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IL-18 does not increase allergic airway disease in mice when produced by BCG.

Amniai L, Biet F, Marquillies P, Locht C, Pestel J, Tonnel AB, Duez C - J. Biomed. Biotechnol. (2007)

Bottom Line: Whilst BCG inhibits allergic airway responses in murine models, IL-18 has adversary effects depending on its environment.BCG-IL-18 and BCG were shown to similarly inhibit the development of AHR, mucus production, eosinophil influx, and local Th2 cytokine production in BAL, both after the primary and secondary challenge.These data show that IL-18 did not increase allergic airway responses in the context of the mycobacterial infection, and suggest that BCG-IL-18 and BCG are able to prevent the development of local Th2 responses and therefore inhibit allergen-induced airway responses even after restimulation.

View Article: PubMed Central - PubMed

Affiliation: INSERM, Institut National de la Santé et de la Recherche Médicale U774, Lille 59019, France.

ABSTRACT
Whilst BCG inhibits allergic airway responses in murine models, IL-18 has adversary effects depending on its environment. We therefore constructed a BCG strain producing murine IL-18 (BCG-IL-18) and evaluated its efficiency to prevent an asthma-like reaction in mice. BALB/cByJ mice were sensitized (day (D) 1 and D10) by intraperitoneal injection of ovalbumin (OVA)-alum and primary (D20-22) and secondary (D62, 63) challenged with OVA aerosols. BCG or BCG-IL-18 were intraperitonealy administered 1 hour before each immunization (D1 and D10). BCG-IL-18 and BCG were shown to similarly inhibit the development of AHR, mucus production, eosinophil influx, and local Th2 cytokine production in BAL, both after the primary and secondary challenge. These data show that IL-18 did not increase allergic airway responses in the context of the mycobacterial infection, and suggest that BCG-IL-18 and BCG are able to prevent the development of local Th2 responses and therefore inhibit allergen-induced airway responses even after restimulation.

No MeSH data available.


Related in: MedlinePlus

BCG and BCG-IL-18 decreaseOVA-specific IgE, but do not modify serum total IgE. IgE weremeasured after primary (a), (c) or secondary (b), (d) challenge. Results areexpressed as mean ± SEM ng/mL for total IgE (a), (b), and mean ± sem ELISA units/mL(EU/mL) for OVA-specific IgE (c), (d). *P < .01.
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fig5: BCG and BCG-IL-18 decreaseOVA-specific IgE, but do not modify serum total IgE. IgE weremeasured after primary (a), (c) or secondary (b), (d) challenge. Results areexpressed as mean ± SEM ng/mL for total IgE (a), (b), and mean ± sem ELISA units/mL(EU/mL) for OVA-specific IgE (c), (d). *P < .01.

Mentions: Serum from OVA-sensitizedmice showed elevated total IgE levels and OVA-specific IgE antibodies comparedto nonsensitized mice following the primary and the secondary challengeprotocol (see Figure 5). Treatment with BCG and BCG-IL-18 did not affect totalIgE measured after the primary and the secondary challenge (see Figures 5(a) and 5(b)). OVA-specific IgE measured after the primary or the secondarychallenge were not modified after BCG treatment (see Figures 5(c) and 5(d)). Incontrast, treatment with BCG-IL-18 significantly increased levels ofOVA-specific IgE after the primary and decreased them after the secondarychallenge compared to OVA-sensitized mice (see Figures 5(c), 5(d)).


IL-18 does not increase allergic airway disease in mice when produced by BCG.

Amniai L, Biet F, Marquillies P, Locht C, Pestel J, Tonnel AB, Duez C - J. Biomed. Biotechnol. (2007)

BCG and BCG-IL-18 decreaseOVA-specific IgE, but do not modify serum total IgE. IgE weremeasured after primary (a), (c) or secondary (b), (d) challenge. Results areexpressed as mean ± SEM ng/mL for total IgE (a), (b), and mean ± sem ELISA units/mL(EU/mL) for OVA-specific IgE (c), (d). *P < .01.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2235931&req=5

fig5: BCG and BCG-IL-18 decreaseOVA-specific IgE, but do not modify serum total IgE. IgE weremeasured after primary (a), (c) or secondary (b), (d) challenge. Results areexpressed as mean ± SEM ng/mL for total IgE (a), (b), and mean ± sem ELISA units/mL(EU/mL) for OVA-specific IgE (c), (d). *P < .01.
Mentions: Serum from OVA-sensitizedmice showed elevated total IgE levels and OVA-specific IgE antibodies comparedto nonsensitized mice following the primary and the secondary challengeprotocol (see Figure 5). Treatment with BCG and BCG-IL-18 did not affect totalIgE measured after the primary and the secondary challenge (see Figures 5(a) and 5(b)). OVA-specific IgE measured after the primary or the secondarychallenge were not modified after BCG treatment (see Figures 5(c) and 5(d)). Incontrast, treatment with BCG-IL-18 significantly increased levels ofOVA-specific IgE after the primary and decreased them after the secondarychallenge compared to OVA-sensitized mice (see Figures 5(c), 5(d)).

Bottom Line: Whilst BCG inhibits allergic airway responses in murine models, IL-18 has adversary effects depending on its environment.BCG-IL-18 and BCG were shown to similarly inhibit the development of AHR, mucus production, eosinophil influx, and local Th2 cytokine production in BAL, both after the primary and secondary challenge.These data show that IL-18 did not increase allergic airway responses in the context of the mycobacterial infection, and suggest that BCG-IL-18 and BCG are able to prevent the development of local Th2 responses and therefore inhibit allergen-induced airway responses even after restimulation.

View Article: PubMed Central - PubMed

Affiliation: INSERM, Institut National de la Santé et de la Recherche Médicale U774, Lille 59019, France.

ABSTRACT
Whilst BCG inhibits allergic airway responses in murine models, IL-18 has adversary effects depending on its environment. We therefore constructed a BCG strain producing murine IL-18 (BCG-IL-18) and evaluated its efficiency to prevent an asthma-like reaction in mice. BALB/cByJ mice were sensitized (day (D) 1 and D10) by intraperitoneal injection of ovalbumin (OVA)-alum and primary (D20-22) and secondary (D62, 63) challenged with OVA aerosols. BCG or BCG-IL-18 were intraperitonealy administered 1 hour before each immunization (D1 and D10). BCG-IL-18 and BCG were shown to similarly inhibit the development of AHR, mucus production, eosinophil influx, and local Th2 cytokine production in BAL, both after the primary and secondary challenge. These data show that IL-18 did not increase allergic airway responses in the context of the mycobacterial infection, and suggest that BCG-IL-18 and BCG are able to prevent the development of local Th2 responses and therefore inhibit allergen-induced airway responses even after restimulation.

No MeSH data available.


Related in: MedlinePlus