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Lorena Capriotti,1,* Marco Iuliano,1,* Roberto Lande,2 Loredana Frasca,2 Mario Falchi,3 Paolo Rosa,1 Giorgio Mangino,1 Giovanna Romeo1 1Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome – Polo Pontino, Latina, Italy; 2Pharmacological Research and Experimental Therapy Section, National Center for Drug Research and Evaluation, Istituto Superiore di Sanità , Rome, Italy; 3National AIDS Center, Istituto Superiore di Sanità , Rome, Italy*These authors contributed equally to this workCorrespondence: Giorgio Mangino, Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome – Polo Pontino, C.so della Repubblica, 79, Latina, 04100, Italy, Tel +39 0773 1757271, Email giorgio.mangino@uniroma1.itPurpose: Extracellular Vesicles (EVs) are a heterogeneous group of cell-derived membranous nanoparticles involved in several physiopathological processes. EVs play a crucial role in the definition of the extracellular microenvironment through the transfer of their cargo. Psoriasis is a prototypical chronic inflammatory disease characterized by several secreted mediators, among which antimicrobial peptides (AMPs) are considered pivotal in the development of the psoriatic inflammatory microenvironment. The role of EVs in the pathogenesis of psoriasis has not been elucidated yet, even if emerging evidence demonstrated that interleukin-17A (IL-17A), the psoriasis-related principal cytokine, modifies EVs release and cargo content. The aim of this work was to analyze whether, besides IL-17A, other psoriasis-related cytokines (ie, IFN-γ, TNF-α, IL-22 and IL-23) could affect EVs release and their AMPs mRNAs cargo as well as to analyze the potential biological effect due to EVs internalization by different acceptor cells.Methods: Nanoparticle tracking analysis (NTA) was performed on supernatants of HaCaT cells stimulated with IL-17A, IFN-γ, TNF-α, IL-22 or IL-23 to enumerate EVs. Real-Time RT-PCR was used for gene expression analysis in cells and EVs. Confocal microscopy and Flow cytometry were used to, respectively, study Netosis and EVs internalization.Results: IL-17A and IFN-γ increased EVs release by HaCaT cells. All the tested cytokines modulated AMPs mRNA expression in parental cells and in their respective EVs. S100A12 and hBD2 mRNAs were upregulated following IL-17A and IL-22 treatments. Interestingly, EVs derived from cytokine treated HaCaT cells induced Netosis in freshly isolated neutrophils. Upregulation of S100A12 and hBD2 mRNA was also detectable in acceptor cells incubated with EVs derived from cells treated with psoriasis-related cytokines.Conclusion: The obtained results highlighted the role of EVs in the composition of psoriasis-associated secretome and microenvironment also suggesting the EV involvement in the spreading of the disease mediators and in the possible associated comorbidities.Keywords: extracellular vesicles, antimicrobial peptides, cytokines, keratinocytes, pathogenesis of psoriasis, comorbidities

Actinic keratosis (AK) is a carcinoma in situ precursor of cutaneous squamous cell carcinoma (cSCC), the second most common cancer affecting the Caucasian population. AK is frequently present in the sun-exposed skin of the elderly population, UV radiation being the main cause of this cancer, and other risk factors contributing to AK incidence. The dysregulation of microRNAs (miRNAs) observed in different cancers leads to an improper expression of miRNA targets involved in several cellular pathways. The TaqMan Array Human MicroRNA Card assay for miRNA expression profiling was performed in pooled AK compared to healthy skin scraping samples from the same patients. Forty-three miRNAs were modulated in the AK samples. The expression of miR-19b (p < 0.05), -31, -34a (p < 0.001), -126, -146a (p < 0.01), -193b, and -222 (p < 0.05) was validated by RT-qPCR. The MirPath tool was used for MiRNA target prediction and enriched pathways. The top DIANA-mirPath pathways regulated by the targets of the 43 miRNAs are TGF-beta signaling, Proteoglycans in cancer, Pathways in cancer, and Adherens junction (7.30 × 10−10 < p < 1.84 × 10−8). Selected genes regulating the KEGG pathways, i.e., TP53, MDM2, CDKN1A, CDK6, and CCND1, were analyzed. MiRNAs modulated in AK regulate different pathways involved in tumorigenesis, indicating miRNA regulation as a critical step in keratinocyte cancer.

