Articles de revues : « Long pentraxin PTX3 »

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Bonacina, Fabrizia, Andrea Baragetti, Alberico Luigi Catapano et Giuseppe Danilo Norata. « Long Pentraxin 3 : Experimental and Clinical Relevance in Cardiovascular Diseases ». Mediators of Inflammation 2013 (2013) : 1–10. http://dx.doi.org/10.1155/2013/725102.

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Pentraxin 3 (PTX3) is an essential component of the humoral arm of innate immunity and belongs, together with the C-reactive protein (CRP) and other acute phase proteins, to the pentraxins' superfamily: soluble, multifunctional, pattern recognition proteins. Pentraxins share a common C-terminal pentraxin domain, which in the case of PTX3 is coupled to an unrelated long N-terminal domain. PTX3 in humans, like CRP, correlates with surrogate markers of atherosclerosis and is independently associated with the risk of developing vascular events. Studies addressing the potential physiopathological role of CRP in the cardiovascular system were so far inconclusive and have been limited by the fact that the sequence and regulation have not been conserved during evolution between mouse and man. On the contrary, the conservation of sequence, gene organization, and regulation of PTX3 supports the translation of animal model findings in humans. While PTX3 deficiency is associated with increased inflammation, cardiac damage, and atherosclerosis, the overexpression limits carotid restenosis after angioplasty. These observations point to a cardiovascular protective effect of PTX3 potentially associated with the ability of tuning inflammation and favor the hypothesis that the increased levels of PTX3 in subjects with cardiovascular diseases may reflect a protective physiological mechanism, which correlates with the immunoinflammatory response observed in several cardiovascular disorders.

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Kunes, P., Z. Holubcova, M. Kolackova et J. Krejsek. « Pentraxin 3(PTX 3) : An Endogenous Modulator of the Inflammatory Response ». Mediators of Inflammation 2012 (2012) : 1–10. http://dx.doi.org/10.1155/2012/920517.

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Inflammatory or anti-inflammatory? That is the question as far as the acute-phase response and its mediators, the pentraxins, are concerned. Only some ten years ago, the classical or short pentraxin C-reactive protein and the newly discovered long pentraxin PTX3 were considered to exert most of the detrimental effects of acute inflammation, whether microbial or sterile in origin. However, accumulating evidence suggests an at least dichotomous, context-dependent outcome attributable to the pentraxins, if not a straightforward anti-inflammatory nature of the acute-phase response. This paper is focused on the inherent effects of pentraxin 3 in inflammatory responses, mainly in coronary artery disease and inAspergillus fumigatusinfection. Both are examples of inflammatory reactions in which PTX3 is substantially involved; the former sterile, the latter infectious in origin. Apart from different inducing noxae, similarities in the pathogenesis of the two are striking. All the same, the introductory question still persists: is the ultimate impact of PTX3 in these conditions inflammatory or anti-inflammatory, paradoxical as the latter might appear? We try to provide an answer such as it emerges in the light of recent findings.

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Rovere, Patrizia, Giuseppe Peri, Fausto Fazzini, Barbara Bottazzi, Andrea Doni, Attilio Bondanza, Valérie S. Zimmermann et al. « The long pentraxin PTX3 binds to apoptotic cells and regulates their clearance by antigen-presenting dendritic cells ». Blood 96, n^o 13 (15 décembre 2000) : 4300–4306. http://dx.doi.org/10.1182/blood.v96.13.4300.

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Abstract Pentraxins are acute-phase proteins produced in vivo during inflammatory reactions. Classical short pentraxins, C-reactive protein, and serum amyloid P component are generated in the liver in response to interleukin (IL)–6. The long pentraxin PTX3 is produced in tissues under the control of primary proinflammatory signals, such as lipopolysaccharide, IL-1β, and tumor necrosis factor-α, which also promote maturation of dendritic cells (DCs). Cell death commonly occurs during inflammatory reactions. In this study, it is shown that PTX3 specifically binds to dying cells. The binding was dose dependent and saturable. Recognition was restricted to extranuclear membrane domains and to a chronological window after UV irradiation or after CD95 cross-linking–induced or spontaneous cell death in vitro. PTX3 bound to necrotic cells to a lesser extent. Human DCs failed to internalize dying cells in the presence of PTX3, while they took up normally soluble or inert particulate substrates. These results suggest that PTX3 sequesters cell remnants from antigen-presenting cells, possibly contributing to preventing the onset of autoimmune reactions in inflamed tissues.

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Rovere, Patrizia, Giuseppe Peri, Fausto Fazzini, Barbara Bottazzi, Andrea Doni, Attilio Bondanza, Valérie S. Zimmermann et al. « The long pentraxin PTX3 binds to apoptotic cells and regulates their clearance by antigen-presenting dendritic cells ». Blood 96, n^o 13 (15 décembre 2000) : 4300–4306. http://dx.doi.org/10.1182/blood.v96.13.4300.h8004300_4300_4306.

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Pentraxins are acute-phase proteins produced in vivo during inflammatory reactions. Classical short pentraxins, C-reactive protein, and serum amyloid P component are generated in the liver in response to interleukin (IL)–6. The long pentraxin PTX3 is produced in tissues under the control of primary proinflammatory signals, such as lipopolysaccharide, IL-1β, and tumor necrosis factor-α, which also promote maturation of dendritic cells (DCs). Cell death commonly occurs during inflammatory reactions. In this study, it is shown that PTX3 specifically binds to dying cells. The binding was dose dependent and saturable. Recognition was restricted to extranuclear membrane domains and to a chronological window after UV irradiation or after CD95 cross-linking–induced or spontaneous cell death in vitro. PTX3 bound to necrotic cells to a lesser extent. Human DCs failed to internalize dying cells in the presence of PTX3, while they took up normally soluble or inert particulate substrates. These results suggest that PTX3 sequesters cell remnants from antigen-presenting cells, possibly contributing to preventing the onset of autoimmune reactions in inflamed tissues.

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Rusnati, Marco, Maura Camozzi, Emanuela Moroni, Barbara Bottazzi, Giuseppe Peri, Stefano Indraccolo, Alberto Amadori, Alberto Mantovani et Marco Presta. « Selective recognition of fibroblast growth factor-2 by the long pentraxin PTX3 inhibits angiogenesis ». Blood 104, n^o 1 (1 juillet 2004) : 92–99. http://dx.doi.org/10.1182/blood-2003-10-3433.

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Abstract The long pentraxin PTX3 is a soluble pattern recognition receptor produced by monocytes and endothelial cells that plays a nonredundant role in inflammation. Several pathologic conditions are characterized by local production of both PTX3 and the angiogenic fibroblast growth factor-2 (FGF2). Here, solid-phase binding assays demonstrated that PTX3 binds with high affinity to FGF2 but not to a panel of cytokines and growth factors, including FGF1, FGF4, and FGF8. Accordingly, PTX3 prevented 125I-FGF2 binding to endothelial cell receptors, leading to specific inhibition of FGF2-induced proliferation. PTX3 hampered also the motogenic activity exerted by endogenous FGF2 on a wounded endothelial cell monolayer. Moreover, PTX3 cDNA transduction in FGF2-transformed endothelial cells inhibited their autocrine FGF2-dependent proliferation and morphogenesis in vitro and their capacity to generate vascular lesions when injected in nude mice. Finally, PTX3 suppressed neovascularization triggered by FGF2 in the chick embryo chorioallantoic membrane with no effect on physiologic angiogenesis. In contrast, the short pentraxin C-reactive protein was a poor FGF2 ligand/antagonist. These results establish the selective binding of a member of the pentraxin superfamily to a growth factor. PTX3/FGF2 interaction may modulate angiogenesis in various physiopathologic conditions driven by inflammation, innate immunity, and/or neoplastic transformation.

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He, Xiaolin, Bing Han et Mingyao Liu. « Long pentraxin 3 in pulmonary infection and acute lung injury ». American Journal of Physiology-Lung Cellular and Molecular Physiology 292, n^o 5 (mai 2007) : L1039—L1049. http://dx.doi.org/10.1152/ajplung.00490.2006.

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Long pentraxin 3 (PTX3) is a newly discovered acute phase protein produced at the sites of infection and inflammation by tissue cells, macrophages, monocytes, and dendritic cells. PTX3 plays an important role in preventing infection of certain fungi, bacteria, and viruses in the lung. Recombinant PTX3 has been proposed as a potential antifungal molecule for therapy. However, under certain experimental conditions, such as intestinal ischemia-reperfusion, high volume mechanical ventilation, or severe bacterial infection, increased expression of PTX3 is associated with more severe lung injury. Therefore, it is necessary to further explore the sources of PTX3 in the lung and the regulatory mechanisms of its expression. It is also essential to further determine how PTX3 binds to pathogens, complement, and apoptotic cells, and to determine whether PTX3 has a specific receptor in targeted cells. These studies will provide insight into the pathological processes of pulmonary infection and acute lung injury and provide potential novel therapeutic strategies to control pulmonary infections without severe lung injury.

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Szymkowiak, Martyna, Piotr Surmiak et Małgorzata Baumert. « Pentraxin 3 – possible uses in neonatology and paediatrics ». Pediatria i Medycyna Rodzinna 16, n^o 3 (30 octobre 2020) : 247–50. http://dx.doi.org/10.15557/pimr.2020.0045.

