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Infection of mice with Mycobacterium bovis-Bacillus Calmette-Guérin (BCG) suppresses allergen-induced airway eosinophilia

Infection of mice with Mycobacterium bovis-Bacillus Calmette-Guérin (BCG) suppresses allergen-induced airway eosinophilia
Infection of mice with Mycobacterium bovis-Bacillus Calmette-Guérin (BCG) suppresses allergen-induced airway eosinophilia
It has been proposed that the increase in prevalence and severity of atopic disorders inversely correlates with exposure to infectious diseases such as tuberculosis. We have investigated this issue by combining an intranasal Mycobacterium bovis-Bacillus Calmette-Guérin (BCG) infection with a murine model of allergen, (ovalbumin [OVA]) induced airway eosinophilia. BCG infection either 4 or 12 wk before allergen airway challenge resulted in a 90-95 and 60-70% reduction in eosinophilia within the lungs, respectively, compared to uninfected controls. The inhibition of airway eosinophilia correlated with a reduced level of IL-5 production by T cells from the lymph node draining the site of OVA challenge. Interestingly, BCG infection of the lung had no effect on IgG1 and IgE OVA-specific serum immunoglobulin or blood eosinophil levels. Furthermore, BCG-induced inhibition of airway eosinophilia was strongly reduced in interferon (IFN)-gamma receptor-deficient mice and could be partially reversed by intranasal IL-5 application. Intranasal BCG infections could also reduce the degree of lung eosinophilia and IL-5 produced by T cells after Nippostrongylus brasiliensis infection. Taken together, our data suggest that IFN-gamma produced during the T helper cell (Th)1 immune response against BCG suppresses the development of local inflammatory Th2 responses in the lung. Most importantly, this inhibition did not extend to the systemic immunoglobulin response against OVA. Our data support the view that mycobacterial infections have the potential to suppress the development of atopic disorders in humans.
0022-1007
561-569
Erb, K.J.
2eaffe26-1f4e-4216-9576-53386966d8fc
Holloway, J.W.
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Sobeck, A.
c2e07094-a15e-4b58-b910-a9ecc5dee4f2
Moll, H.
3257b37e-9e4c-43a2-ac7d-aad73a55a75f
Le Gros, G.
937643ee-4f0a-42e3-8450-632be0de85aa
Erb, K.J.
2eaffe26-1f4e-4216-9576-53386966d8fc
Holloway, J.W.
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Sobeck, A.
c2e07094-a15e-4b58-b910-a9ecc5dee4f2
Moll, H.
3257b37e-9e4c-43a2-ac7d-aad73a55a75f
Le Gros, G.
937643ee-4f0a-42e3-8450-632be0de85aa

Erb, K.J., Holloway, J.W., Sobeck, A., Moll, H. and Le Gros, G. (1998) Infection of mice with Mycobacterium bovis-Bacillus Calmette-Guérin (BCG) suppresses allergen-induced airway eosinophilia. The Journal of Experimental Medicine, 187 (4), 561-569.

Record type: Article

Abstract

It has been proposed that the increase in prevalence and severity of atopic disorders inversely correlates with exposure to infectious diseases such as tuberculosis. We have investigated this issue by combining an intranasal Mycobacterium bovis-Bacillus Calmette-Guérin (BCG) infection with a murine model of allergen, (ovalbumin [OVA]) induced airway eosinophilia. BCG infection either 4 or 12 wk before allergen airway challenge resulted in a 90-95 and 60-70% reduction in eosinophilia within the lungs, respectively, compared to uninfected controls. The inhibition of airway eosinophilia correlated with a reduced level of IL-5 production by T cells from the lymph node draining the site of OVA challenge. Interestingly, BCG infection of the lung had no effect on IgG1 and IgE OVA-specific serum immunoglobulin or blood eosinophil levels. Furthermore, BCG-induced inhibition of airway eosinophilia was strongly reduced in interferon (IFN)-gamma receptor-deficient mice and could be partially reversed by intranasal IL-5 application. Intranasal BCG infections could also reduce the degree of lung eosinophilia and IL-5 produced by T cells after Nippostrongylus brasiliensis infection. Taken together, our data suggest that IFN-gamma produced during the T helper cell (Th)1 immune response against BCG suppresses the development of local inflammatory Th2 responses in the lung. Most importantly, this inhibition did not extend to the systemic immunoglobulin response against OVA. Our data support the view that mycobacterial infections have the potential to suppress the development of atopic disorders in humans.

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More information

Published date: 16 February 1998
Organisations: Human Development & Health

Identifiers

Local EPrints ID: 192095
URI: https://eprints.soton.ac.uk/id/eprint/192095
ISSN: 0022-1007
PURE UUID: ec408862-ddec-47bc-be78-a48cdd3deb40
ORCID for J.W. Holloway: ORCID iD orcid.org/0000-0001-9998-0464

Catalogue record

Date deposited: 18 Dec 2012 11:40
Last modified: 06 Jun 2018 12:59

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