Cellular basis of host defence in pyelonephritis. I. Chronic infection.
Infection persists for long periods in chronic pyelonephritis, but the cellular basis of the host-parasite relationship is poorly understood. We have obtained quantitative data on the relationship between the pathogen (E. coli) and cellular defence mechanisms. Depletion of cellular components was carried out using whole body irradiation, methylprednisolone, cyclophosphamide or carrageenan and silica particles. A system of administering cyclophosphamide and methylprednisolone through the use of a slow release carrier, as well as graded doses of irradiation, was then developed to allow the controlled reduction of cellular competence. Quantitative studies in a host with chronic pyelonephritis and normal cellular defence reserves showed that severe depletion of granulocytic cells is necessary before host defence mechanisms are adversely affected. This finding conflicts with the observation that microorganisms survive and persist in the kidney for extended periods. Additionally, noncellular factors may also limit bacterial growth.
D000818:Animals; D000917:Antibody Formation; D002908:Chronic Disease; D003520:Cyclophosphamide / Q000494:pharmacology; D004927:Escherichia coli Infections / Q000276:immunology*; D006790:Host-Parasite Interactions; D007111:Immunity, Cellular; D007121:Immunocompetence / Q000187:drug effects; D008212:Lymphocyte Depletion; D008775:Methylprednisolone / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects; D011704:Pyelonephritis / Q000276:immunology* / Q000382:microbiology; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors; D014916:Whole-Body Irradiation
D003520:Cyclophosphamide; D008775:Methylprednisolone