Background: Low-dose-medicine is based on the administration of low doses of biological regulators to restore the immunologic balance altered in the disease. Cytokines are pivotal regulators of cellular and tissue functions and impaired crosstalk, due to an imbalance between specific cytokines, it is fundamental in acute inflammation and diseases correlated to low-grade chronic inflammation. Osteoarthritis is the most prevalent arthritic disease and a leading cause of disability. In the treatment of muscle-skeletal pathologies, the therapeutic integration of conventional medicine with homotoxicology, or low-dose-medicine appears to be beneficial. Objective: This study aims to get more insights into the role of inflammatory cytokines and chemokines during the development of osteoarthritis and to evaluate a possible blocking strategy using anti-inflammatory molecules, we resort to an in vitro experimental model using an established human chondrosarcoma cell line that underwent to a well known pro-inflammatory stimulus as bacterial lipopolysaccharide. Method: We tested the production of inflammatory-related cytokines and chemokines, and the efficacy of low-dose (LD) administration of anti-inflammatory compounds, namely IL-10 and anti-IL-1, to block inflammatory cellular pathways. Results: Following an inflammatory insult, chondrocytes upregulated the expression of several pro-inflammatory cyto-/chemokines and this induction could be counteracted by LD IL-10 and anti-IL-1. We reported that these effects could be ascribed to an interfering effect of LD drugs with the NF-κB signaling. Conclusion: Our results provided a good indication that LD drugs can be effective in inhibiting the inflammatory response in chondrocytes opening the way to new therapies for the treatment of diseases such as osteoarthritis.

Objectives Extracellular vesicles (EVs) are key biological mediators of several physiological functions within the cell microenvironment. Platelets are the most abundant source of EVs in the blood. Similarly, platelet lysate (PL), the best platelet derivative and angiogenic performer for regenerative purposes, is enriched of EVs, but their role is still too poorly discovered to be suitably exploited. Here, we explored the contribution of the EVs in PL, by investigating the angiogenic features extrapolated from that possessed by PL. Methods We tested angiogenic ability and molecular cargo in 3D bioprinted models and by RNA sequencing analysis of PL-derived EVs. Results A subset of small vesicles is highly represented in PL. The EVs do not retain aggregation ability, preserving a low redox state in human umbilical vein endothelial cells (HUVECs) and increasing the angiogenic tubularly-like structures in 3D endothelial bioprinted constructs. EVs resembled the miRNome profile of PL, mainly enriched with small RNAs and a high amount of miR-126, the most abundant angiogenic miRNA in platelets. The transfer of miR-126 by EVs in HUVEC after the in vitro inhibition of the endogenous form, restored angiogenesis, without involving VEGF as a downstream target in this system. Conclusion PL is a biological source of available EVs with angiogenic effects involving a miRNAs-based cargo. These properties can be exploited for targeted molecular/biological manipulation of PL, by potentially developing a product exclusively manufactured of EVs.

Objectivesextracellular vesicles (EVs) are key biological mediators of several physiological functions within the cell microenvironment. Platelets are the most abundant source of EVs in the blood. Similarly, platelet lysate (PL), the best platelet derivative and angiogenic performer for regenerative purposes, is enriched of EVs, but their role is still too poorly discovered to be suitably exploited. Here we explored the contribution of the EVs in PL, by investigating the angiogenic features extrapolated from that possessed by PL.Methodswe tested angiogenic ability and molecular cargo in 3D bioprinted models and by RNA sequencing analysis of PL-derived EVs.Resultsa subset of small vesicles is highly represented in PL. The EVs do not retain aggregation ability, preserving a low redox state in HUVEC and increasing the angiogenic tubularly-like structures in 3D endothelial bioprinted constructs. EVs resembled the miRNome profile of PL, mainly enriched of small RNAs and a high amount of miR-126, the most abundant angiogenic miRNA in platelets. The transfer of miR-126 by EVs in HUVEC after the in vitro inhibition of the endogenous form, restored angiogenesis, without involving VEGF as downstream target in this system.ConclusionsPL is a biological source of available EVs with angiogenic effects involving a miRNAs-based cargo. These properties can be exploited for targeted molecular/biological manipulation of PL, by potentially developing a product exclusively manufactured of EVs.

