophic factor, leukemia inhibitory factor and interleukin-6: class-I cytokines involved in the neuroendocrine regulation of the reproductive function.

Class-I cytokines represent a large group of molecules involved in different physiological processes including host defence, immune regulation, food intake, energy metabolism and, relevant for this review, reproduction. In this latter respect, here, we focus the attention on four of these molecules, specifically leptin, ciliary neurotrophic factor (CNTF), leukemia inhibitory factor (LIF) and interleukin-6 (IL-6). These cytokines present similar three-dimensional fold structure, interact with related class-I receptors, which are expressed in the same regions (i.e., hypothalamus), and activate similar intracellular pathways. Leptin and CNTF share functional similarities, by acting at hypothalamic and pituitary levels, and their receptors are colocalized in the arcuate and paraventricular nuclei of the hypothalamus. For both these molecules, no effect on GnRH migration has been described. LIF has also been shown to affect gonadotropin secretion and here we present the novel observation that it is also able to stimulate GnRH secretion in vitro. Moreover, in the mouse, LIF is prenatally expressed in nasal regions where GnRH neurons originate and start their migration, and in vitro it stimulates intrinsic cell motility and directional migration. The role of the prototypical cytokine, IL-6, on the GnRH-LH axis is not fully clear and additional information seem necessary to better clarify this aspect. In conclusion, the data here discussed suggest that this family of cytokines appears to participate to the complex control of the reproductive function by affecting the development and function of the hypothalamus-pituitary system at different ontogenic times and anatomical sites.

Chemokines and bone remodeling.

Bone remodeling is characterized by spatial and temporal coupling of bone resorption and formation and is necessary for skeletal growth and normal bone structure maintenance. Imbalance of this process is related to metabolic bone disorders such as osteoporosis or rheumatoid arthritis. For this reason, bone remodeling is under the control of several local and systemic factors, including molecules of the immune system. The importance of the interplay of both the skeletal and immune systems is reflected by the emerging interdisciplinary research field, called osteoimmunology, focused on common aspects of osteology and immunology. This review focuses on the role of inflammatory mediators, such as cytokines in bone remodeling and, in particular, a subfamily of chemotactic cytokines or chemokines which are involved not only in several aspects of physiological bone remodeling but also in pathological bone disorders, such as rheumatoid arthritis or osteoporosis. Understanding the role of inflammation and chemokines will provide new insights for the treatment of diseases affecting both skeletal and immune systems, by the development of new therapeutic strategies targeting common inflammatory mediators.

Protein biochip array of adhesion molecule expression in peripheral blood of patients with nasal polyposis.

Nasal polyposis is a chronic non-infectious inflammatory disease of the nasal and paranasal cavity mucosa of unknown multifactorial origin in which inflammatory cells, and in particular eosinophils, seem to play a pivotal role. Eosinophil migration from the bloodstream to nasal polyps is considered to be specific and is a complex process involving several different molecules such as ICAM-1, VCAM-1, and L-, P- and E-selectins. The aim of this study was to investigate, using a protein biochip array technology, the concentrations of these molecules in the peripheral blood of a group of patients affected by nasal polyposis. Patients exhibited a significantly higher expression of VCAM-1, E-selectin, and L-selectin compared to healthy controls, and Spearman's rank correlation test limited to the molecules with significant betweengroup differences demonstrated a significant correlation between VCAM-1 and E-selectin, VCAM-1 and L-selectin, and Eselectin and L-selectin. The results of this investigation are in line with those coming from various imunohistochemical analyses, and seem to confirm the role of inflammation in the pathogenesis of nasal polyposis. These molecules may also represent novel therapeutic targets in the treatment of nasal polyps, and may allow the selection of pharmacological prophylactics that would allow effective inhibition of the inflammation induced by a given allergen.