S100B Induces the Release of Pro-Inflammatory Cytokines in Alveolar Type I-like Cells

Piazza, Ornella; Leggiero, Eleonora; Benedictis, G. De; Pastore, Lucio; Salvatore, Francesco; Tufano, R; Robertis, Edoardo De

doi:10.1177/039463201302600211

Cited by 30 publications

(19 citation statements)

References 36 publications

(47 reference statements)

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“…In the case of dendritic and lymphoid cell types, their role in in ammatory processes is widely known [34,35], so that the mechanistic involvement of S100B in their function would merely increase the breadth of knowledge in this respect. It is interesting to note that, under pulmonary in ammation, S100B has been reported to be upregulated in bronchiolar epithelial cells and airway dendritic cells [36,37]. Moreover, as shown in alveolar cell types, S100B can stimulate the secretion of pro-in ammatory cytokines, that are commonly involved in lung in ammation, following a similar process suspected to be present also in Covid-19 [19][20][21][22]36,37].…”

Section: Discussionmentioning

confidence: 83%

“…It is interesting to note that, under pulmonary in ammation, S100B has been reported to be upregulated in bronchiolar epithelial cells and airway dendritic cells [36,37]. Moreover, as shown in alveolar cell types, S100B can stimulate the secretion of pro-in ammatory cytokines, that are commonly involved in lung in ammation, following a similar process suspected to be present also in Covid-19 [19][20][21][22]36,37]. Additional studies will be needed in order to de ne the source of serum S100B in patients affected by SARS-CoV-2, but the nding of increased serum levels of the protein, correlated with the gravity of the disease and in ammatory processes, offers a novel biomarker potentially useful to monitor the disease.…”

Section: Discussionmentioning

confidence: 99%

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Serum S100B protein as a marker of severity in Covid-19 patients

Aceti

Margarucci

Scaramucci

et al. 2020

Preprint

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SARS-CoV-2 infection shows a wide-ranging clinical severity, requiring prognostic markers. We focused on S100B, a calcium-binding protein present in biological fluids, being a reliable biomarker in disorders having inflammatory processes as common basis and RAGE as main receptor. Since Covid-19 is characterized by a potent inflammatory response also involving RAGE, we tested if S100B serum levels were related to disease severity.Serum samples (n=74) were collected from hospitalized SARS-CoV-2 positive patients admitted to Covid center. Illness severity was established by admission clinical criteria and Covid risk score. Treatment protocols followed WHO guidelines available at the time. Circulating S100B was determined by ELISA assay. Statistical analysis used Pearson’s χ2 test, t-Test, and ANOVA, ANCOVA, Linear Regression.S100B was detected in serum from Covid-19 patients, significantly correlating with disease severity as shown both by the level of intensity of care (p<0.006) as well by the value of Covid score (Multiple R-squared: 0.3751); the correlation between Covid-Score and S100B was 0.61 (p<0.01). S100B concentration was associated with inflammation markers (Ferritin, C-Reactive Protein, Procalcitonin), and organ damage markers (Alanine Aminotransferase, Creatinine). Serum S100B plays a role in Covid-19 and can represent a prognostic marker in Sars-CoV-2 infected patients.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Serum S100B protein as a marker of severity in Covid-19 patients

Aceti

Margarucci

Scaramucci

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…Nanomolar S100B concentrations produce low amounts of signaling oxygen radicals that lead to the activation of the anti-apoptotic factor Bcl-2 ). In contrast, toxic/proinflammatory effects have been shown to be induced by S100B at high (micromolar) concentrations Lam et al 2001;Valencia et al 2004;Schmitt et al 2007;Piazza et al 2013;Fujiya et al 2014;Niven et al 2015). Persistent activation of RAGE by micromolar concentrations of S100B produces increased amounts of oxygen radicals, and this could lead to mitochondrial dysfunction and induction of apoptosis.…”

