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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 effect on mucushyperplasia after primary and secondary challenge. Mucus production was detected using PeriodicAcid Schiff staining on lung sectionfrom nonsensitized mice (a), (e), sensitized mice (b), (f), sensitized mice treatedwith BCG (c), (g), or BCG-IL-18 (d), (h), after primary (a)–(d) or secondary (e)–(h) OVAchallenge.
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fig3: BCG and BCG-IL-18 effect on mucushyperplasia after primary and secondary challenge. Mucus production was detected using PeriodicAcid Schiff staining on lung sectionfrom nonsensitized mice (a), (e), sensitized mice (b), (f), sensitized mice treatedwith BCG (c), (g), or BCG-IL-18 (d), (h), after primary (a)–(d) or secondary (e)–(h) OVAchallenge.

Mentions: Lung tissue wasobtained and processed 48 hours after allergen provocation. To assess thedegree of goblet cell hyperplasia, tissue sections were stained with PAS. Afterprimary (see Figures 3(a)–3(d)) and secondary (see Figures 3(e)–3(h)) challenge,nonsensitized mice showed no PAS-positive cells, whereas nontreated OVA-sensitizedmice showed many PAS-positive cells (92% and 81% of PAS positive cells/mmbasement membrane for the primary and secondary challenge protocol,resp.). In contrast, sensitized and BCG- or BCG-IL-18-treated miceshowed only scattered PAS-positive cells (71% and 66% of PAS-positive cells/mmbasement membrane for BCG-treated mice in the primary and secondary challengeprotocol, resp., and 48% and 40% of PAS-positive cells/mm basementmembrane for BCG-IL-18-treated mice in the primary and secondary challengeprotocol, resp.), with a stronger inhibition for BCG-IL-18 treatmentafter the secondary challenge (Figure 3(h)).


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 effect on mucushyperplasia after primary and secondary challenge. Mucus production was detected using PeriodicAcid Schiff staining on lung sectionfrom nonsensitized mice (a), (e), sensitized mice (b), (f), sensitized mice treatedwith BCG (c), (g), or BCG-IL-18 (d), (h), after primary (a)–(d) or secondary (e)–(h) OVAchallenge.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: BCG and BCG-IL-18 effect on mucushyperplasia after primary and secondary challenge. Mucus production was detected using PeriodicAcid Schiff staining on lung sectionfrom nonsensitized mice (a), (e), sensitized mice (b), (f), sensitized mice treatedwith BCG (c), (g), or BCG-IL-18 (d), (h), after primary (a)–(d) or secondary (e)–(h) OVAchallenge.
Mentions: Lung tissue wasobtained and processed 48 hours after allergen provocation. To assess thedegree of goblet cell hyperplasia, tissue sections were stained with PAS. Afterprimary (see Figures 3(a)–3(d)) and secondary (see Figures 3(e)–3(h)) challenge,nonsensitized mice showed no PAS-positive cells, whereas nontreated OVA-sensitizedmice showed many PAS-positive cells (92% and 81% of PAS positive cells/mmbasement membrane for the primary and secondary challenge protocol,resp.). In contrast, sensitized and BCG- or BCG-IL-18-treated miceshowed only scattered PAS-positive cells (71% and 66% of PAS-positive cells/mmbasement membrane for BCG-treated mice in the primary and secondary challengeprotocol, resp., and 48% and 40% of PAS-positive cells/mm basementmembrane for BCG-IL-18-treated mice in the primary and secondary challengeprotocol, resp.), with a stronger inhibition for BCG-IL-18 treatmentafter the secondary challenge (Figure 3(h)).

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