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Pentraxin 3 (PTX3) is a multifunctional acute phase protein belonging to the family of long pentraxins, which is synthesised in numerous cells of the body under the influence of proinflammatory factors and locally at the site of inflammation. Under physiological conditions, PTX3 is stored in neutrophil granules, where there is a constant pool of glycoproteins. Increased pentraxin 3 levels in blood serum are observed as early as 1 hour after a damaging stimulus. Elevation of PTX3 serum levels can be used to diagnose fertility disorders in women as well as in pregnancy pathology, women at risk of pre-eclampsia, gestational diabetes, premature rupture of membrane and preterm delivery. The biological function of PTX3 is not fully understood, especially in the population of newborns and children. So far, no reference values for PTX3 levels in newborns and children have been developed. This protein can be used as a marker of pulmonary hypertension in newborns as well as to assess the degree of respiratory failure in premature infants. In older children, it is useful in the assessment of the severity of meningococcal disease and sepsis as well as in the treatment of childhood asthma. There are studies available in which blood levels of PTX3 significantly correlate with the severity of kidney damage in Henoch–Schönlein macular degeneration in children, and the evaluation of this protein in urine is used to detect renal parenchymal destruction after pyelonephritis.

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Moalli, Federica, Sebastien Jaillon, Antonio Inforzato, Marina Sironi, Barbara Bottazzi, Alberto Mantovani et Cecilia Garlanda. « Pathogen Recognition by the Long Pentraxin PTX3 ». Journal of Biomedicine and Biotechnology 2011 (2011) : 1–15. http://dx.doi.org/10.1155/2011/830421.

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Innate immunity represents the first line of defence against pathogens and plays key roles in activation and orientation of the adaptive immune response. The innate immune system comprises both a cellular and a humoral arm. Components of the humoral arm include soluble pattern recognition molecules (PRMs) that recognise pathogen-associated molecular patterns (PAMPs) and initiate the immune response in coordination with the cellular arm, therefore acting as functional ancestors of antibodies. The long pentraxin PTX3 is a prototypic soluble PRM that is produced at sites of infection and inflammation by both somatic and immune cells. Gene targeting of this evolutionarily conserved protein has revealed a nonredundant role in resistance to selected pathogens. Moreover, PTX3 exerts important functions at the cross-road between innate immunity, inflammation, and female fertility. Here, we review the studies on PTX3, with emphasis on pathogen recognition and cross-talk with other components of the innate immune system.

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Matarazzo, Sara, Laura Melocchi, Sara Rezzola, Elisabetta Grillo, Federica Maccarinelli, Arianna Giacomini, Marta Turati et al. « Long Pentraxin-3 Follows and Modulates Bladder Cancer Progression ». Cancers 11, n^o 9 (30 août 2019) : 1277. http://dx.doi.org/10.3390/cancers11091277.

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Bladder tumors are a diffuse type of cancer. Long pentraxin-3 (PTX3) is a component of the innate immunity with pleiotropic functions in the regulation of immune response, tissue remodeling, and cancer progression. PTX3 may act as an oncosuppressor in different contexts, functioning as an antagonist of the fibroblast growth factor/fibroblast growth factor receptor (FGF/FGFR) system, rewiring the immune microenvironment, or acting through mechanisms not yet fully clarified. In this study we used biopsies and data mining to assess that PTX3 is differentially expressed during the different stages of bladder cancer (BC) progression. BC cell lines, representative of different tumor grades, and transgenic/carcinogen-induced models were used to demonstrate in vitro and in vivo that PTX3 production by tumor cells decreases along the progression from low-grade to high-grade advanced muscle invasive forms (MIBC). In vitro and in vivo data revealed for the first time that PTX3 modulation and the consequent impairment of FGF/FGR systems in BC cells have a significant impact on different biological features of BC growth, including cell proliferation, motility, metabolism, stemness, and drug resistance. PTX3 exerts an oncosuppressive effect on BC progression and may represent a potential functional biomarker in BC evolution. Moreover, FGF/FGFR blockade has an impact on drug resistance and stemness features in BC.

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Mantovani, Alberto, Cecilia Garlanda, Barbara Bottazzi, Giuseppe Peri, Andrea Doni, Yeny Martinez de la Torre et Roberto Latini. « The long pentraxin PTX3 in vascular pathology ». Vascular Pharmacology 45, n^o 5 (novembre 2006) : 326–30. http://dx.doi.org/10.1016/j.vph.2006.08.011.

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Pilling, Darrell, Nehemiah Cox, Varsha Vakil, J. Sjef Verbeek et Richard H. Gomer. « The Long Pentraxin PTX3 Promotes Fibrocyte Differentiation ». PLOS ONE 10, n^o 3 (16 mars 2015) : e0119709. http://dx.doi.org/10.1371/journal.pone.0119709.

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Sasaki, Mitsuhito, Shunsuke Kondo, Hiroko Hosoi, Futa Koga, Yasunari Sakamoto, Chigusa Morizane, Hideki Ueno et Takuji Okusaka. « A pooled analysis of long pentraxin for patients with advanced pancreatic cancer. » Journal of Clinical Oncology 34, n^o 4_suppl (1 février 2016) : 251. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.251.

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251 Background: Pancreatic carcinoma is one of the most lethal cancers and is the fourth leading cause of cancer-related death in Japan. Inflammatory responses play decisive roles at different stages of tumor development, including initiation, promotion, malignant conversion, invasion, and metastasis, affecting immune surveillance and response to therapy. We previously reported that pentraxin family members, especially long pentraxin (PTX3), are promising biomarkers for the prognosis of pancreatic carcinoma patients. The objective of the present study was to determine whether PTX3 levels could be a prognostic factor for patients with unresectable or recurrent pancreatic carcinoma. Methods: We analyzed data from two clinical trials (UMIN000002323 and UMIN000009474) using the Kaplan-Meier method and Cox proportional hazards model. We included data from patients who were chemo-naïve pancreatic invasive ductal carcinoma patients, had a 0–2 performance status score, and had adequate organ function. PTX3 levels and other laboratory and clinical data were assessed before initial treatment. Results: Overall, 181 patients with unresectable or recurrent pancreatic carcinoma were evaluated for the baseline plasma PTX3 level (median, mean, and range PTX3: 3.54 ng/mL, 4.34 ng/mL, and 0.9–17.7 ng/mL, respectively). In this study population, the median overall survival was 327 days (95% confidence interval, 281–372 days). The median overall survival was significantly shorter at high PTX3 levels( > 4.34ng/mL) than at low PTX3 levels ( < 4.34ng/mL)(223days vs 409 days; log rank test, P < 0.0001). In a multivariate analysis, the PTX3, C-reaction protein (CRP), and cancer antigen (CA) 19-9 levels, and performance status were independent predictors of survival. High PTX3 levels were associated with high CA19-9 and high CRP levels. Conclusions: We confirmed that a high PTX3 level may be a useful prognostic marker for advanced pancreatic carcinoma. However, the mechanism of tumor inflammation and the exact nature of the role of PTX3 expression remain unclear, calling for investigation of the mechanisms underlying PTX3 activity in carcinoma cells and in the tumor environment. Clinical trial information: UMIN000002323 and UMIN000009474.

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Liu, Haibo, Xiaofang Guo, Kang Yao, Chunming Wang, Guozhong Chen, Wei Gao, Jie Yuan, Wangjun Yu et Junbo Ge. « Pentraxin-3 Predicts Long-Term Cardiac Events in Patients with Chronic Heart Failure ». BioMed Research International 2015 (2015) : 1–7. http://dx.doi.org/10.1155/2015/817615.

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The aim of this study was to investigate the long-term prognostic value of pentraxin-3 (PTX3) in patients with chronic heart failure (CHF). 377 patients were prospectively followed up for 3 years to determine cardiac events including cardiac death or rehospitalization for worsening heart failure. The plasma PTX3 levels were significantly higher in CHF patients than in healthy subjects (p<0.001), and they increased with advancing New York Heart Association (NYHA) Functional Classification (p<0.001). Plasma PTX3 levels in CHF patients with cardiac events were significantly higher than in event-free patients (p<0.001). We determined the normal upper limit of plasma PTX3 levels from the mean + 2 SD value of 64 control subjects (3.64 ng/mL). A Kaplan-Meier analysis revealed that patients with increased PTX3 (≥3.64 ng/mL) were at a higher risk for cardiac events than those without increased PTX3 (p<0.01). A multifactorial Cox proportional hazards model showed that increased PTX3 (≥3.64 ngImL) was an independent risk factor for cardiac events in CHF patients (hazard ratio (HR) = 4.224,p<0.01; 95% CI: 1.130–15.783). Plasma PTX3 levels are a long-term independent predictor of prognosis in patients with CHF.

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Guerra, Jessica, Paola Chiodelli, Chiara Tobia, Claudia Gerri et Marco Presta. « Long-Pentraxin 3 Affects Primary Cilium in Zebrafish Embryo and Cancer Cells via the FGF System ». Cancers 12, n^o 7 (1 juillet 2020) : 1756. http://dx.doi.org/10.3390/cancers12071756.

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Primary cilium drives the left-right asymmetry process during embryonic development. Moreover, its dysregulation contributes to cancer progression by affecting various signaling pathways. The fibroblast growth factor (FGF)/FGF receptor (FGFR) system modulates primary cilium length and plays a pivotal role in embryogenesis and tumor growth. Here, we investigated the impact of the natural FGF trap long-pentraxin 3 (PTX3) on the determination of primary cilium extension in zebrafish embryo and cancer cells. The results demonstrate that down modulation of the PTX3 orthologue ptx3b causes the shortening of primary cilium in zebrafish embryo in a FGF-dependent manner, leading to defects in the left-right asymmetry determination. Conversely, PTX3 upregulation causes the elongation of primary cilium in FGF-dependent cancer cells. Previous observations have identified the PTX3-derived small molecule NSC12 as an orally available FGF trap with anticancer effects on FGF-dependent tumors. In keeping with the non-redundant role of the FGF/FGR system in primary cilium length determination, NSC12 induces the elongation of primary cilium in FGF-dependent tumor cells, thus acting as a ciliogenic anticancer molecule in vitro and in vivo. Together, these findings demonstrate the ability of the natural FGF trap PTX3 to exert a modulatory effect on primary cilium in embryonic development and cancer. Moreover, they set the basis for the design of novel ciliogenic drugs with potential implications for the therapy of FGF-dependent tumors.