Section: S100b As An Active Factor In Neural Injurymentioning

confidence: 99%

The S100B story: from biomarker to active factor in neural injury

Michetti

D’Ambrosi

Toesca

et al. 2018

Journal of Neurochemistry

290

238

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S100B is a Ca -binding protein mainly concentrated in astrocytes. Its levels in biological fluids (cerebrospinal fluid, peripheral and cord blood, urine, saliva, amniotic fluid) are recognized as a reliable biomarker of active neural distress. Although the wide spectrum of diseases in which the protein is involved (acute brain injury, neurodegenerative diseases, congenital/perinatal disorders, psychiatric disorders) reduces its specificity, its levels remain an important aid in monitoring the trend of the disorder. Mounting evidence now points to S100B as a Damage-Associated Molecular Pattern molecule which, when released at high concentration, through its Receptor for Advanced Glycation Endproducts, triggers tissue reaction to damage in a series of different neural disorders. This review addresses this novel scenario, presenting data indicating that S100B levels and/or distribution in the nervous tissue of patients and/or experimental models of different neural disorders, for which the protein is used as a biomarker, are directly related to the progress of the disease: acute brain injury (ischemic/hemorrhagic stroke, traumatic injury), neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis), congenital/perinatal disorders (Down syndrome, spinocerebellar ataxia-1), psychiatric disorders (schizophrenia, mood disorders), inflammatory bowel disease. In many cases, over-expression/administration of the protein induces worsening of the disease, whereas its deletion/inactivation produces amelioration. This review points out that the pivotal role of the protein resulting from these data, opens the perspective that S100B may be regarded as a therapeutic target for these different diseases, which appear to share some common features reasonably attributable to neuroinflammation, regardless their origin.

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“…In normal physiological concentrations, S100B has been shown to have trophic effects on neurons, but following injury and rise in concentration, this protein could exacerbate the damage. Increased S100B secretion also induces interleukin-6 (IL-6) secretion in CSF, which has been shown to contribute to neuroinflammation and further damage (Piazza et al , 2013). S100B also functions as an inhibitor of glial fibrillary acidic protein (GFAP), the structural intermediate filament (IF) exclusive to astrocytes, by inhibiting the phosphorylation and assembly of GFAP (Sorci et al , 1998).…”

Section: Csf Biomarkers For Hiv/neuroaidsmentioning

confidence: 99%

HIV/neuroAIDS biomarkers

Rahimian

2017

Progress in Neurobiology

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HIV infection often causes neurological symptoms including cognitive and motor dysfunction, which have been collectively termed HIV/neuroAIDS. Neuropsychological assessment and clinical symptoms have been the primary diagnostic criteria for HIV/neuroAIDS, even for the mild cognitive and motor disorder, the most prevalent form of HIV/neuroAIDS in the era of combination antiretroviral therapy. Those performance-based assessments and symptoms are generally descriptive and do not have the sensitivity and specificity to monitor the diagnosis, progression, and treatment response of the disease when compared to objective and quantitative laboratory-based biological markers, or biomarkers. In addition, effects of demographics and comorbidities such as substance abuse, psychiatric disease, nutritional deficiencies, and co-infection on HIV/neuroAIDS could be more readily determined using biomarkers than using neuropsychological assessment and clinical symptoms. Thus, there have been great efforts in identification of HIV/neuroAIDS biomarkers over the past two decades. The need for reliable biomarkers of HIV/neuroAIDS is expected to increase as the HIV-infected population ages and their vulnerability to neurodegenerative diseases, particularly Alzheimer’s disease increases. Currently, three classes of HIV/neuroAIDS biomarkers are being pursued to establish objective laboratory-based definitions of HIV-associated neurologic injury: cerebrospinal fluid biomarkers, blood biomarkers, and neuroimaging biomarkers. In this review, we will focus on the current knowledge in the field of HIV/neuroAIDS biomarker discovery.

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S100B Induces the Release of Pro-Inflammatory Cytokines in Alveolar Type I-like Cells

Cited by 30 publications

References 36 publications

Serum S100B protein as a marker of severity in Covid-19 patients

Serum S100B protein as a marker of severity in Covid-19 patients

The S100B story: from biomarker to active factor in neural injury

HIV/neuroAIDS biomarkers

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