To assess the role of CD3A total of 76 patients (57.6 ± 11.7 years) with chronic plaque-type psoriasis were initially evaluated. Nineteen patients (19 eyes) and 19 healthy volunteers (19 eyes) were subjected to dermatological evaluation with Psoriasis Area Severity Index (PASI) and the Dermatology life quality index (DLQI). Retinal images were processed using an automatized software. On the same day, a venous sample was collected and analyzed using multiparametric flow cytometry. Three out of 6 patients who presented cataract, consented to perform surgery with humor aqueous collection. The samples were analyzed using a Multi-Analyte ELISA kit for the simultaneous quantification of IL1α, IL1β, IL2, IL4, IL6, IL8, IL10, IL12, IL17A, IFNγ, TNF-α, GMCSF.The CD3Our findings demonstrated that CD20

Highlights • A group of mucosal HPVs are the causative agents of cervical cancer and are associated to other cancers. • Certain cutaneous HPVs are involved in the development of cutaneous squamous cell carcinoma. • EVs released by HPV+ cells convey a specific cargo of mRNAs and microRNAs. • The EV delivery from HPV+ cells to non-infected recipient cells may represent a novel mechanism of tumorigenesis promotion., A small group of mucosal Human Papillomaviruses are the causative agents of cervical cancer and are also associated with other types of cancers. Certain cutaneous Human Papillomaviruses seem to have a role as co-factors in the UV-induced carcinogenesis of the skin. The main mechanism of the tumorigenesis induced by Human Papillomaviruses is linked to the transforming activity of the viral E6 and E7 oncoproteins. However, other mechanisms, such as the gene expression control by specific microRNAs expression and deregulation of immune inflammatory mediators, may be important in the process of transformation. In this context, the release of Extracellular Vesicles with a specific cargo (microRNAs involved in tumorigenesis, mRNAs of viral oncoproteins, cytokines, chemokines) appears to play a key role.

A theoretical and experimental study has been carried out on a tunable dual pump-probe optical source for distributed Brillouin optical time-domain analysis (BOTDA). The developed source exploits a modified Brillouin ring laser technology and is capable of a tuning range of ∼200 MHz without using phase-locked loop or optical sideband generation techniques, and exhibits a linewidth smaller than 2.5 MHz and ∼0.5 mW power. In BOTDA experiments, the proposed source has demonstrated to be an efficient solution enabling distributed sensing over 10 km single mode fiber with a spatial resolution of ∼4 m, and a strain and temperature resolutions of ∼10 μ ϵ and ∼0.5 °C respectively.

Simple Summary This review aims to collect recent studies on the complex relationship between the host innate response to oncogenic viruses (i.e., HPV, HTLV-1, MCPyV, JCPyV, Herpesviruses, HBV, HCV) and tumorigenic processes by focusing mainly on regulatory crosstalks between viral components and the type I IFN system. It is a picture of new mechanisms by which type I IFNs may be affected and, in turn, affect signaling pathways to mediate anti-proliferative and antiviral responses in virus-induced tumorigenic context. Studies on cellular and viral miRNAs machinery, as well as cellular communication and microenvironment modification via classical secretion mechanisms and extracellular vesicle-mediated delivery are described. Abstract Oncogenic viruses favor the development of tumors in mammals by persistent infection and specific cellular pathways modifications by deregulating cell proliferation and inhibiting apoptosis. They counteract the cellular antiviral defense through viral proteins as well as specific cellular effectors involved in virus-induced tumorigenesis. Type I interferons (IFNs) are a family of cytokines critical not only for viral interference but also for their broad range of properties that go beyond the antiviral action. In fact, they can inhibit cell proliferation and modulate differentiation, apoptosis, and migration. However, their principal role is to regulate the development and activity of most effector cells of the innate and adaptive immune responses. Various are the mechanisms by which IFNs exert their effects on immune cells. They can act directly, through IFN receptor triggering, or indirectly by the induction of chemokines, the secretion of further cytokines, or by the stimulation of cells useful for the activation of particular immune cells. All the properties of IFNs are crucial in the host defense against viruses and bacteria, as well as in the immune surveillance against tumors. IFNs may be affected by and, in turn, affect signaling pathways to mediate anti-proliferative and antiviral responses in virus-induced tumorigenic context. New data on cellular and viral microRNAs (miRNAs) machinery, as well as cellular communication and microenvironment modification via classical secretion mechanisms and extracellular vesicles-mediated delivery are reported. Recent research is reviewed on the tumorigenesis induced by specific viruses with RNA or DNA genome, belonging to different families (i.e., HPV, HTLV-1, MCPyV, JCPyV, Herpesviruses, HBV, HCV) and the IFN system involvement.

