Intranasal IFNγ extends passive IgA antibody protection of mice against Mycobacterium tuberculosis lung infection

R. Reljic, Simon Clark, Ann Williams, G. Falero-Diaz, M. Singh, S. Challacombe, Phillip Marsh, J. Ivanyi*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

38 Citations (Scopus)

Abstract

Intranasal inoculation of mice with monoclonal IgA against the α-crystallin (acr1) antigen can diminish the tuberculous infection in the lungs. As this effect has been observed only over a short-term, we investigated if it could be extended by inoculation of IFNγ 3 days before infection, and further coinoculations with IgA, at 2 h before and 2 and 7 days after aerosol infection with Mycobacterium tuberculosis H37Rv. This treatment reduced the lung infection at 4 weeks more than either IgA or IFNγ alone (i.e. 17-fold, from 4.2 × 107 to 2.5 × 106 CFU, P = 0.006), accompanied also by lower granulomatous infiltration of the lungs. IFNγ added prior to infection of mouse peritoneal macrophages with IgA-opsonized bacilli resulted in a synergistic increase of nitric oxide and TNFα production and a 2-3 fold decrease in bacterial counts. Our improved results suggest, that combined treatment with IFNγ and IgA could be developed towards prophylactic treatment of AIDS patients, or as an adjunct to chemotherapy.

Original languageEnglish
Pages (from-to)467-473
Number of pages7
JournalClinical and Experimental Immunology
Volume143
Issue number3
DOIs
Publication statusPublished - Mar 2006

Keywords

  • IgA
  • Infection
  • Interferon-γ
  • Intranasal
  • Lungs
  • TB

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