Ivana Marventano

Don Carlo Gnocchi Foundation

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Marina Saresella

Don Carlo Gnocchi Foundation

Mario Clerici

University of Milan

Federica Piancone

University of Foggia

Francesca La Rosa

Don Carlo Gnocchi Foundation

Domenico Caputo

Sapienza University of Rome

Marco Rovaris

Don Carlo Gnocchi Foundation

Raffaello Nemni

Don Carlo Gnocchi Foundation

Laura Mendozzi

Don Carlo Gnocchi Foundation

Franca Rosa Guerini

Don Carlo Gnocchi Foundation

Ambra Hernis

Don Carlo Gnocchi Foundation

Cooperative Institutions

University of Milan

108

Istituti di Ricovero e Cura a Carattere Scientifico

Don Carlo Gnocchi Foundation

Charité - Universitätsmedizin Berlin

German Rheumatism Research Centre

Leibniz Association

Humboldt-Universität zu Berlin

Freie Universität Berlin

Institute of Immunology

Inserm

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Increased Levels of Beta-Endorphin and Noradrenaline after a Brief High-Impact Multidimensional Rehabilitation Program in Multiple Sclerosis

Life (2022)

Alessia d’Arma Marina Saresella Valentina Rossi Ivana Marventano Federica Piancone

Finding new solutions for the management of multiple sclerosis (MS) is crucial: further research is needed to study the effect of non-pharmacological interventions on the symptoms and the course of the disease, especially on lifestyle. Benefits from a proper lifestyle are evident not only on a clinical level but also on immune and neuro-endocrine systems. A brief high-impact multidimensional rehabilitation program (b-HIPE) was proposed for a sample of people with MS (pwMS) with a medium level of disease disability. We tested the change on clinical parameters and quality of life (QoL) after participation in B-HIPE. We furthermore decided to measure beta-endorphin and catecholamines concentrations pre- and post-participation in the b-HIPE program, due to the relationship between these hormones and the immune system in neurodegenerative diseases. Our results showed that after the b-HIPE program, an improvement of clinical parameters and QoL occurred. Moreover, we found higher levels of beta-endorphin and noradrenaline after participation in the program. These findings highlight the importance of implementing lifestyle interventions in the clinical management of MS. Furthermore, we hypothesize that the B-HIPE program increased beta-endorphin and noradrenaline levels, helping to reduce the inflammation related to MS disease.

10.3390/life12050755

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Herpes simplex virus-1 (HSV-1) infection induces a potent but ineffective IFN-λ production in immune cells of AD and PD patients

Journal of Translational Medicine (2019)

Francesca La Rosa Simone Agostini Anna Bianchi Raffaello Nemni Federica Piancone

The sequential activation of immediate early (IE), early (E) and late (L) genes is required to allow productive herpes simplex virus type 1 (HSV-1) infection. Several evidences suggest that, together with inflammation, an immunological response incapable to counteract HSV-1 reactivation plays a role in the pathogenesis of Alzheimer's (AD) and Parkinson's (PD) diseases. IFN-lambda (IFN-λ), a cytokine endowed with a robust antiviral activity, contains HSV-1 reactivation. HSV-1-induced IFN-λ, IL-10 and IL-1β as well as the expression of viral IE, E and L genes were analyzed in vitro in peripheral blood mononuclear cells (PBMC) of AD and PD patients as well as of healthy controls (HC). PBMC of AD, PD and HC were in vitro infected with one multiplicity of infection (1 MOI) HSV-1. IE, E, and L viral genes transcription as well as IFN-λ, IL-10 and IL-1β production were analyzed. In HSV-1-infected cells of AD and PD patients compared to HC: (1) transcription of IE (ICP0, ICP27) genes was reduced whereas that of E (UL41, UL29) and L (UL48, LAT) genes was increased; (2) IFN-λ mRNA expression was increased. IL-1β was augmented and IL-10 was reduced in unstimulated cells of AD and PD compared to HC; HSV-1 infection significantly increased IL-10 production in HC alone. Data herein show that a proinflammatory condition is present in AD and PD, in whom attempts to obstacle viral replication via an initial, possibly more potent IFN-λ-mediated control of IE viral genes is unsuccessful.

