Evidence for a reduced chemokine response in the lungs of beige mice infected with Mycobacterium avium

• Type: Article in International Scientific Journal
• Date: 1997

Authors

Florido, M (Author) Other; Appelberg, R (Author) ICBAS; Orme, IM (Author) Other; Cooper, AM (Author) Other

Journal

Title: Immunology

Vol. 90

Pages: 600-606

ISSN: 0019-2805

Publisher: Wiley-Blackwell

Indexing

ISI Web of Knowledge - 24 Citations

Scopus - 27 Citations

Scientific classification

FOS: Medical and Health sciences > Basic medicine

Other information

Authenticus ID: P-00H-KBA

DOI: 10.1046/j.1365-2567.1997.00206.x

Abstract (EN): The basis of the increased susceptibility of beige mice to Mycobacterium avium infections is still not clearly understood. In this study we examined the growth of three virulent strains of M. avium in beige mice and normal C57BL/6 controls. Depletion of natural killer (NK) cells by administration of anti-asialo GM1 antisera did not affect the growth of M. avium in any of the groups of animals. Similarly, interferon-gamma (IFN-gamma) gene-disrupted mice were more susceptible to infection than control mice but the growth of M. avium was not further affected by NK-cell depletion. In terms of effector immunity, beige mice showed enhanced expression of IFN-gamma and tumour necrosis factor-alpha. (TNF-alpha) when compared with wild-type C57BL/6 mice. In agreement with these results, 1-h and interferon-inducible protein (IP-10) expression was also higher in beige mice than in wild-type animals, as was expression of the chemokines macrophage inflamatory protein-2 (MIP-2) and macrophage chemotactic protein (MCP-1) during latter stages of the infection. However, over the first few weeks of the infection, when the susceptibility of the beige mouse lung first becomes evident, MIP-1 beta and MIP-2 chemokine expression in the lungs was lower in beige mice than in wild-type animals. These data indicate, therefore, that the increased susceptibility of beige mice to M. avium infection in the lung is not due to lack of NK-cell activity, nor can it be explained in terms of the effector cytokine response. Instead, the lower early expression of the neutrophil chemoattractants MIP-1 beta and MIP-2 in the lungs of beige mice tends to suggest that the enhanced susceptibility of these mice to M. avium infection may be due in part to defective recruitment of neutrophils or other cells responsive to these specific chemokines.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 7