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Paffoni, Alessio, Guido Ragni, Andrea Doni, Edgardo Somigliana, Fabio Pasqualini, Liliana Restelli, Giorgio Pardi, Alberto Mantovani et Cecilia Garlanda. « Follicular Fuid Levels of the Long Pentraxin PTX3 ». Journal of the Society for Gynecologic Investigation 13, n^o 3 (avril 2006) : 226–31. http://dx.doi.org/10.1016/j.jsgi.2005.12.008.

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Jaillon, Sébastien, Giuseppe Peri, Yves Delneste, Isabelle Frémaux, Andrea Doni, Federica Moalli, Cecilia Garlanda et al. « The humoral pattern recognition receptor PTX3 is stored in neutrophil granules and localizes in extracellular traps ». Journal of Experimental Medicine 204, n^o 4 (26 mars 2007) : 793–804. http://dx.doi.org/10.1084/jem.20061301.

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The long pentraxin (PTX) 3 is produced by macrophages and myeloid dendritic cells in response to Toll-like receptor agonists and represents a nonredundant component of humoral innate immunity against selected pathogens. We report that, unexpectedly, PTX3 is stored in specific granules and undergoes release in response to microbial recognition and inflammatory signals. Released PTX3 can partially localize in neutrophil extracellular traps formed by extruded DNA. Eosinophils and basophils do not contain preformed PTX3. PTX3-deficient neutrophils have defective microbial recognition and phagocytosis, and PTX3 is nonredundant for neutrophil-mediated resistance against Aspergillus fumigatus. Thus, neutrophils serve as a reservoir, ready for rapid release, of the long PTX3, a key component of humoral innate immunity with opsonic activity.

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Zeybek, S., E. Tepeli, GO Cetin, V. Caner, H. Senol, B. Yildirim et G. Bagci. « Increased expression of pentraxin 3 in placental tissues from patients with unexplained recurrent pregnancy loss ». Balkan Journal of Medical Genetics 22, n^o 1 (28 août 2019) : 21–28. http://dx.doi.org/10.2478/bjmg-2019-0002.

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AbstractPentraxin 3 (PTX3), a prototypical member of the long pentraxin subfamily, is a evolutionarily conserved multimeric pattern recognition receptor involved in the humoral component of the innate immune system. Pentraxin 3 is released when tissue is stressed or damaged, and interacts with many different ligands. Pentraxin 3 exerts a pivotal role both as a regulator and as an indicator of inflammatory response in the pathogenesis of many diseases such as sepsis, vasculitis and preeclampsia. Uncontrolled inflammatory response is considered a major cause of unexplained recurrent pregnancy loss (URPL). We determined the PTX3 messenger ribonucleic acid (mRNA) and protein expression levels in placentai tissues from 50 women with URPL, and made comparison with those in 50 age-matched control subjects. In quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry analyses, PTX3 mRNA and protein levels, respectively, were significantly increased in URPL patients compared with their respective controls (p = 0.0001). Although no significant correlations were identified between PTX3 expression levels and clinical parameters such as maternal age, numbers of previous pregnancy losses, and gestational age at miscarriage, PTX3 mRNA expression was significantly higher in patients with no live births than in women with previous live births (p = 0.0001). Our study suggests that tissue-specific expression of PTX3 is associated with URPL. Further larger studies are required to determine whether PTX3 expression can be used as a biomarker to manage URPL in routine clinical practice.

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Baumert, Małgorzata, Piotr Surmiak, Martyna Szymkowiak et Agnieszka Janosz. « The Assessment of Pentraxin 3 : A Novel Biomarker in Early Detection of Infection in Newborns ». BioMed Research International 2021 (30 juin 2021) : 1–8. http://dx.doi.org/10.1155/2021/6638622.

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Introduction. As the clinical manifestation of neonatal infection is nonspecific and characterised by varied clinical features, it is highly problematic to establish an early diagnosis. Recently, hopes have been raised by the new acute-phase protein—pentraxin 3 (PTX3). PTX3 belongs to the family of long pentraxins, which is synthesized in numerous cells like endothelial cells, macrophages, and monocytes infiltrating sites of inflammation. Material and Methods. In our research, we have enrolled 29 newborns with infection as the study group and 47 healthy ones as the control group, as well as their mothers. The C-reactive protein (CRP), procalcitonin (PCT), and PTX3 levels were determined in venous blood samples from all investigated neonates and their mothers. Moreover, PTX3 concentrations were assessed in the umbilical cord. Results. There were statistically significant differences in PTX3 levels between healthy and sick newborns both in the umbilical cord ( p = 0.02 ) and venous blood ( p = 0.01 ). The highest PTX3 concentrations were observed in children with infection in the presence of premature rupture of membranes (PROM). PTX3 concentrations in this group were significantly higher compared to those in healthy children without PROM. We observed elevated PCT levels in newborns with infection. No differences in CRP levels in 12 hours of life were noticed between the investigated groups. A comparison of ROC curves for PTX3 and PCT concentrations revealed similar sensitivity and specificity in the prediction of infection in neonates. Conclusions. Serum PTX3 is an important and specific biomarker of early infection. It is already elevated in the umbilical cord, so measuring PTX3 concentration might be useful in the early prediction of infection in newborns.

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Ronca, Roberto, Sara Taranto, Michela Corsini, Chiara Tobia, Cosetta Ravelli, Sara Rezzola, Mirella Belleri et al. « Pentraxin 3 Inhibits the Angiogenic Potential of Multiple Myeloma Cells ». Cancers 13, n^o 9 (8 mai 2021) : 2255. http://dx.doi.org/10.3390/cancers13092255.

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During multiple myeloma (MM) progression the activation of the angiogenic process represents a key step for the formation of the vascular niche, where different stromal components and neoplastic cells collaborate and foster tumor growth. Among the different pro-angiogenic players, Fibroblast Growth Factor 2 (FGF2) plays a pivotal role in BM vascularization occurring during MM progression. Long Pentraxin 3 (PTX3), a natural FGF antagonist, is able to reduce the activation of stromal components promoted by FGF2 in various in vitro models. An increased FGF/PTX3 ratio has also been found to occur during MM evolution, suggesting that restoring the “physiological” FGF/PTX3 ratio in plasma cells and BM stromal cells (BMSCs) might impact MM. In this work, taking advantage of PTX3-inducible human MM models, we show that PTX3 produced by tumor cells is able to restore a balanced FGF/PTX3 ratio sufficient to prevent the activation of the FGF/FGFR system in endothelial cells and to reduce the angiogenic capacity of MM cells in different in vivo models. As a result of this anti-angiogenic activity, PTX3 overexpression causes a significant reduction of the tumor burden in both subcutaneously grafted and systemic MM models. These data pave the way for the exploitation of PTX3-derived anti-angiogenic approaches in MM.

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Cappuzzello, Claudia, Andrea Doni, Erica Dander, Fabio Pasqualini, Manuela Nebuloni, Barbara Bottazzi, Alberto Mantovani, Andrea Biondi, Cecilia Garlanda et Giovanna D'Amico. « Role Of Long Pentraxin 3 (PTX3) In Wound Closure Induced By Bone Marrow-Derived Mesenchymal Stromal Cells ». Blood 122, n^o 21 (15 novembre 2013) : 1220. http://dx.doi.org/10.1182/blood.v122.21.1220.1220.

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Abstract Although several studies have shown the capacity of mesenchymal stromal cells (MSCs) to repair and regenerate different tissues, the mechanisms underlying these processes are not understood. Long Pentraxin 3 (PTX3) is a multifunctional protein produced by MSCs and other cell subsets upon activation with inflammatory cytokines. PTX3 is involved in innate immunity, inflammation and extracellular matrix deposition. In the present study we analyzed the potential role of PTX3 in wound repair process induced by MSCs. PTX3 knockout MSCs (PTX3-/-MSCs) were collected from bone marrow of PTX3-/- mice. After 3-5 culture passages the expression of surface markers was analyzed by flow cytometry and their osteogenic and adipogenic differentiation capacity was detected by alizarin red O and oil red S staining, respectively. The ability of PTX3-/-MSCs to abrogate T cell proliferation was evaluated by co-culturing MSCs and PBMCs previously activated with Phytohaemagglutinin. Finally, equal number of both PTX3-/-MSCs and wild type (WT) MSCs were implanted into excisional wounds created by a biopsy punch on the back of allogenic WT and PTX3-/- mice. Wound area was measured up to 14 day and calculated using an image analysis program. The wound specimens were collected at 2, 7 and 14 days and processed for histological analysis. We demonstrated that PTX3-/-MSCs, similarly to WT MSCs, displayed typical fibroblastoid morphology, they expressed common MSC markers and were able to differentiate into adipocytes and osteoblasts. In addition, they drastically decreased the mitogen-induced proliferation of lymphocyte. Importantly, in a mouse model of wound healing, PTX3-/- MSCs showed a highly significant defect in wound closure compared to WT MSCs at each time point. Histological evaluation of skin samples treated with PTX3-/- MSCs showed a reduction of the granulation tissue and a significant increase of neutrophils (GR-1+) in the wound bed. Moreover, wounds treated with PTX3-/- MSCs were characterized by an excessive accumulation of fibrin at the 2nd day after injury. Accordingly, PTX3-/- MSCs showed a defective ability to degrade the fibrin matrix in vitro. Finally, PTX3-/- MSCs failed to close the ulcers in PTX3-/- mice. In conclusion, we demonstrated that PTX3 deficiency does not alter the phenotype and the capacity of MSCs to differentiate into mesengetic lineages; however, the production of PTX3 represents an essential requirement for MSC ability of enhancing tissue repair. Disclosures: No relevant conflicts of interest to declare.