Multiplicity of infection

Proinflammatory cytokine

Pathogenesis

10.1186/s12967-019-2034-9

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Citations (15)

FoxP3 mRNA Expression in Regulatory T Cells from Patients with Tuberculosis

American Journal of Respiratory and Critical Care Medicine (2006)

Lidia Gazzola Camilla Tincati Andrea Gori Marina Saresella Ivana Marventano

We read with great interest the article by Guyot-Revol and colleagues (1) assessing the role of T regulatory cells (Tregs) in tuberculosis (TB) pathogenesis. Guyot-Revol and coworkers found that in patients with TB, percentages of CD4 CD25 T cells and levels of FoxP3 mRNA expression in peripheral blood mononuclear cells were both significantly higher in comparison with controls. To better comprehend Tregs’ mechanism of action, the authors investigated whether the increased levels of FoxP3 mRNA that they had observed were effectively caused by increased gene expression, or were simply the result of increasedCD4 CD25high frequency.FoxP3mRNAinCD4 CD25 T cells was compared between patients with TB and control subjects. As no quantitative difference was observed, the authors suggest that the greater levels of FoxP3 mRNA are simply an effect of increases in Treg frequency rather than a result of an up-regulated gene expression. The transcription factor FoxP3 is the most specific molecular marker for Tregs available to date, and its correct evaluation is crucial (2–4). In the analysis of Treg dynamics, an assessment of what happens in the frequency and level of FoxP3 mRNA expression at the single cell level is mandatory. The recent literature demonstrates a strong correlation between levels of CD25 expression and the frequency of FoxP3-positive cells in healthy donors (4), and suggests that to correctly evaluate FoxP3 expression in Tregs, mRNA should be quantified in CD4 CD25 rather than in CD4 CD25 T cells (5). We are currently performing a prospective study to evaluate Tregs in patients with TB. Analysis of CD4 CD25 percentage on CD4 T cells at TB diagnosis showed similar levels of Tregs among patients with TB and controls (median percentage: 2.1% [IQR, 1.8–6.6] vs. 1.9% [IQR, 1.5–2.2]). Unlike Guyot-Revol and coworkers, we evaluated FoxP3 mRNA expression by real-time polymerase chain reaction in CD4 CD25 T cells, purified using an EPICSALTRACell Sorter (Beckman-Coulter; purity 93.6%). A considerable increase of FoxP3 mRNA expression in patients with TB with respect to control subjects was clearly observed (median: 39.1 [IQR, 5.1–109] vs. 1.6 [IQR, 0.8–2.8]; p 0.0062). These data implicate FoxP3 gene overexpression as a probable mechanism involving Tregs in the pathogenesis of TB, and suggest a possible role of FoxP3 gene up-regulation in the outcome of chronic infections. Our results underscore the importance of using the correct methodology in evaluating Treg cell dynamics, and prove that an accurate evaluation of FoxP3 mRNA expression in Treg cells may lead to the identification of previously unknown mechanisms of Treg cell involvement in disease pathogenesis.

Expression (computer science)

10.1164/ajrccm.174.3.356

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Citations (12)

P3‐115: Neuroinflammation Correlates with Hippocampus Atrophy in Alzheimer’s Disease

Alzheimer s & Dementia (2016)

Marina Saresella Francesca Baglio Monica Cabinio Federica Piancone Francesca La Rosa

The pathogenesis of Alzheimer's disease (AD) is characterized by two alterations that are the consequence of b-amyloid accumulation: neuroinflammation and hippocampus atrophy. We investigated possible correlations between these two AD-associated phenomena using structural Magnetic Resonance Imaging (MRI) to evaluate hippocampal volume (Hv) and immunologic analyses to analyze neuroinflammation. Immunological analyses were performed using peripheral blood mononuclear cells; MRI analyses were based on high resolution 3D images acquired on a 1.5 T scanner using dedicated softwares (FSL – First). Results obtained in 30 AD individuals showed the presence of statistically significant: 1) positive correlations between left Hv and b-amyloid-stimulated CD14+ cells that produce IL-10 producing or express CD200; and 2) negative correlation between left Hv and b-amyloid specific-CD4+ ROR+ T cells. These correlations are immunologically sound as: 1) Interleukin -10 is an anti-inflammatory cytokine; 2) the interaction of CD200 protein with CD200R, its receptor, on glia cell, inhibits immune stimulatory responses in CNS and enhance microglia-mediated b-amyloid clearance; and 3) CD4+ ROR+ T cells identify the proinflammatory TH17 subset of circulating lymphocytes. The observation that reduced Hv correlates with an impairment of anti-inflammatory b-amyloid -specific peripheral monocytes and, conversely, with a higher percentage of circulating proinflammatory TH17 b-amyloid-specific T lymphocytes strongly suggest that neuroinflammation and hippocampus atrophy are indeed correlated in AD and indicate that monitoring of immune cells in peripheral blood could have a prognostic value in this disease.

