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The Journal of Immunology, 2003, 171: 4758-4764.
Copyright © 2003 by The American Association of Immunologists

Mice Lacking Myeloid Differentiation Factor 88 Display Profound Defects in Host Resistance and Immune Responses to Mycobacterium avium Infection Not Exhibited by Toll-Like Receptor 2 (TLR2)- and TLR4-Deficient Animals

Carl G. Feng1,*, Charles A. Scanga*, Carmen M. Collazo-Custodio2,*, Allen W. Cheever{dagger}, Sara Hieny*, Patricia Caspar* and Alan Sher*

* Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and {dagger} Biomedical Research Institute, Rockville, MD 20852

To assess the role of Toll-like receptor (TLR) signaling in host resistance to Mycobacterium avium infection, mice deficient in the TLR adaptor molecule myeloid differentiation factor 88 (MyD88), as well as TLR2-/- and TLR4-/- animals, were infected with a virulent strain of M. avium, and bacterial burdens and immune responses were compared with those in wild-type (WT) animals. MyD88-/- mice failed to control acute and chronic M. avium growth and succumbed 9–14 wk postinfection. Infected TLR2-/- mice also showed increased susceptibility, but displayed longer survival and lower bacterial burdens than MyD88-/- animals, while TLR4-/- mice were indistinguishable from their WT counterparts. Histopathological examination of MyD88-/- mice revealed massive destruction of lung tissue not present in WT, TLR2-/-, or TLR4-/- mice. In addition, MyD88-/- and TLR2-/-, but not TLR4-/-, mice displayed marked reductions in hepatic neutrophil infiltration during the first 2 h of infection. Although both MyD88-/- and TLR2-/- macrophages showed profound defects in IL-6, TNF, and IL-12p40 responses to M. avium stimulation in vitro, in vivo TNF and IL-12p40 mRNA induction was impaired only in infected MyD88-/- mice. Similarly, MyD88-/- mice displayed a profound defect in IFN-{gamma} response that was not evident in TLR2-/- or TLR4-/- mice or in animals deficient in IL-18. These findings indicate that resistance to mycobacterial infection is regulated by multiple MyD88-dependent signals in addition to those previously attributed to TLR2 or TLR4, and that these undefined elements play a major role in determining bacterial induced proinflammatory as well as IFN-{gamma} responses.


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