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Gruszka, Wojciech, Katarzyna Wyskida, Jerzy Chudek et Magdalena Olszanecka-Glinianowicz. « Pentraxin 3 – a potential link between inflammation, obesity and cardiovascular complications in polycystic ovary syndrome ». Postępy Higieny i Medycyny Doświadczalnej 72 (18 juillet 2018) : 634–41. http://dx.doi.org/10.5604/01.3001.0012.2025.

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Polycystic ovary syndrome (PCOS) is the most frequently diagnosed endocrine disorder among women in reproductive age. Metabolic disturbances in PCOS include among others increased incidence of insulin resistance and hyperinsulinemia, type 2 diabetes, dyslipidemia, pre-thrombotic state, hypertension, sleep apnea, atherosclerosis and cardiovascular diseases. Adipose tissue disturbances, including inflammation, were shown to play an important role in the development of both endocrine and metabolic disturbances, accelerating the progression of arteriosclerosis, which leads to premature cardiovascular disease development in PCOS. Pentraxin 3 (PTX3) seems to be one of the factors linking obesity and cardiovascular complications observed in PCOS. PTX3 belongs to a family of long pentraxin proteins. It primarily plays a role in acute immunological response; however, some data suggests that it may also be involved in oocyte maturation. In contrast to the short pentraxin, C-reactive protein, which is primarily produced in the liver, PTX3 is produced locally in the site of the inflammation by several types of cells, for example, adipose tissue during development of inflammation. Increased PTX3 expression was found in visceral fat tissue in obese subjects, and was shown to be under TNF-α control. PTX3 expression has not been tested in PCOS women, yet. Up to now there are only 5 studies investigating PTX3 in PCOS. Only in one study PTX3 level in PCOS women was increased compared to the control groups, in two other studies – decreased, and in two – similar. Also, the association between PTX3, PCOS and obesity remains uncertain. Further research, including ones with a greater number of subjects, especially obese and older women, are necessary to assess the role of PTX3 as a potential link between the inflammation, obesity and polycystic ovary syndrome.

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Mantovani, Alberto, Cecilia Garlanda, Andrea Doni et Barbara Bottazzi. « Pentraxins in Innate Immunity : From C-Reactive Protein to the Long Pentraxin PTX3 ». Journal of Clinical Immunology 28, n^o 1 (9 septembre 2007) : 1–13. http://dx.doi.org/10.1007/s10875-007-9126-7.

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Balhara, Jyoti, Lianyu Shan et Abdelilah Soussi Gounni. « PTX3 modulates airway hyperresponsiveness and immune response to OVA in a murine model of asthma (P6011) ». Journal of Immunology 190, n^o 1_Supplement (1 mai 2013) : 120.6. http://dx.doi.org/10.4049/jimmunol.190.supp.120.6.

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Abstract Pentraxin-3 (PTX3) is a member of the long pentraxins family. It activates the innate and adaptive immune systems, playing an important role in providing immunity against various pulmonary infections. Considering its role in fostering lung immunity, we examined the role of PTX3 in asthma. We have recently demonstrated an enhanced expression of PTX3 in bronchial biopsies of allergic asthmatics that correlated with the disease severity. In this report, we assessed the effect of PTX3 deficiency in a murine model of OVA-induced asthma. Sensitized PTX3 Knockout (KO) mice exhibited an enhanced airway and tissue resistance in response to methacholine (MCh) in contrast to their WT counterparts. We observed an increase in the infiltration of inflammatory cells in BALF obtained from PTX3 KO mice upon OVA sensitization/challenge as compared to their WT littermates. However peribronchial and perivascular inflammation and goblet cells hyperplasia showed no significant difference in both mouse strains. Further we found an enhanced induction of IL-4, IFN-gamma, IL-17 and IL-10 production in the lungs of PTX3 KO mice as compared to WT mice upon OVA challenge. In lymph node, IL-17A recall response was found to be greater in PTX3 KO mice than WT mice but no difference was observed in term of IL-4, IFN-gamma and IL-10 production. Taken together, we conclude that lack of PTX3 predisposes mice to airway hyperresponsiveness and an enhanced inflammation.

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Liu, Siguan, Xin Qu, Feng Liu et Chunting Wang. « Pentraxin 3 as a Prognostic Biomarker in Patients with Systemic Inflammation or Infection ». Mediators of Inflammation 2014 (2014) : 1–9. http://dx.doi.org/10.1155/2014/421429.

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Purpose. The long pentraxin 3 (PTX3) is a key component of the humoral arm of the innate immune system. PTX3 is produced locally in response to proinflammatory stimuli. We reviewed the usefulness of systemic levels of PTX3 in critically ill patients with systemic inflammatory response syndrome (SIRS), sepsis, and bacteremia, focusing on its diagnostic and prognostic value.Methods. A PubMed search on PTX3 was conducted. The list of papers was narrowed to original studies of critically ill patients. Eleven papers on original studies of critically ill patients that report on PTX3 in SIRS, sepsis, or bacteremia were identified.Results. Systematic levels of PTX3 have little diagnostic value in critically ill patients with SIRS, sepsis, or bacteremia. Systemic levels of PTX3, however, have superior prognostic power over other commonly used biological markers in these patients. Systemic levels of PTX3 correlate positively with markers of organ dysfunction and severity-of-disease classification system scores. Finally, systemic levels of PTX3 remain elevated in the acute phase and decreased on recovery. Notably, the age of the patients and underlying disease affect systemic levels of PTX3.Conclusions. The diagnostic value of PTX3 is low in patients with sepsis. Systemic levels of PTX3 have prognostic value and may add to prognostication of patients with SIRS or sepsis, complementing severity-of-disease classification systems and other biological markers.

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Meron-Sudai, Shiri, Arava Reizis, Sophy Goren, Anya Bialik, Amit Hochberg et Dani Cohen. « Pentraxin 3 and Shigella LPS and IpaB Antibodies Interplay to Defeat Shigellosis ». Journal of Clinical Medicine 11, n^o 15 (28 juillet 2022) : 4384. http://dx.doi.org/10.3390/jcm11154384.

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Shigella causes moderate to severe diarrhea or dysentery after invading the colon mucosa. Long Pentraxin 3 (PTX3) is recognized as the humoral component of the innate immune response to bacterial pathogens. We examined the interplay between levels of PTX3 and levels of anti-Shigella lipopolysaccharide (LPS) and anti-Shigella type 3 secretion system protein-IpaB antibodies in children during acute shigellosis and after recovery. PTX3 concentrations in serum and stool extracts were determined by sandwich ELISA using commercial anti-PTX3 antibodies. Serum IgG, IgM, and IgA anti-S. sonnei LPS or anti-S. sonnei IpaB were measured using in house ELISA. Children with acute shigellosis (n = 60) had elevated PTX3 levels in serum and stools as compared with recovered subjects (9.6 ng/mL versus 4.7 ng/mL, p < 0.009 in serum and 16.3 ng/g versus 1.1 ng/g in stool, p = 0.011). Very low levels of PTX3 were detected in stools of healthy children (0.3 ng/g). Increased serum levels of PTX3 correlated with high fever accompanied by bloody or numerous diarrheal stools characteristic of more severe shigellosis while short pentraxin; C-Reactive Protein (CRP) did not show such a correlation. PTX3 decreased in convalescence while anti-Shigella antibodies increased, switching the response from innate to adaptive toward the eradication of the invasive organism. These data can inform the development of Shigella vaccines and treatment options.

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Bonacina, Fabrizia, Annalisa Moregola, Rémi Porte, Andrea Baragetti, Eduardo Bonavita, Alice Salatin, Liliana Grigore et al. « Pentraxin 3 deficiency protects from the metabolic inflammation associated to diet-induced obesity ». Cardiovascular Research 115, n^o 13 (12 mars 2019) : 1861–72. http://dx.doi.org/10.1093/cvr/cvz068.

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Abstract Aims Low-grade chronic inflammation characterizes obesity and metabolic syndrome. Here, we aim at investigating the impact of the acute-phase protein long pentraxin 3 (PTX3) on the immune-inflammatory response occurring during diet-induced obesity. Methods and results PTX3 deficiency in mice fed a high-fat diet for 20 weeks protects from weight gain and adipose tissue deposition in visceral and subcutaneous depots. This effect is not related to changes in glucose homeostasis and lipid metabolism but is associated with an improved immune cell phenotype in the adipose tissue of Ptx3 deficient animals, which is characterized by M2-macrophages polarization and increased angiogenesis. These findings are recapitulated in humans where carriers of a PTX3 haplotype (PTX3 h2/h2 haplotype), resulting in lower PTX3 plasma levels, presented with a reduced prevalence of obesity and decreased abdominal adiposity compared with non-carriers. Conclusion Our results support a critical role for PTX3 in the onset of obesity by promoting inflammation and limiting adipose tissue vascularization and delineate PTX3 targeting as a valuable strategy for the treatment of adipose tissue-associated inflammatory response.