10.1016/j.jalz.2016.06.1773

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TH17-Driven Inflammation is Present in All Clinical Forms of Multiple Sclerosis; Disease Quiescence is Associated with Gata3-Expressing Cells

European Journal of Inflammation (2013)

Marina Saresella Paola Tortorella Ivana Marventano Nasser M. Al‐Daghri Federica Piancone

Multiple Sclerosis (MS) presents in a variety of clinical forms associated with a diverse grade of neurological impairment, different prognosis and, possibly, multiple pathogenic mechanisms. Thus, whereas relapsing-remitting (RR) MS appears to be largely driven by inflammatory processes, neurodegeneration, partially independent from inflammation, drives primary progressive (PP) and secondary progressive (SP) MS. An extensive analysis of neuroinflammation in the different forms of MS was performed by evaluating immunophenotypic and functional parameters in MBP-stimulated T lymphocytes of 103 MS patients (26 benign (BE) MS, 30 RRMS, 33 SPMS and 14 PPMS) and 40 healthy controls (HC). Results showed that: i) IL-17-producing and RORC/γt-expressing CD4+ T cells (TH17 lymphocytes), as well as IL-6 expressing CD14+ cell were augmented in all patients; ii) IL-22-expressing cells were increased in all forms of MS with the exception of PPMS; iii) TGF-β-expressing B cells were increased only in RRMS; and iv) GATA3-, NFATc-1, IL-13-, and IL-25-expressing cells (TH2 lymphocytes) were augmented in RRMS and BEMS patients alone. Data herein indicate a pivotal pathogenic role of TH17-driven inflammation in all clinical forms of MS and suggest that control over disease (RRMS and BEMS) is associated not with lack of inflammation per se, but rather with the activation of immune-mediated anti-inflammatory mechanisms. These results could help the design of novel diagnostic and therapeutic approaches.

GATA3

10.1177/1721727x1301100121

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Citations (7)

Muscle & Nerve (2011)

M. Gironi Marina Saresella Ivana Marventano Franca Rosa Guerini Andrea Gatti

Foundation (evidence)

10.1002/mus.22064

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Glibenclamide-Loaded Nanoparticles Reduce NLRP3 Inflammasome Activation and Modulate miR-223-3p/miR-7-1-5p Expression in THP-1 Cells

Pharmaceuticals (2023)

Roberta Mancuso Lorenzo Agostino Citterio Simone Agostini Ivana Marventano Francesca La Rosa

The anti-hyperglycemic drug glibenclamide (Glb) might represent an interesting therapeutic option in human neurodegenerative diseases because of its anti-inflammatory activity and its ability to downregulate activation of the NLRP3 inflammasome. Bi-functionalized liposomes that can cross the blood-brain barrier (BBB) may be used to release Glb into the central nervous system (CNS), overcoming its poor solubility and bioavailability. Here, we analyzed in vitro the effect of Glb-loaded nanovectors (GNVs) and Glb itself on NLRP3 inflammasome activation using a lipopolysaccharide- and nigericine-activated THP-1 cell model. Apoptosis-associated speck-like protein containing a CARD (ASC) aggregation and NLRP3-related cytokine (IL-1β, caspase 1, and IL-18) production and gene expression, as well as the concentration of miR-223-3p and miR-7-1-5p, known to modulate the NLRP3 inflammasome, were evaluated in all conditions. Results showed that both GNVs and Glb reduced significantly ASC-speck oligomerization, transcription and translation of NLRP3, as well as the secretion of caspase 1 and IL-1β (p < 0.05 for all). Unexpectedly, GNVs/Glb significantly suppressed miR-223-3p and upregulated miR-7-1-5p expression (p < 0.01). These preliminary results thus suggest that GNVs, similarly to Glb, are able to dampen NLRP3 inflammasome activation, inflammatory cytokine release, and modulate miR-223-3p/miR-7-1-5p. Although the mechanisms underlying the complex relation among these elements remain to be further investigated, these results can open new roads to the use of GNVs as a novel strategy to reduce inflammasome activation in disease and rehabilitation.