Psoriasis is a chronic inflammatory systemic disease caused by deregulation of the interleukin-23/-17 axis that allows the activation of Th17 lymphocytes and the reprogramming of keratinocytes proliferative response, thereby inducing the secretion of cyto-/chemokines and antimicrobial peptides. Beside cell-to-cell contacts and release of cytokines, hormones and second messengers, cells communicate each other through the release of extracellular vesicles containing DNA, RNA, microRNAs and proteins. It has been reported the alteration of extracellular vesicles trafficking in several diseases, but there is scarce evidence of the involvement of extracellular vesicles trafficking in the pathogenesis of psoriasis. The main goal of the study was to characterize the release, the cargo content and the capacity to transfer bioactive molecules of extracellular vesicles produced by keratinocytes following recombinant IL-17A treatment if compared to untreated keratinocytes. A combined approach of standard ultracentrifugation, RNA isolation and real-time RT-PCR techniques was used to characterize extracellular vesicles cargo. Flow cytometry was used to quantitatively and qualitatively analyse extracellular vesicles and to evaluate cell-to-cell extracellular vesicles transfer. We report that the treatment of human keratinocytes with IL-17A significantly modifies the extracellular vesicles cargo and release. Vesicles from IL-17A-treated cells display a specific pattern of mRNA which is undid by IL-17A neutralization. Extracellular vesicles are taken up by acceptor cells irrespective of their content but only those derived from IL-17A-treated cells enable recipient cells to express psoriasis-associated mRNA. The results imply a role of extracellular vesicles in amplifying the pro-inflammatory cascade induced in keratinocyte by pro-psoriatic cytokines.

Objective To assess the role of CD3+ CD20+ CD4- CD8- double-negative (DN) or CD3+CD20+ CD4/CD8+ T cells and the related pro-inflammatory cytokines in the humor aqueous, in mediating retinal microvascular changes in patients with chronic plaque-type moderate to severe psoriasis. Design. A total of 76 patients (57.6 ± 11.7 years) with chronic plaque-type psoriasis were initially evaluated. Nineteen patients (19 eyes) and 19 healthy volunteers (19 eyes) were subjected to dermatological evaluation with Psoriasis Area Severity Index (PASI) and the Dermatology life quality index (DLQI). Retinal images were processed using an automatized software. On the same day, a venous sample was collected and analyzed using multiparametric flow cytometry. Three out of 6 patients who presented cataract, consented to perform surgery with humor aqueous collection. The samples were analyzed using a Multi-Analyte ELISA kit for the simultaneous quantification of IL1α, IL1β, IL2, IL4, IL6, IL8, IL10, IL12, IL17A, IFNγ, TNF-α, GMCSF. Results The CD3+CD4+/CD8+CD20+CD56- T cells expression was greater in the psoriatic patients (+73.9%, P Conclusion Our findings demonstrated that CD20+ T cell subpopulation is highly represented in psoriasis regardless of the use of immunomodulatory therapies, and the diffuse microvascular alterations suggested possible endothelial damage as mainstream for the genesis of psoriatic-mediated complications as further supported by the comparable concentrations of cytokines, at least as humor aqueous content, with respect to healthy eyes.

The connection between chronic inflammation and risk of cancer has been supported by several studies. The development of cancer might be a process driven by the presence of a specific combination of inflammatory mediators, including cytokines, chemokines and enzymes, in the tumor microenvironment. Virus-induced tumors, like HPV-induced Squamous Cell Carcinomas, represent a paradigmatic example of the interplay between inflammation, as integral part of the innate antiviral response, and malignant transformation. Here, the role of inflammatory microenvironment in the HPV-induced carcinogenesis is addressed, with a specific focus on the involvement of the immune molecules as well as their delivery through the microvesicle cargo possibly correlated to the different HPV genotype. The expression of the inflammatory mediators in HPV positive cells has been analyzed in primary human foreskin keratinocytes and keratinocytes transduced by E6 and E7 from mucosal HPV-16 or cutaneous HPV-38 genotypes. HPV E6 and E7 proteins can modulate the expression of immune mediators in HPV-infected cells and can affect the levels of immune molecules, mainly chemokines, in the extracellular milieu. HPV-16 E6 and E7 oncoproteins have been silenced to confirm the specificity of the modulation of the inflammatory microenvironment. Our results suggest that the expression of HPV oncoproteins allows the modification of the tumor milieu through the synthesis and release of specific pro-inflammatory cytokines and chemokines, affecting the efficacy of the immune response. The microenvironment can also be conditioned by an altered mRNA cargo delivered by extracellular vesicles, thereby efficiently affecting the surrounding cells with possible implication for tumorigenesis and tumor diagnosis.