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Lerzo, Franco, Giuseppe Peri, Andrea Doni, Paola Bocca, Fabio Morandi, Angela Pistorio, Anna Maria Carleo, Alberto Mantovani, Vito Pistoia et Ignazia Prigione. « Dexamethasone Prophylaxis in Pediatric Open Heart Surgery Is Associated with Increased Blood Long Pentraxin PTX3 : Potential Clinical Implications ». Clinical and Developmental Immunology 2011 (2011) : 1–6. http://dx.doi.org/10.1155/2011/730828.

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Glucocorticoid administration before cardiopulmonary bypass (CPB) can reduce the systemic inflammatory response and improve clinical outcome. Long pentraxin PTX3 is a novel inflammatory parameter that could play a protective cardiovascular role by regulating inflammation. Twenty-nine children undergoing open heart surgery were enrolled in the study. Fourteen received dexamethasone (1st dose 1.5 mg/Kg i.v. or i.m. the evening before surgery; 2nd dose 1.5 mg/kg i.v. before starting bypass) and fifteen children served as control. Blood PTX3, short pentraxin C-reactive protein (CRP), interleukin-1 receptor II (IL-1RII), fibrinogen and partial thromboplastin time (PTT) were assayed at different times. PTX3 levels significantly increased during CPB in dexamethasone-treated (+D) and dexamethasone-untreated (−D) subjects, but were significantly higher in +D than −D patients. CRP levels significantly increased both in +D and −D patients in the postoperative days, with values significantly higher in −D than +D patients. Fibrinogen and PTT values were significantly higher in −D than +D patients in the 1st postoperative day. IL-1RII plasma levels increased in the postoperative period in both groups. Dexamethasone prophylaxis in pediatric patients undergoing CPB for cardiac surgery is associated with a significant increase of blood PTX3 that could contribute to decreasing inflammatory parameters and improving patient clinical outcome.

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Brügger-Andersen, Trygve, Volker Pönitz, Harry Staines, Heidi Grundt, Mina Sagara, Dennis W. T. Nilsen et Frederic Kontny. « The long pentraxin 3 (PTX3) : a novel prognostic inflammatory marker for mortality in acute chest pain ». Thrombosis and Haemostasis 102, n^o 09 (2009) : 555–63. http://dx.doi.org/10.1160/th09-02-0137.

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SummaryThe long pentraxin 3 (PTX3) is a recently identified member of the pentraxin protein family that includes C-reactive protein. PTX3 is produced by the major cell types involved in atherosclerotic lesions in response to inflammatory stimuli, and elevated plasma levels are found in several conditions including acute coronary syndromes (ACS). The aim of this study was to assess the value of PTX3 as a prognostic marker of mortality and recurrent ischaemic events in a consecutive series of patients admitted with acute chest pain and potential ACS.The patients received follow-up for 24 months. Blood samples were taken on admission for measurement of PTX3, high sensitive C-reactive protein (hsCRP), B-type natriuretic peptide (BNP), and troponin T. All-cause mortality at 24 months in the study cohort was 15.2%. Patients in the upper PTX3 quartiles had a significantly higher death risk than those in the lowest quartile (Q3: hazard ratio [HR] 2.36; 95% CI 1.12–4.99; p=0.024, and Q4: HR 3.60; 95% CI 1.68–7.72; p=0.001). Elevated BNP levels were also significantly associated with a fatal outcome (Q3: HR 3.05; 95% CI 1.16–7.99; p=0.024; and Q4: HR 3.90; 95% CI 1.48–10.26; p=0.006). Elevation in hsCRP was not associated with increased death risk. As PTX3 predicted mortality independently of BNP, the combination of these two biomarkers showed an incremental prognostic value.PTX3 is a new biomarker related to inflammation that, independently of BNP, strongly predicts long-term all-cause mortality in patients with acute chest pain. The combination of these two biomarkers enhances the prognostic value over either marker alone.

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Nauta, Alma J., Simone De Haij, Barbara Bottazzi, Alberto Mantovani, Maria C. Borrias, J. A. N. Aten, Maria P. I. A. Rastaldi, Mohamed R. Daha, Cees Van Kooten et Anja Roos. « Human renal epithelial cells produce the long pentraxin PTX3 ». Kidney International 67, n^o 2 (février 2005) : 543–53. http://dx.doi.org/10.1111/j.1523-1755.2005.67111.x.

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Deban, Livija, Remo Castro Russo, Marina Sironi, Federica Moalli, Margherita Scanziani, Vanessa Zambelli, Ivan Cuccovillo et al. « Regulation of leukocyte recruitment by the long pentraxin PTX3 ». Nature Immunology 11, n^o 4 (7 mars 2010) : 328–34. http://dx.doi.org/10.1038/ni.1854.

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Gupta, Gaurav, Ping Jia, Rohit Sharma, Romaniya Zayats, Lianyu Shan, Zhirong Mou, Thomas Murooka, Abdelilah Soussi-Gounni, Camila I. de Oliveira et Jude E. Uzonna. « Long Pentraxin 3 (PTX3) Regulates IL-17A Mediated Immunity to Primary and Secondary Leishmania major Infection ». Journal of Immunology 202, n^o 1_Supplement (1 mai 2019) : 190.21. http://dx.doi.org/10.4049/jimmunol.202.supp.190.21.

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Abstract Resolution of cutaneous leishmaniasis (CL), caused by the protozoan parasite Leishmania (L) major, relies on the nature of the host immune response. The long pentraxin 3 (PTX3), a soluble pattern recognition molecule, is critical for wound healing by regulating tissue repair and also in innate and adaptive responses during infection and inflammation. Here, we show that PTX3 regulates disease pathogenesis and immunity to CL. PTX3 expression is increased in active skin lesions in patients and mice during CL, with higher levels being expressed in individuals with severe disease. PTX3−/− mice were highly resistant to primary and secondary L. major infection. Interestingly, the enhanced resistance of PTX3−/− mice to primary or secondary L. major infection was not associated with enhanced IFN-γ or decreased IL-10 response. Instead, L. major-infected PTX3−/− mice displayed strong IL-17 response and in vivo neutralization of IL-17A abolished their enhanced resistance. Naïve CD4+ T cells from PTX3−/− mice displayed increased differentiation into Th17 cells and this was associated with increased expression of Th17-specific transcription factors including RORγt, AhR and STAT3. Addition of recombinant PTX3 significantly inhibited the expression of Th17-specific transcription factors and the frequency of Th17 cells in Th17 polarizing cultures of PTX3−/− CD4+ T cells. Similarly, healed PTX3−/− mice had higher frequencies of effector memory CD4+ T cells that rapidly proliferate and differentiate into IL-17A-producing CD4+ T cells upon secondary challenge. Collectively, our results show that PTX3 contributes to pathogenesis of CL by negatively regulating protective Th17 and IL-17 responses.

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Moalli, Federica, Andrea Doni, Livija Deban, Teresa Zelante, Silvia Zagarella, Barbara Bottazzi, Luigina Romani, Alberto Mantovani et Cecilia Garlanda. « Role of complement and Fcγ receptors in the protective activity of the long pentraxin PTX3 against Aspergillus fumigatus ». Blood 116, n^o 24 (9 décembre 2010) : 5170–80. http://dx.doi.org/10.1182/blood-2009-12-258376.

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AbstractPentraxin 3 (PTX3) is a soluble pattern recognition molecule playing a nonredundant role in resistance against Aspergillus fumigatus. The present study was designed to investigate the molecular pathways involved in the opsonic activity of PTX3. The PTX3 N-terminal domain was responsible for conidia recognition, but the full-length molecule was necessary for opsonic activity. The PTX3-dependent pathway of enhanced neutrophil phagocytic activity involved complement activation via the alternative pathway; Fcγ receptor (FcγR) IIA/CD32 recognition of PTX3-sensitized conidia and complement receptor 3 (CR3) activation; and CR3 and CD32 localization to the phagocytic cup. Gene targeted mice (ptx3, FcR common γ chain, C3, C1q) validated the in vivo relevance of the pathway. In particular, the protective activity of exogenous PTX3 against A fumigatus was abolished in FcR common γ chain-deficient mice. Thus, the opsonic and antifungal activity of PTX3 is at the crossroad between complement, complement receptor 3-, and FcγR-mediated recognition. Because short pentraxins (eg, C-reactive protein) interact with complement and FcγR, the present results may have general significance for the mode of action of these components of the humoral arm of innate immunity.

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Loppini, Mattia, Marco Di Maio, Roberta Avigni, Roberto Leone, Antonio Inforzato, Guido Grappiolo, Alberto Mantovani et Barbara Bottazzi. « Long Pentraxin 3 as a New Biomarker for Diagnosis of Hip and Knee Periprosthetic Joint Infections ». Journal of Clinical Medicine 12, n^o 3 (29 janvier 2023) : 1055. http://dx.doi.org/10.3390/jcm12031055.