THP1 cell line

Proinflammatory cytokine

10.3390/ph16111590

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Citations (3)

Increased activity of Th-17 and Th-9 lymphocytes and a skewing of the post-thymic differentiation pathway are seen in Alzheimer’s disease

Brain Behavior and Immunity (2010)

Marina Saresella Elena Calabrese Ivana Marventano Federica Piancone Andrea Gatti

10.1016/j.bbi.2010.12.004

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Citations (174)

Neuroinflammation and Brain Functional Disconnection in Alzheimer’s Disease

Frontiers in Aging Neuroscience (2013)

Francesca Baglio Marina Saresella Maria Giulia Preti Monia Cabinio Ludovica Griffanti

Neuroinflammation and brain functional disconnection result from β-amyloid (Aβ) accumulation and play fundamental roles in the pathogenesis of Alzheimer's disease (AD). We investigated possible correlations between these two AD-associated phenomena using DTI-based tractography and immunologic analyses in people with amnestic mild cognitive impairment (aMCI) and AD. DTI-Analyses focused on corpus callosum (CC). We found that frontal CC regions were preserved with respect to the posterior ones in aMCI; in these individuals significant correlations were seen between DTI-derived metrics in frontal-parietal CC areas and Aβ42-stimulated BDNF-producing CD4+ T lymphocytes and PDL-1-expressing CD14+ cells. These associations were lost in AD where DTI data involving the same CC areas correlated instead with Aβ42-stimulated interleukin (IL)-21 producing CD4+ T lymphocytes. Higher susceptibility to PDL-1-mediated apoptosis of Aβ42-specific lymphocytes and BDNF-associated survival of existing neurons could contribute to the relative CC structure preservation seen in aMCI. These potentially protective mechanisms are lost in frank AD, when severe alterations in the CC are mirrored in peripheral blood by proinflammatory cytokines-producing T cells. Monitoring of immune cells in peripheral blood could have a prognostic value in AD.

Disconnection

Proinflammatory cytokine

Pathogenesis

10.3389/fnagi.2013.00081

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Citations (27)

P2‐179: STAVUDINE INHIBITS INFLAMMASOME ACTIVATION MOLECULAR INHIBITOR IN PERIPHERAL‐MONOCYTES OF AD PATIENTS

Alzheimer s & Dementia (2018)

Francesca La Rosa Marina Saresella Federica Piancone Ivana Marventano Chiara Fenoglio

Alzheimer's disease(AD) is a chronic neuroinflammation disorder and the first cause of dementia. Deposition of phospho tau(τ) and beta-amyloid(Aß) plaques-formed possibly as a consequence of an impairment of Aß-phagocytosis-are the core neuropathological features of AD; this is accompanied by neuroinflammation. Recent results demonstrated that neuroinflammation in AD is driven by the activation of the NLRP3 inflammosome, resulting in the downstream production of Caspase1, IL1ß and IL18. We verified whether NLRP3 activation is also involved in altering Aß-phagocytosis, and if Stavudine, a well known antiviral originally used in HIV infection, could dampen NLRP3 activation and increase Aß-clearence in human peripheral monocytes of AD patients Twenty AD patients (MMSE 19±1.9) characterized by Apo E genotype, Aß42, P-T and total T CSF levels were selected within a cohort of well characterized individuals; results were compared to those of 20 healthy sex and age matched healthy controls(HC). Mechanisms regulating inflammasome signaling involves the priming signal to upregulate the expression of NLRP3 and signal 2 to activate the functional NLRP3; thus monocytes were either primed with LPS(1mg/ml for 2h) and stimulated with Aß42 AlexaFluor488 (FAM)-labeled (10mg/ml) for 24h or stimulated with Aß42 FAM alone for 24h in the presence/absence of Stavudine (50mM) for 22h. Aß-phagocytosis was analyzed by Imagines–FlowCitometry; caspase1 and cytokines were quantified by ELISA. Results showed that: 1) Caspase1, IL1ß and IL18 production by LPS and Aß42 stimulated monocytes of AD patients was significantly increased compared to HC (for all p<0.05); 2) Aß-phagocytosis was significantly reduced in LPS-primed and Aß42 stimulated cells of AD and HC individuals compared to those stimulated with Aß42 alone (for both p<0.05); 3) Stavudine resulted in a drastic reduction of Caspase1, IL1ß and IL18 production (p<0.05) but did not modify the Aß-phagocytosis capacity of monocytes. NLRP3 inflammasome-driven inflammation reduces monocytes mediated Aß phagocytosis in AD and HC. Stavudine dampens NLRP3 activation and downstream inflammation but does not significantly modify Aß-phagocytosis. These results suggest that, even if Stavudine could be useful in modulating neuroinflammation in AD, AD-associated impairments in Aß-phagocytosis are not a consequence of a direct consequence of inflammation.

Stavudine

10.1016/j.jalz.2018.06.866

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