Human Papilloma Viruses (HPVs) are the causative agents of cervical cancer although other types of cancers are associated with HPV infection. Type I Interferons can interfere with HPV E6- and/or E7-dependent transformation and can affect microRNA (miRNA) expression. Cancer cells show a specific pattern of miRNA expression and HPVs are able to modulate miRNAs expressed in infected cells. Keratinocytes transduced with E6 and E7 from mucosal HPV-16 or cutaneous HPV-38 (K16 and K38) were studied to analyze the involvement of HPV oncoproteins in the anti-proliferative activity of IFN-β. In view of our previous data showing senescence induction by the cytokine in K38 cells, we observe that IFN-β treatment leads to p53-indipendent apoptosis in K16 cells whereas induces senescence in K16 cells if E6 is silenced and p53 expression is restored. The levels of selected miRNAs, deregulated in K16 and K38 cells, can be modulated by IFN-β when E6 and E7 proteins of HPV-16, but not HPV-38, are expressed.

More than 15% of the global cancer burden is attributable to infectious agents. Pathogens that cause persistent infections are strongly associated with cancer, inflammation being a major component of the chronic infections as revealed by basic, clinical and epidemiological studies. Persistent infection and viral oncoproteins induce specific cellular pathways modifications that promote tumorigenesis. Deregulated and continuous immune response leads to severe tissue and systemic damage, impaired tumor surveillance and consequent carcinogenesis promotion by selecting for metastatic and therapeutically resistant tumor phenotypes. In this review, the role of inflammatory microenvironment in the HPV-induced carcinogenesis is addressed, with a specific focus on the involvement of the immune molecules and microRNAs as well as their delivery through the microvesicle cargo.

Human papillomaviruses (HPVs) are the causative agents of cervical cancer and are also associated with other types of cancers. HPVs can modulate microRNAs (miRNAs) expressed by infected cells. The production of extracellular vesicles is deregulated in cancer, and their cargo delivered to the microenvironment can promote tumorigenesis. The involvement of HPV oncoproteins on miRNA expression in cells and exosomes was analyzed in keratinocytes transduced with E6 and E7 from mucosal HPV-16 or cutaneous HPV-38 (K16 and K38).MiRNAs were investigated through the TaqMan Array Human MicroRNA Cards, followed by real-time RT-PCR assay for specific miRNAs. Selected miRNA targets were analyzed by Western blot and correlated to the HPV oncoproteins by specifically silencing E6 and E7 expression. Exosomes, isolated from K16 and K38 supernatants by differential centrifugations, were quantified through the vesicle-associated acetylcholinesterase activity.MiRNAs deregulated in K16 and K38 cells were identified. HPV-16 and/or HPV-38 E6 and E7 single proteins can modify the expression of selected miRNAs involved in the tumorigenesis, in particular miR-18a, -19a, -34a and -590-5p. The analysis of the content of exosomes isolated from HPV-positive cells revealed the presence of E6 and E7 mRNAs and few miRNAs. MiR-222, a key miRNA deregulated in many cancers, was identified in exosomes from K16 cells.HPV E6 and/or E7 oncoprotein expression can induce the deregulation of some miRNAs. Through the production and function of exosomes, HPV oncogenes as well as HPV-deregulated miRNAs can potentiate the virus oncogenic effects in the tumor cell microenvironment.

The inception of tumor microenvironment (TME), a complex and dynamic system constituted by different types of cells engaged by tumor and extracellular matrix surrounding cancer cells, is a way for them to elude the immune surveillance. Dendritic cells (DCs), as a sentinel, are able to recognize alteration in the microenvironment and predispose the immune system response. The relationship between cancer and virus infection is well documented. High-risk Human Papillomavirus (HR-HPV) has a well-characterized transforming property and has been associated with squamous cell carcinoma of the ano-genital and oral tracts. Transforming ability of HR-HPVs is based on the function of E6 and E7 viral oncoproteins, which interact and inactivate p53 and pRb oncosuppressors, respectively. Recently, it was demonstrated that HPV oncoproteins are also able to affect a number of microRNAs (miRNAs) regulating the expression of genes involved in proliferative control. For these reasons DC-based vaccines targeting oncogenic E6 and E7 are ideal candidates to elicit strong immune responses. Here we summarize significant data about the analysis of TME in HPV-induced tumorigenesis. We also report original results produced by cytotoxic T lymphocyte (CTL) in vitro priming against E6 and E7 HPV16 antigens, performed using human monocyte-derived dendritic cells. Dendritic cells, maturated by the exposition to necrotic or apoptotic keratinocytes expressing both oncoproteins of HPV16, show different expression levels of specific maturation markers. Evidence indicating the ability of necrotic keratinocytes to alter the microRNA profile in DCs, macrophages (MΦ) and Langerhans cells (LCs) compared to prototypical stimuli as bacterial lipopolysaccharide was also provided. We can speculate that, based on transformed cells death pathway (i.e. apoptosis versus necrosis), virus-induced immune alterations might show different results in creating an immunotolerogenic microenvironment during the carcinogenesis process.