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Background: Preoperative diagnosis of periprosthetic joint infections (PJIs) poses an unmet clinical challenge. The long pentraxin PTX3 is a component of the innate immune system involved in infection immunity. This study evaluated the potential of synovial and plasmatic PTX3 in the diagnosis of hip and knee PJIs. Methods: Consecutive total hip and knee arthroplasty (THA/TKA) revisions were prospectively included and classified as septic or aseptic according to the European Bone and Joint Infection Society (EBJIS) and Musculoskeletal Infection Society (MSIS) criteria. The concentration of PTX3 in plasma and synovial fluid samples was measured with ELISA. The AUC, threshold value, sensitivity, specificity, and positive and negative likelihood ratios were calculated using the ROC (receiver operating characteristic) curve method. Results: The study population included 128 patients (94 THAs; 34 TKAs). The AUC of the synovial PTX3 based on EBJIS criteria was 0.85 (p < 0.0001), with a sensitivity of 81.13% and a specificity of 93.33%. The AUC based on MSIS criteria was 0.95 (p < 0.001), with a sensitivity of 91.43% and a specificity of 89.25%. Plasmatic PTX3 failed to discriminate infected from non-infected patients. Conclusions: Synovial PTX3 demonstrated an excellent diagnostic potential in hip and knee PJIs, with a very high specificity irrespective of the diagnostic criteria for PJI.

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Bozza, Silvia, Francesco Bistoni, Roberta Gaziano, Lucia Pitzurra, Teresa Zelante, Pierluigi Bonifazi, Katia Perruccio et al. « Pentraxin 3 protects from MCMV infection and reactivation through TLR sensing pathways leading to IRF3 activation ». Blood 108, n^o 10 (15 novembre 2006) : 3387–96. http://dx.doi.org/10.1182/blood-2006-03-009266.

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AbstractReactivation of latent human cytomegalovirus (HCMV) following allogeneic transplantation is a major cause of morbidity and mortality and predisposes to severe complications, including superinfection by Aspergillus species (spp). Antimicrobial polypeptides, including defensins and mannan-binding lectin, are known to block viral fusion by cross-linking sugars on cell surface. Pentraxin 3 (PTX3), a member of the long pentraxin family, successfully restored antifungal immunity in experimental hematopoietic transplantation. We assessed here whether PTX3 binds HCMV and murine virus (MCMV) and the impact on viral infectivity and superinfection in vivo. We found that PTX3 bound both viruses, reduced viral entry and infectivity in vitro, and protected from MCMV primary infection and reactivation as well as Aspergillus superinfection. This occurred through the activation of interferon (IFN) regulatory factor 3 (IRF3) in dendritic cells via the TLR9/MyD88-independent viral recognition sensing and the promotion of the interleukin-12 (IL-12)/IFN-γ–dependent effector pathway.

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Suzuki, Satoshi, Tetsuro Shishido, Akira Funayama, Shunsuke Netsu, Mitsunori Ishino, Tatsuro Kitahara, Toshiki Sasaki et al. « Long Pentraxin PTX3 Exacerbates Pressure Overload–Induced Left Ventricular Dysfunction ». PLoS ONE 8, n^o 1 (23 janvier 2013) : e53133. http://dx.doi.org/10.1371/journal.pone.0053133.

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Bottazzi, Barbara, Valérie Vouret-Craviari, Antonio Bastone, Luca De Gioia, Cristian Matteucci, Giuseppe Peri, Fabio Spreafico et al. « Multimer Formation and Ligand Recognition by the Long Pentraxin PTX3 ». Journal of Biological Chemistry 272, n^o 52 (26 décembre 1997) : 32817–23. http://dx.doi.org/10.1074/jbc.272.52.32817.

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Braunschweig, Anne, et Mihály Józsi. « Interaction of the long pentraxin PTX3 with soluble complement inhibitors ». Molecular Immunology 47, n^o 13 (août 2010) : 2234–35. http://dx.doi.org/10.1016/j.molimm.2010.05.114.

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Kato, Shingo, Mitsuko Ochiai, Tomoya Sakurada, Shino Ohno, Kyoko Miyamoto, Mina Sagara, Masataka Ito et al. « Increased Expression of Long Pentraxin PTX3 in Inflammatory Bowel Diseases ». Digestive Diseases and Sciences 53, n^o 7 (8 novembre 2007) : 1910–16. http://dx.doi.org/10.1007/s10620-007-0075-z.

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Koh, Seo Hyun, Seul Gi Shin, Maria Jose Andrade, Ryun-hee Go, Seonghee Park, Chang-Hoon Woo et Jae Hyang Lim. « Long pentraxin PTX3 mediates acute inflammatory responses against pneumococcal infection ». Biochemical and Biophysical Research Communications 493, n^o 1 (novembre 2017) : 671–76. http://dx.doi.org/10.1016/j.bbrc.2017.08.133.

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Han, Bing, Jack J. Haitsma, Yu Zhang, Xiaohui Bai, Matthew Rubacha, Shaf Keshavjee, Haibo Zhang et Mingyao Liu. « Long pentraxin PTX3 deficiency worsens LPS-induced acute lung injury ». Intensive Care Medicine 37, n^o 2 (12 novembre 2010) : 334–42. http://dx.doi.org/10.1007/s00134-010-2067-2.

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Coltrini, Daniela, Adwaid Manu Krishna Chandran, Mirella Belleri, Pietro L. Poliani, Manuela Cominelli, Francesca Pagani, Miriam Capra et al. « β-Galactosylceramidase Deficiency Causes Upregulation of Long Pentraxin-3 in the Central Nervous System of Krabbe Patients and Twitcher Mice ». International Journal of Molecular Sciences 23, n^o 16 (21 août 2022) : 9436. http://dx.doi.org/10.3390/ijms23169436.

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Globoid cell leukodystrophy (GLD), or Krabbe disease, is a neurodegenerative sphingolipidosis caused by genetic deficiency of lysosomal β-galactosylceramidase (GALC), characterized by neuroinflammation and demyelination of the central (CNS) and peripheral nervous system. The acute phase protein long pentraxin-3 (PTX3) is a soluble pattern recognition receptor and a regulator of innate immunity. Growing evidence points to the involvement of PTX3 in neurodegeneration. However, the expression and role of PTX3 in the neurodegenerative/neuroinflammatory processes that characterize GLD remain unexplored. Here, immunohistochemical analysis of brain samples from Krabbe patients showed that macrophages and globoid cells are intensely immunoreactive for PTX3. Accordingly, Ptx3 expression increases throughout the course of the disease in the cerebrum, cerebellum, and spinal cord of GALC-deficient twitcher (Galctwi/twi) mice, an authentic animal model of GLD. This was paralleled by the upregulation of proinflammatory genes and M1-polarized macrophage/microglia markers and of the levels of PTX3 protein in CNS and plasma of twitcher animals. Crossing of Galctwi/twi mice with transgenic PTX3 overexpressing animals (hPTX3 mice) demonstrated that constitutive PTX3 overexpression reduced the severity of clinical signs and the upregulation of proinflammatory genes in the spinal cord of P35 hPTX3/Galctwi/twi mice when compared to Galctwi/twi littermates, leading to a limited increase of their life span. However, this occurred in the absence of a significant impact on the histopathological findings and on the accumulation of the neurotoxic metabolite psychosine when evaluated at this late time point of the disease. In conclusion, our results provide the first evidence that PTX3 is produced in the CNS of GALC-deficient Krabbe patients and twitcher mice. PTX3 may exert a protective role by reducing the neuroinflammatory response that occurs in the spinal cord of GALC-deficient animals.

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Zhang, Jingbo, Latifa Koussih, Lianyu Shan et Abdelilah Soussi Gounni. « Glucocorticoid induces pentraxin 3 expression through mitogen-activated protein kinase pathway in human airway smooth muscle cells (P6013) ». Journal of Immunology 190, n^o 1_Supplement (1 mai 2013) : 120.7. http://dx.doi.org/10.4049/jimmunol.190.supp.120.7.

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Abstract Long pentraxin 3 (PTX3) is a multifunctional soluble pattern recognition receptor that links innate immunity, inflammation, and matrix deposition. Glucocorticoids (GC) are an important anti-inflammatory treatment in asthma. Previous studies have demonstrated that GC had divergent effects on PTX3 production in diverse cell types. In this study, we first evaluated whether GC alone induced and, under inflammatory conditions, enhanced and extended PTX3 production in Human airway smooth muscle cells (HASMC) and investigated the plausible molecule mechanism regulating the induction of PTX3. HASMC transfected with PTX3 promoter constructs were treated with dexamethasone (Dex) or and TNF. We demonstrated Dex induced and synergized with TNF to augment PTX3 protein levels. However, Dex does not influence the mRNA levels and promoter activity of PTX3 alone, but it decreased the effect of TNF-induced PTX3 promoter activity. Further results had shown that Dex increased TNF-induced PTX3 mRNA stability. Primary HASMC pretreated with inhibitors of p42/p44 ERK, but not p38 or JNK-MAPK, significant decrease in PTX3 release on Dex- and TNF-treatment. Taken together, our data provide the first evidence of Dex-induced PTX3 expression in HASMC maybe occurred posttranscriptional mechanisms and via p42/p44-MAPK signaling pathways. Our results raise the possibility that HASMC may play a role in airway inflammation via PTX3-dependent pathway.

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Chen, Xuehai, Jiao Luo, Minmin Wu, Zhuo Pan, Yue Xie, Hongwei Wang, Bicheng Chen et Hong Zhu. « Study on Association of Pentraxin 3 and Diabetic Nephropathy in a Rat Model ». Journal of Diabetes Research 2018 (2018) : 1–10. http://dx.doi.org/10.1155/2018/8968573.

