Adoptive transfer of resistance to pulmonary tuberculosis in guinea pigs is altered by protein deficiency

Abstract

Adoptive transfer of lymphoid cells was used to study the influence of dietary protein deficiency on the development and expression of resistance in inbred strain 2 guinea pigs infected by the respiratory route with virulent Mycobacterium tuberculosis H37Rv. Cells from the bronchotracheal lymph nodes of aerosol-infected donors and from the spleens of intravenously-infected donors transferred a significant level of protection when injected (0.5–1.0 × 10 8 cells) into syngeneic recipients by the intraperitoneal route. Nylon wool enrichment of T cells from both cell populations resulted in a marked increase in the level of resistance transferred. Adoptively-protected guinea pigs were as resistant, as measured by control of viable M. tuberculosis in the lungs, as animals actively vaccinated with M. bovis BCG. Donor lymphocytes were more effective when transferred into the recipients by the intraperitoneal, as compared to the subcutaneous, route of injection. Reciprocal adoptive transfer between well-nourished or protein-deficient donors and recipients revealed that protein deficiency prevented guinea pigs from generating a population of immune lymphocytes as indicated by the relative inability of such cells to protect normally-nourished recipients. However, protein-deprived recipients were perfectly capable of being protected by immune cells from well-nourished donors. Adoptively protected protein-deficient guinea pigs developed large, well-circumscribed tuberculous granulomas in their lungs, in contrast to their non-protected counterparts which developed numerous, small, poorly-defined granulomata. Our data suggest that the cellular and humoral environment of the protein-deficient guinea pig is not intrinsically suppressive, but that protein deficiency prevents infected animals from generating a population of protective lymphocytes.