Inflammation is a critical component of tumorigenesis. Tumor microenvironment participates in the neoplastic process fostering proliferation, survival and migration. Virus-induced tumors, like HPV-induced Squamous Cell Carcinomas, represent a paradigmatic example of the interplay between inflammation, as integral part of the innate antiviral response, and malignant transformation. To study the tumorigenic role of inflammatory mediators in HPV + cells, we analyzed by real time RT-PCR the expression of selected inflammatory cytokines, chemokines and related molecules in human foreskin keratinocytes transduced by E6 and E7 from mucosalHPV-16 (K16) or cutaneousHPV-38 (K38) genotypes comparing them to primary Human Foreskin Keratinocytes. We also performed silencing experiments by using E6/E7 siRNA in HPV + SiHa carcinoma cells to verify the involvement of the viral proteins. IL-1 α and IL-1 β mRNAs are downregulated in K16 and K38 cells, whereas IL-1R1 mRNA level is comparable in all cell lines. IL-6 mRNA level is unchanged in K16 and downregulated in K38. E6/E7 silencing in SiHa confirms the effect specificity. MIP-3 α , CCL-17 and CCl-22 mRNA levels in K16 cells are also deregulated. Deregulation of MIP-3 α mRNA appears to be related to miR-21 over-expression detected in both K16 and K38. The effect of the IFN- β on the levels of these pro-inflammatory mediators will be also discussed. Experiments on paraffin embedded tissues are in progress to verify MIP-3 α deregulation in vivo. Our results suggest that HPV is able to modify the tumor microenvironment through the synthesis and release of specific pro-inflammatory cytokines and chemokines possibly to interfere with the leucocytes trafficking and/or allowing a better tumor growth and infiltration.

A partire dagli anni settanta del Quattrocento si sviluppa in Italia un grande interesse per il «ritratto » di città. Venezia, Napoli, Firenze, Roma e le principali capitali europee sono riprodotte in dipinti su tavola, incisioni e affreschi che si diffondono rapidamente. Per Napoli la prima immagine di questo tipo è senza dubbio la nota Tavola Strozzi, ma per osservare il prototipo di veduta replicato fino al Settecento bisognerà attendere quasi un secolo, quando verranno incise le vedute di Carlo Theti (1560) e Dupérac-Lafréry (1566). La rappresentazione di Napoli oggetto del presente studio è parte del ricco ciclo di affreschi commissionato da Gentile Virginio Orsini, capitano della flotta pontificia, di ritorno dalla vincente spedizione di Tunisi (1535). Orsini fa rappresentare nella sala maggiore del suo palazzo di Anguillara Sabazia il «ritratto » di Napoli, che ha un duplice valore documentario : costituisce il più antico esempio dell’impostazione in pianta assonometrica della città e restituisce l’immagine della struttura urbana rinascimentale alla vigilia dei consistenti interventi che saranno attuati dal vicerè Pedro de Toledo., Iuliano Marco. Napoli a volo d’uccello. Un affresco per lo studio della topografia aragonese. In: Mélanges de l'École française de Rome. Italie et Méditerranée, tome 113, n°1. 2001. Alle origini della biografia femminile : dal modello alla storia. Actes du colloque organisé par le Dipartimento di storia dell’Università degli studi di Firenze, l’École française de Rome et le Comune di Firenze «Progetto donna», Florence 11 et 12 juin 1999. pp. 287-311.

Lo scritto descrive l'architettura del LIdo delle Sirene sul litorale di Bagnoli attraverso le fotografie dell'Archivio Parisio di Napoli.

La storia dell'Accademia Aeronautica di Pozzuoli attraverso le fotografie dell'Archivio Parisio di Napoli