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Diabetic nephropathy (DN) is a serious microvascular complication of diabetes. Compared with other therapies for diabetic patients, islet transplantation can effectively prevent and reverse diabetes-induced microvascular disease, such as diabetic retinopathy and nephropathy. PTX3 is the only long pentraxin that can be detected in renal tissue. In this study, we investigated the expression of PTX3 when early DN was reversed after islet transplantation.Methods. Diabetes was induced in rats by injecting streptozotocin (STZ). Twelve weeks later, the diabetic rats were divided into 2 groups: the islet transplantation group (IT) and the diabetic nephropathy group (DN). Renal injury, renal function, and the expression of PTX3 in the plasma and the kidneys were assessed with urinalysis, immunohistochemical staining, and Western blot, respectively.Results. The expression of PTX3 in the kidney was significantly decreased in the DN group but increased in the IT group because of the reversal of DN.Conclusions. Our data showed that the level of PTX3 in renal tissue is closely related to renal injury in DN. This may be used to quantify the extent of renal injury in DN, provide a potential early indicator of renal tubular injury in early DN patients, and assess DN clinical progression.

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Tsai, Yih-Jeng, Ping-Hung Shen, Sheng-Dean Luo et Wen-Bin Wu. « Liver X Receptor Expression and Pentraxin 3 Production in Chronic Rhinosinusitis and Sinonasal Mucosal Fibroblast Cells ». Journal of Clinical Medicine 10, n^o 3 (25 janvier 2021) : 452. http://dx.doi.org/10.3390/jcm10030452.

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The long pentraxin 3 (PTX3) is a prototypic molecule for recognizing pathogens. Liver X receptors (LXRs), belonging to nuclear receptors (NRs) for cholesterol metabolism through heterodimerizing with other NRs, were recently reported to participate in inflammation. However, their roles in chronic rhinosinusitis without nasal polyps (CRSsNP) are unclear. Therefore, this study was sought to explore roles of LXRs in chronic rhinosinusitis (CRS) sinonasal tissues and derived fibroblasts. Immunohistochemistry indicated that LXRα and β expression and lipid/fat deposition were differentially expressed in the control and CRSsNP nasal mucosa. GW7647 (a peroxisome proliferator activated receptor α (PPARα) agonist) and GW3965 (a dual agonist for LXRα and β) significantly caused PTX3 induction in the fibroblast cells. GW3965 induced PTX3 mRNA and protein expression, and the induction substantially led to PTX3 secretion. Meanwhile, an endogenous agonist-cholesterol had a similar enhancing effect on the induction of PTX3 protein. LXR siRNA knockdown to lower LXRα or β expression significantly compromised PTX3 induction. Interestingly, GW3965 also induced phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) activation and its inhibition reduced PTX3 expression. Collectively, we demonstrated here for the first time that CRSsNP nasal mucosa differentially expresses LXRα and β and deposits lipids/fats that may contain cholesterol metabolites to activate LXRs. Activation of LXRs leads to PTX3 production in sinonasal mucosa-derived fibroblasts. Our previous study showed PTX3 overexpression in the nasal cavity of CRSsNP, whereas this study highlights that cholesterol metabolites and LXR activation regulate PTX3 production and may contribute to antimicrobial activity and tissue repair during CRSsNP progression.

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Kawasugi, Kazuo, Tadashi Yamamoto, Ryosuke Shirasaki, Haruko Tashiro et Naoki Shirafuji. « Increased Levels of PTX3 in Human Plasma in Septic Patients with DIC ». Blood 118, n^o 21 (18 novembre 2011) : 4347. http://dx.doi.org/10.1182/blood.v118.21.4347.4347.

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Abstract Abstract 4347 Sepsis is a life-threatening condition that is characterized by a whole-body inflammatory state (called a systemic inflammatory response syndrome, SIRS). Long pentraxin PTX3 is an inflammatory mediator and a component of the humoral arm of innate immunity produced by neutrophils, macrophages, myeloid dendritic and endothelial cells. During sepsis a massive inflammatory activation and coagulation/fibrinolysis dysfunction occur. However, little is known about PTX3 in septic patients with DIC. Therefore, we measured PTX3s in the plasma from septic patients with DIC (n=20). Also, we investigated PTX3 in the plasma from septic patients without DIC (n=8) and acute promyelocytic leukemia (APL)-induced DIC (n=5). PTX3 in the plasma from human were measured using enzyme-linked immunosorbent assay (ELISA) kits (Perseus Proteomics Inc, Japan). The thrombin antithrombin complexes (TAT) levels were higher in both DIC patients as reported by others. We detected high levels of PTX3 in the plasma of all septic patients with DIC. Also, plasma levels of PTX3 were positive in septic patients without DIC. However, plasma levels of PTX3 were significantly higher in septic patients with DIC than in septic patients without DIC. Plasma levels of PTX3 ware significantly correlated with severity of septic DIC (platelet count and TAT level). We did not find any difference plasma levels of PTX3 in the APL patients with DIC. Moreover, high-mobility group box 1 (HMGB1) concentrations in the human plasma were determined using ELISA kit (Shino-Test, Japan). Plasma levels of HMBG1 were positive for 14 cases in 20 septic patients with DIC. Also, we did not find any difference plasma levels of HMGB1 in the APL patients with DIC. These results suggest that assess of PTX3 and HMBG1 in the plasma may be helpful in the making the diagnosis in septic patients with DIC. However, PTX3 seemed to be a better biomarker than HMGB1. It appears that PTX3 may contribute to the severity of septic DIC. Disclosures: No relevant conflicts of interest to declare.

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Haibo, Liu, Guo Xiaofang, Wang Chunming, Yuan Jie, Chen Guozhong, Zhang Limei, Cao Yong et al. « Prognostic Value of Plasma Pentraxin-3 Levels in Patients with Stable Coronary Artery Disease after Drug-Eluting Stent Implantation ». Mediators of Inflammation 2014 (2014) : 1–7. http://dx.doi.org/10.1155/2014/963096.

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Pentraxin-3 (PTX3) is an inflammatory marker thought to be more specific to cardiovascular inflammation than C-reactive protein (CRP). Our aim was to assess the prognostic value of PTX3 in patients with stable coronary artery disease (CAD) after drug eluting stent (DES) implantation. Plasma PTX3 levels were measured before percutaneous coronary intervention (PCI) and at 24 h post-PCI in 596 consecutive patients with stable CAD. Patients were followed up for a median of 3 years (range 1–5) for major adverse cardiovascular events (MACEs). We found that the post-PCI plasma PTX3 levels were significantly higher at 24 h after PCI than pre-PCI, patients with MACEs had higher post-PCI PTX3 levels compared with MACEs-free patients, patients with higher post-PCI PTX3 levels (median > 4.384 ng/mL) had a higher risk for MACEs than those with PTX3 < 4.384 ng/mL, and post-PCI PTX3, cTnI, multiple stents, and age but not high-sensitivity CRP (hsCRP) were independently associated with the prevalence of MACEs after DES implantation. The present study shows that post-PCI PTX3 may be a more reliable inflammatory predictor of long-term MACEs in patients with stable CAD undergoing DES implantation than CRP. Measurement of post-PCI PTX3 levels could provide a rationale for risk stratification of patients with stable CAD after DES implantation.

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Targonska-Stepniak, B., A. Drelich-Zbroja et K. Grzechnik. « AB0782 Serum pentraxin 3 as a biomarker in patients with spondyloarthritis. » Annals of the Rheumatic Diseases 81, Suppl 1 (23 mai 2022) : 1517.2–1518. http://dx.doi.org/10.1136/annrheumdis-2022-eular.606.

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BackgroundA proper evaluation and management of patients with spondyloarthritis (SpA) requires the use of biomarkers, facilitating early diagnosis, reflecting disease activity and clinical response to therapies. The chronic, systemic inflammatory process is responsible for increased CV risk in SpA patients. Pentraxin 3 (PTX3) is an inflammatory marker, a member of long pentraxin superfamily, argued to be involved in pathogenesis of both inflammation and atherosclerosis. PTX3 is produced locally in the inflamed tissue, by different cell types including macrophages, endothelial cells, synoviocytes, but not hepatocytes. PTX3 is produced in walls of blood vessels, in atherosclerotic plaques, as a response to pro-inflammatory cytokines.ObjectivesThe aim of the study was to assess the role of PTX3 as a biomarker in patients with SpA and to evaluate the relationship between PTX3 and CV risk markers (carotid intima-media thickness (cIMT), lipid profile).MethodsThe study group consisted of 40 consecutive patients with SpA: 29 patients with psoriatic arthritis (PsA) and 11 patients with ankylosing spondylitis (AS). The group consisted of 16 (40%) women and 24 (60%) men, with the mean (SD) age 43.9 (12.0) (range 25–68) and disease duration 7,8 (7,6) years (range 1–32). An assessment of the disease activity included: laboratory inflammatory parameters (erythrocyte sedimentation rate (ESR), C-reactive protein, CRP) and clinical assessment (in patients with peripheral SpA (pSpA) joints counts and disease activity score in 28 joints (DAS28); in patients with axial SpA (axSpA) Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI) and pain of the spine according to the patient in visual analogue scale (VAS). A measurement of carotid intima-media thickness (cIMT) was performed using high-resolution B-mode ultrasonography to estimate features of atherosclerosis (cIMT> 0.9 mm and/or presence of atherosclerotic plaques).ResultsThe median (IQR) PTX3 concentration in SpA patients was 3.39 (2.22-3.88) ng/ml. The mean (SD) value of ESR was 27.7 (28.3) mm/h and CRP concentration 13.6 (19.9) mg/l.The mean values of clinical indices were as follows: DAS28 3.8 (1.1), BASDAI 4.02 (2.1), BASFI 4.22 (2.2), VAS spine pain 41.4 (24.0).The mean (SD) cIMT value was 0.77 (0.23) mm (range 0.48-1.33). The features of atherosclerosis were detected in 7 (17.5%) patients.No significant correlations were found between PTX3 and other inflammatory markers (ESR, CRP). There were no correlations between PTX3 concentration the clinical indices of the disease activity (DAS28, BASDAI, BASFI, VAS spine pain). No differences of PTX3 concentrations were detected between pSpA and axSpA patients.The PTX3 concentrations were significantly higher in patients with definite atherosclerosis (cIMT > 0.9 mm) than in patients with subclinical or no atherosclerosis (cIMT=< 0.9) (5.79 (3.84-8.59) vs 3.06 (2.0-3.52) ng/ml, p=0.01), as well as in patients with atherosclerotic plaques in comparison with no plaques (6.79 (4.86-8.59) vs 3.26 (2.0-3.71) ng/ml, p=0.02) (Figure 1).ConclusionThe results of our study suggest that in patients with SpA, PTX3 could be regarded as a biomarker indicating intensity of atherosclerosis. However PTX3 was not associated with parameters of disease activity in patients with SpA.References[1]Maksymowych WP. Biomarkers in axial spondyloarthritis. Curr Opin Rheumatol. 2015 Jul;27(4):343-8. doi: 10.1097/BOR.0000000000000180.[2]Nisihara R, Skare TL, Zeni JO, Rasera H, Lidani K, Messias-Reason I. Plasma levels of pentraxin 3 in patients with spondyloarthritis. Biomarkers. 2018 Feb;23(1):14-17. doi: 10.1080/1354750X.2016.1278265.Disclosure of InterestsNone declared

