About: Th2 Responses in OVA-Sensitized BALB/c Mice Are Down-Modulated By Mycobacterium bovis BCG Treatment

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About: Th2 Responses in OVA-Sensitized BALB/c Mice Are Down-Modulated By Mycobacterium bovis BCG Treatment Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Th2 Responses in OVA-Sensitized BALB/c Mice Are Down-Modulated By Mycobacterium bovis BCG Treatment
Creator	Ferreira, Ana Gameiro, Jacy Cláudia, Ana Alves, Souza Brugiolo, Singer Castro, Márcia César, Caio Flávia, & Gouveia, Carvalho Pereira, Felipe Sin, Alessa
source	Medline; PMC
abstract	OBJECTIVE: This study aimed to determine whether Mycobacterium bovis Bacillus Calmette-Guérin (BCG) treatment can reverse an established allergic airway inflammation in a BALB/c mouse model of ovalbumin (OVA)-induced airway inflammation. METHODS: OVA sensitized BALB/c mice were challenged with aerosolized OVA on days 28 to 30, 34, 41 and 63. Mice were intranasal treated with BCG on days 35 and 42. Twenty-four hours after the last challenge, blood samples were collected to detect anti-OVA immunoglobulin isotypes, and bronchoalveolar lavage (BAL) was harvested for cell count. Additionally, lungs were collected for histological analysis, detection of the eosinophil peroxidase (EPO) activity and measurement of cytokines and CCL11. The expression of CTLA-4, Foxp3 and IL-10 was also determined in lung tissue by flow cytometry. RESULTS: BCG treatment was able to inhibit an established allergic Th2-response, by decreasing the allergen-induced eosinophilic inflammation, EPO activity, levels of CCL11 and IL-4, serum levels of IgE and IgG1. Mycobacteria treatment increased lung levels of IFN-γ, IL-10 and TGF-β, and expressions of Foxp3 and CTLA-4 in CD4(+)T cells. Additionally, an increased production of IL-10 by CD8(+) T cells was observed, even though no detectable changes in CD4(+)IL-10(+) was noticed. CONCLUSION: BCG treatment inhibits features of allergic airway inflammation and the results suggest that the mechanism underlying the down-regulatory effects of BCG on OVA-induced airway inflammation appear to be associated with the induction of both Th1 and T regulatory immune responses.
has issue date	2012-08-04(xsd:dateTime)
bibo:doi	10.1007/s10875-012-9746-4
bibo:pmid	22864629
has license	no-cc
sha1sum (hex)	72ceb06d0b4409dda06adb1d24bec24a42b0db96
schema:url	https://doi.org/10.1007/s10875-012-9746-4
resource representing a document's title	Th2 Responses in OVA-Sensitized BALB/c Mice Are Down-Modulated By Mycobacterium bovis BCG Treatment
has PubMed Central identifier	PMC7086714
has PubMed identifier	22864629
schema:publication	J Clin Immunol
resource representing a document's body	covid:72ceb06d0b4409dda06adb1d24bec24a42b0db96#body_text
is schema:about of	named entity 'OVA' named entity 'Responses' covid:arg/72ceb06d0b4409dda06adb1d24bec24a42b0db96 named entity 'Bacillus' named entity 'Mycobacterium bovis' named entity 'BCG' named entity 'inflammation' named entity 'airway' named entity 'OVA' named entity 'BCG' named entity 'Th2' named entity 'Mice' named entity 'goblet cells' named entity 'regulatory T cells' named entity 'BCG' named entity 'allergy' named entity 'Th2' named entity 'IL-10' named entity 'transcription factor' named entity 'inflammatory cell' named entity 'CD8' named entity 'intraperitoneally' named entity 'mycobacteria' named entity 'IgG1' named entity 'Th1' named entity 'BCG' named entity 'IgE' named entity 'C57BL/6' named entity 'TGF-β' named entity 'OVA' named entity 'CD4 +' named entity 'hygiene hypothesis' named entity 'BCG' named entity 'allergic' named entity 'inflammation' named entity 'CCL11' named entity 'inflammatory processes' named entity 'CD4 +' named entity 'IL-10' named entity 'BCG' named entity 'IgE' named entity 'cytokines' named entity 'immune response' named entity 'inflammation' named entity 'CD152' named entity 'PBS' named entity 'RPMI' named entity 'PAS' named entity 'hygiene hypothesis' named entity 'allergic' named entity 'immune response' named entity 'CTLA-4' named entity 'BCG' named entity 'IgE' named entity 'experimental evidence' named entity 'IL-10' named entity 'IgG2a' named entity 'inflammatory responses' named entity 'IgE' named entity 'IgE' named entity 'significance level' named entity 'IL-10' named entity 'lung' named entity 'allergic' named entity 'allergic' named entity 'optical microscope' named entity 'allergic' named entity 'liquid nitrogen' named entity 'BCG' named entity 'Kolmogorov-Smirnov' named entity 'CCL11'

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