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Immunotherapy of experimental asthma by agonists of toll-like receptors, infection or tolerance

Abstract

Allergy prevalence and severity of asthma are increasing worldwide. Asthma is a chronic lung inflammatory syndrome and its classical phenotype is associated with deregulated activity of Thelper2 (Th2) cells. The current therapies to asthmatic patients are basically symptomatic and not therapeutic. Murine models have been developed to study asthma mechanisms and ovalbumin (OVA) is the most widely used allergen. However, OVA is considered a food- and not an airway born-allergen. Therefore, animal models of lung allergies have been adapted to airway born allergens, such as to those derived from mites present in household dust. We have recently developed an asthma model of allergic asthma using allergens from Blomia tropicalis (Bt), one of the most prevalent mite in tropical countries. Previous and recent work of our group using the OVA-model showed two potent immunotherapic mechanisms for the attenuation of allergic reactions: activation of the immune system by toll-like receptor (TLR) agonists or by mycobacteria infection and by the induction of specific- or cross-immunological tolerance. Based on these studies and in unpublished recent data we postulated that these immune mechanisms attenuate allergic responses by direct or indirect inhibition of Th2 cells' activities. I.e., our experiments with TLR agonists, infection with mycobacteria and tolerance indicate that experimental asthma could be controlled by inhibiting the development Th2 immunity or by suppressing its activities. The present project aims to outline prophylactic but mainly therapeutic applications of TLR agonists and/or mycobacteria conjunctly or not with cross-tolerance in regulating OVA or Bt-induced experimental asthma. (AU)

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Scientific publications (7)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
ALBERCA, RICARDO W.; GOMES, ELIANE; MORETTI, EDUARDO H.; RUSSO, MOMTCHILO; STEINER, ALEXANDRE A. Naturally occurring hypothermia promotes survival in severe anaphylaxis. Immunology Letters, v. 237, p. 27-32, SEP 2021. Web of Science Citations: 0.
ALBERCA, RICARDO WESLEY; GOMES, ELIANE; RUSSO, MOMTCHILO. CpG-ODN Signaling via Dendritic Cells-Expressing MyD88, but Not IL-10, Inhibits Allergic Sensitization. VACCINES, v. 9, n. 7 JUL 2021. Web of Science Citations: 0.
ALBERCA-CUSTODIO, RICARDO WESLEY; FAUSTINO, LUCAS D.; GOMES, ELIANE; NUNES, FERNANDA PEIXOTO BARBOSA; DE SIQUEIRA, MIRIAN KRYSTEL; LABRADA, ALEXIS; ALMEIDA, RAFAEL RIBEIRO; CAMARA, NIELS OLSEN SARAIVA; DA FONSECA, DENISE MORAIS; RUSSO, MOMTCHILO. Allergen-Specific Immunotherapy With Liposome Containing CpG-ODN in Murine Model of Asthma Relies on MyD88 Signaling in Dendritic Cells. FRONTIERS IN IMMUNOLOGY, v. 11, APR 23 2020. Web of Science Citations: 0.
ALBERCA CUSTODIO, RICARDO W.; MIROTTI, LUCIANA; GOMES, ELIANE; NUNES, FERNANDA P. B.; VIEIRA, RAQUEL S.; GRACA, LUIS; ALMEIDA, RAFAEL R.; CAMARA, NIELS O. S.; RUSSO, MOMTCHILO. Dendritic Cells Expressing MyD88 Molecule Are Necessary and Sufficient for CpG-Mediated Inhibition of IgE Production In Vivo. CELLS, v. 8, n. 10 OCT 2019. Web of Science Citations: 0.
NUNES, FERNANDA P. B.; ALBERCA-CUSTODIO, RICARDO WESLEY; GOMES, ELIANE; FONSECA, DENISE M.; YOKOYAMA, NICOLE H.; LABRADA, ALEXIS; RUSSO, MOMTCHILO. TLR9 agonist adsorbed to alum adjuvant prevents asthma-like responses induced by Blomia tropicalis mite extract. Journal of Leukocyte Biology, v. 106, n. 3, SI JULY 2019. Web of Science Citations: 0.
MIROTTI, LUCIANA CRISTINA; ALBERCA CUSTDIO, RICARDO WESLEY; GOMES, ELIANE; RAMMAURO, FLORENCIA; DE ARAUJO, ELISEU FRANK; GARCIA CALICH, VERA LUCIA; RUSSO, MOMTCHILO. CpG-ODN Shapes Alum Adjuvant Activity Signaling via MyD88 and IL-10. FRONTIERS IN IMMUNOLOGY, v. 8, FEB 3 2017. Web of Science Citations: 9.
NASCIMENTO, FLAVIA R. F.; GOMES, ELIANE A.; RUSSO, MOMTCHILO; LEPIQUE, ANA P. Interferon Regulatory Factor (IRF)-1 Is a Master Regulator of the Cross Talk between Macrophages and L929 Fibrosarcoma Cells for Nitric Oxide Dependent Tumoricidal Activity. PLoS One, v. 10, n. 2 FEB 6 2015. Web of Science Citations: 9.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.
Filed patent(s) as a result of this research project

Solicitação em análise e dentro do prazo legal de sigilo previsto na legislação BR1020180703390 - Universidade de São Paulo (USP) . Solicitação em análise e dentro do prazo legal de sigilo previsto na legislação - October 2018, 02