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Kathariya, Rahul, Hansa Jain, Dnyneshwari Gujar, Archana Singh, Himanshu Ajwani et Devendra Mandhyan. « Pentraxins as Key Disease Markers for Periodontal Diagnosis ». Disease Markers 34, n^o 3 (2013) : 143–51. http://dx.doi.org/10.1155/2013/259273.

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Periodontal diseases are characterized by a complex set of biologic interactions between a diverse and dynamic microbial ecosystem and the host’s multifaceted and responsive immune and inflammatory machinery. Such interactions between microbial pathogens and various host response systems play a critical role in the development and progression of periodontal disease via the release of inflammatory and immune mediators. Advances in periodontal disease diagnostic are moving toward methods whereby periodontal risk can be identified and quantified by detecting such inflammatory mediators in its sequential pathophysiology. Pentraxins (PTXs) are classical mediators of inflammation and markers of acute-phase reaction. They are a super family of multifunctional molecules characterized by multimeric structure, divided into “short” PTXs and “long” PTXs. C-reactive protein (CRP) and pentraxin-3 (PTX3) are prototypic molecules of the short and long PTX family, respectively. Evidence suggests that PTXs acts as a non-redundant component of the humoral arm of innate immunity, downstream of, and complementary to, cellular recognition, as well as a tuner of inflammation. CRP is a cheaper biomarker and more readily available in everyday clinical practice compared with other inflammatory markers, on the other hand, PTX3 is believed to be the true independent indicator of disease activity and could have clinical implication in diagnosing the “at site” inflammatory status of the periodontal disease. These pentraxins are sensitive and specific in the diagnosis and prognosis of chronic diseases. Thus the pentraxins could be used as preferred biomarkers in periodontal disease diagnosis.

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Assandri, R., G. Martellosio et A. Montanelli. « AB0051 SERUM AMYLOID A AND PENTRAXIN 3 : INNATE IMMUNE RESPONSE AND DISEASE ACTIVITY IN SYSTEMIC LUPUS ERYTHEMATOSUS ». Annals of the Rheumatic Diseases 79, Suppl 1 (juin 2020) : 1328.1–1328. http://dx.doi.org/10.1136/annrheumdis-2020-eular.1933.

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Background:Systemic Lupus Erythematosus (SLE) is an autoimmune disease that involves several molecular patterns with a wide spectrum of clinical manifestations and symptoms. Inflammation and related pathway play a role in SLE pathogenesis. The pentraxin superfamily including long and short pentraxin, C Reactive Protein CRP, Serum amyloid A (SAA), Pentraxin 3 (PTX3) are key components of innate immune system and induce a variety of inflammation associated pathway. However Literature provides several evidences that CRP serum levels not correlated with clinical and immunological manifestations. This situation affected clinical practice and the patient follow up. PTX3 have been identified as a component of inflammatory status in several autoimmune conditions. SAA is an acute phase protein secreted in large quantity during inflammation.Objectives:We want to evaluated SAA, PTX3 and CRP concentrations, their correlation between SLE Disease Activity Index (SLEDAI), that including complement fractions C3, C4.Methods:We enrolled fifty patients that fulfilled the SLE American College of Rheumatology criteria and fifty healthy subjects. The SLE disease activity was classified with the SLEDAI (0 to 12). Patients were divided into two groups according to SLEDAI score: inactive group (Group 1, 25 patients, 50%: SLEDAI < 4) and active group (Group 2, 25 patients, 50%: SLEDAI 5 to 12). PTX3 concentration was measured by a sandwich ELISA kit (Hycult) with 2.8 ng/mL cut-off point. SAA concentration was detected by nephelometry performed on a BN ProSpec System (Siemens, Germany), with assay kit based on polyclonal antibodies (Siemens Healthcare Diagnostics Products, Germany, 6.5 mg/L cut-off point). High sensitive CRP concentrations were determined using the ci8200 platform (Abbott Laboratories Chicago, Illinois).Results:Plasma PTX3 and serum SAA levels was significantly higher in SLE patients than in the healthy subjects (PTX311.5 ± 7.3 ng/mL vs 2.3 ± 1.1; p < 0.001; SAA: 87 ±77 mg/L vs 2.6±2.5; p < 0.001). These differences were not evident in CRP levels (8.5 ± 7.8 mg/L vs 6.2± 2.5). Considering two groups, there were statistical differences in PTX3 level (Group 2: 14.9 ± 12 ng/mL vs Group 1: 2.16 ±0.5 ng/mL, p<0,05) and SAA concentration (Group 2: 114 ± 89 ng/mL vs Group 1: 3.6 ±1.7 ng/mL, p<0,05) but not in CRP concentration (Group 2: 11.5 ± 8.4 mg/L vs Group 1: 9.5 ±3.5). There was a significantly negative correlation between C3, C4 fractions, PTX3 and SSA levels (respectively r = −0.74, p=<0.05, and r = −0.79, p<0.05). No statistical correlation were appeared between C3, C4 fractions and CRP serum levels (r= −0,12., p= 0.82, and r= −0.18, p= 0,21). We noted a positive significant correlation between SLEDAI, PTX3 and SAA concentration (r = 0.79, p < 0.05, 0.83, p < 0.05, respectively) an increase in PTX3 and SAA levels followed the lupus flare and symptoms. No significant correlation appeared between SLEDAI and CRP (r= 0.15, p=0.89)Conclusion:PTX3 and SAA concentration was significantly higher in SLE patients than the healthy control subjects and their levels reflected disease activity. We showed a direct correlation between PTX3 and SAA. In SLE patients PTX3 and SAA concentrations were correlated with SLEDAI. We suggest an integrate viewpoint in witch SAA and PTX3 may play a role as a biomarker of disease activity, with synergic work during SLE events. Evidences suggested that PTX3 and SAA could trigger the same molecular pathway, by TLR4, via NF-kB.References:[1]Assandri R, Monari M Montanelli A. Pentraxin 3 in Systemic Lupus Erithematosus: Questions to be Resolved, Translational Biomedicine (2015)Disclosure of Interests:None declared

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Baranova, Natalia S., Antonio Inforzato, David C. Briggs, Viranga Tilakaratna, Jan J. Enghild, Dhruv Thakar, Caroline M. Milner, Anthony J. Day et Ralf P. Richter. « Incorporation of Pentraxin 3 into Hyaluronan Matrices Is Tightly Regulated and Promotes Matrix Cross-linking ». Journal of Biological Chemistry 289, n^o 44 (4 septembre 2014) : 30481–98. http://dx.doi.org/10.1074/jbc.m114.568154.

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Mammalian oocytes are surrounded by a highly hydrated hyaluronan (HA)-rich extracellular matrix with embedded cumulus cells, forming the cumulus cell·oocyte complex (COC) matrix. The correct assembly, stability, and mechanical properties of this matrix, which are crucial for successful ovulation, transport of the COC to the oviduct, and its fertilization, depend on the interaction between HA and specific HA-organizing proteins. Although the proteins inter-α-inhibitor (IαI), pentraxin 3 (PTX3), and TNF-stimulated gene-6 (TSG-6) have been identified as being critical for COC matrix formation, its supramolecular organization and the molecular mechanism of COC matrix stabilization remain unknown. Here we used films of end-grafted HA as a model system to investigate the molecular interactions involved in the formation and stabilization of HA matrices containing TSG-6, IαI, and PTX3. We found that PTX3 binds neither to HA alone nor to HA films containing TSG-6. This long pentraxin also failed to bind to products of the interaction between IαI, TSG-6, and HA, among which are the covalent heavy chain (HC)·HA and HC·TSG-6 complexes, despite the fact that both IαI and TSG-6 are ligands of PTX3. Interestingly, prior encounter with IαI was required for effective incorporation of PTX3 into TSG-6-loaded HA films. Moreover, we demonstrated that this ternary protein mixture made of IαI, PTX3, and TSG-6 is sufficient to promote formation of a stable (i.e. cross-linked) yet highly hydrated HA matrix. We propose that this mechanism is essential for correct assembly of the COC matrix and may also have general implications in other inflammatory processes that are associated with HA cross-linking.

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