Ines Benedetti

Dr. Ines Benedetti

Medicine, Universidad de Cartagena, Cartagena, Bolívar, Colombia
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Research Focus & Metrics

Academic Career Length

14Years (2013-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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5 December 2013 in International Archives of Allergy and Immunology
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JJJosefina Josefina
Josefina Josefina
IBInes Benedetti
Ines Benedetti
EFEnrique Fernández-Caldas
Enrique Fernández-Caldas
LCLuis Caraballo
Luis Caraballo
Background: Information about the biological properties of Blomia tropicalis allergens is scarce. It is predicted that Blo t 12, an allergen with two described isoforms, contains a chitin-binding domain, similar to that found in peritrophins. Th2 adjuvant properties have been described for chitin. Therefore, it is feasible that binding to this carbohydrate influences its allergenicity. We aimed to evaluate the chitin-binding activity of Blo t 12 isoallergens and its effect on airway inflammation and antibody responses in a murine model of allergen sensitization. Methods: Chitin-binding assays were conducted with the recombinant isoallergens Blo t 12.0101 and Blo t 12.0102. BALB/c mice were sensitized via i.p. with any of the two isoforms (alone, with chitin or alum) and then challenged intranasally. Methacholine-induced bronchial hyperreactivity was tested by whole-body plethysmography and lung sections were stained with hematoxylin and eosin and periodic-acid Schiff. Total IgE and allergen-specific IgE, IgG1 and IgG2 levels were measured by ELISA. Results: The two isoforms bound chitin, but Blo t 12.0101 showed a stronger binding capacity. Both isoforms induced total and allergen-specific IgE, airway hyperreactivity, bronchial inflammation and mucus secretion without any adjuvant; however, when administered with chitin, Blo t 12.0101 induced higher total IgE levels. The IgG1/IgG2a ratio was significantly higher in mice immunized with Blo t 12.0101 than those immunized with Blo t 12.0102. As peritrophins, Blo t 12 was detected in mite feces. Conclusions: Blo t 12 isoforms are chitin-binding proteins that induce airway inflammation and bronchial hyperreactivity. However, for Blo t 12.0101, chitin reinforces its effects on total IgE production.

18 January 2016 in Cancer Biomarkers
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NRNiradiz Reyes
Niradiz Reyes
IBInes Benedetti
Ines Benedetti
ABAlfonso Bettin
Alfonso Bettin
JRJuan Rebollo
Juan Rebollo
JGJan Geliebter
Jan Geliebter
BACKGROUND: Fibromodulin is a small leucine-rich proteoglycan important for extracellular matrix organization and essential for tissue repair in multiple organs. The main function of this proteoglycan is the regulation of collagen fibrillogenesis; ho

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EMErnesto Carlos Mondol Miranda
Ernesto Carlos Mondol Miranda
Karen DonadoKaren Donado
Karen Donado
RRRonald Regino
Ronald Regino
KVkaren margerita hernandez villar
karen margerita hernandez villar
DMDilia Mercado
Dilia Mercado
LCLuis Caraballo
Luis Caraballo
Only few allergens derived from house dust mite (HDM) species have been evaluated in terms of their potential to induce allergic inflammation. In this study, we aimed to evaluate different aspects of the allergenicity and allergenic activity of Blo t 2, a Blomia tropicalis allergen. Blo t 2 was produced as a recombinant protein in Escherichia coli. Its allergenic activity was tested in humans by skin prick test and basophil activation assays, and in mice, by passive cutaneous anaphylaxis and a model of allergic airway inflammation. Sensitization rate to Blo t 2 (54.3%) was similar to that found to Blo t 21 (57.2%) and higher than to Der p 2 (37.5%). Most Blo t 2-sensitized patients showed a low intensity response (99.5%). Blo t 2 elicited CD203c upregulation and allergen induced skin inflammation. Additionally, immunized animals produced anti-Blo t 2 IgE antibodies and passive transfer of their serum to non-immunized animals induced skin inflammation after allergen exposure. Immunized animals developed bronchial hyperreactivity and a strong inflammatory lung reaction (eosinophils and neutrophils). These results confirm the allergenic activity of Blo t 2 and supports its clinical relevance.

1 October 2016 in Annals of Diagnostic Pathology
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Journal Article
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IBInes Benedetti
Ines Benedetti
ABAlfonso Bettin
Alfonso Bettin
NRNiradiz Reyes
Niradiz Reyes

1 August 2017 in International Journal of Experimental Pathology
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IBInes Benedetti
Ines Benedetti
AMAngelo M. De Marzo
Angelo M. De Marzo
JGJan Geliebter
Jan Geliebter
NRNiradiz Reyes
Niradiz Reyes

24 June 2020 in Cancer Prevention Research
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LHLauren Hurwitz
Lauren Hurwitz
IKIbrahim Kulac
Ibrahim Kulac
BGBerrak Gumuskaya
Berrak Gumuskaya
JVJavier A. Baena Del Valle
Javier A. Baena Del Valle
IBInes Benedetti
Ines Benedetti
EPElizabeth A. Platz
Elizabeth A. Platz
Aspirin and statin use may lower the risk of advanced/fatal prostate cancer, possibly by reducing intraprostatic inflammation. To test this hypothesis, we investigated the association of aspirin and statin use with the presence and extent of intraprostatic inflammation, and the abundance of specific immune cell types, in benign prostate tissue from a subset of men from the placebo arm of the Prostate Cancer Prevention Trial. Men were classified as aspirin or statin users if they reported use at baseline or during the 7-year trial. Presence and extent of inflammation were assessed, and markers of specific immune cell types (CD4, CD8, FoxP3, CD68, and c-KIT) were scored, in slides from end-of-study prostate biopsies taken irrespective of clinical indication, per trial protocol. Logistic regression was used to estimate associations between medication use and inflammation measures, adjusted for potential confounders. Of 357 men included, 61% reported aspirin use and 32% reported statin use. Prevalence and extent of inflammation were not associated with medication use. However, aspirin users were more likely to have low FoxP3, a T regulatory cell marker [OR, 5.60; 95% confidence interval (CI), 1.16–27.07], and statin users were more likely to have low CD68, a macrophage marker (OR, 1.63; 95% CI, 0.81–3.27). If confirmed, these results suggest that these medications may alter the immune milieu of the prostate, which could potentially mediate effects of these medications on advanced/fatal prostate cancer risk.