Abstract
Abstract An assay procedure was developed to assess resistance to cytopathic damage by virulent H37Rv in oil-induced peritoneal macrophages of normal and bacillus Calmette Guérin-immunized rabbits utilizing 51Cr. Immune serum was required for potentiation of maximal resistance. The radiolabeling procedure was standardized in terms of cultural and labeling conditions to obtain maximal radiochromate uptake with minimal nonspecific release, absence of re-utilization of released radiochro-mate and the low standard deviation of radiorelease in replicate cultures. Whereas functionally immune cells released only little more label than did their controls (sometimes less), nonimmune cells released appreciably greater amounts than did corresponding control cells. The radioassay demonstrated the importance of immune serum in potentiating cellular resistance to necrotization by tubercle bacilli, for effective immunity required the conjoint action of immune cells and immune serum. Immune macrophages in normal serum released significantly more isotope than in immune serum; normal cells in immune serum exhibited increased resistance by diminished label release. However, cells and sera reacted interdependently so that some immune sera enhanced the antimicrobial activity of certain normal cells nearly to the immune cell level; conversely, a number of immune cells in normal sera reacted in a manner comparable to that of normal cells. Further evidence that release of radiolabel reflects cellular damage was obtained through the use of an obligate intracellular parasite, poliovirus, type I, capable of rapid cytopathogenesis over a 48- to 72-hr period. When used to infect labeled monkey kidney cells, patterns of isotope release clearly indicated a close correlation between isotope escape and virus-initiated cytolysis.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
