Experimental evidence for molecular exchanges between a dependent trypanosome cell and its host

Abstract Evidence in support of the general working hypothesis that dependent (parasitic) cells and organisms exchange chemical substances with their environment ( Lincicome, 1963 ) is presented in this study. The test system was the laboratory rat with its natural parasite Trypanosoma lewisi. The rat was made experimentally deficient in thiamine before introduction of the dependent cell (T. lewisi). The following categories of evidence were examined: (1) host body weight gains, (2) host food consumption, (3) host longevity, (4) oxygen consumption of host liver and kidney slices, and (5) transketolase activities of host liver and kidney homogenates. Accelerated body weight gains of T. lewisi infected rats, maintained on an adequate diet, ranged from 0–19% over uninfected rats. Weight advantages of infected thiamine-deficient rats over uninoculated thiamine-deficient ones were more consistent and ranged from 0–11%. No significant advantages were observed in weights of infected over noninfected inanition control rats. The amount of food consumed by uninfected thiamine-deficient rats decreased from about 6 gm per rat a day (initially) to about 1.5 gm (just prior to death). During the same period, food consumption of infected deficient rats decreased from 6 to 2.5 gm. Infected deficient rats lived approximately 46 days after initiation of the diet and 7 days longer than uninfected rats. The survival time of inoculated deficient rats ranged from 35 to 64 days; that of uninoculated rats was from 31 to 51 days. Liver slices from T. lewisi infected control diet rats consumed 4.5 μl of O2, which was not significantly different from the amount utilized by uninfected rat liver slices. The QO2 values for liver slices from thiamine-deficient uninfected rats decreased as the deficiency progressed from about 3.5 to 1.5 μl; liver from infected thiamine-deficient rats had QO2 values of about 4.5-1.9, but during the second week of infection the value for uninfected rat liver slices was 3 μl; that of liver from infected rats was about 4.3 μl. The QO2 values of liver slices from rats having 3-week-old infections were 3.3 μl and that of controls, 2.2 μl. Kidney slices from thiamine-deficient infected rats consumed 7.9 μl of oxygen per gram of tissue per hour during the second week of trypanosome infection; kidney slices of uninfected rats used 5.4 μl. Transketolase assays showed that this enzyme and its cofactors were more active in tissue homogenates from T. lewisi-infected rats than those from noninfected rats. Liver of infected rats, deficient in thiamine formed 23 mg of hexose per gram of tissue per hour as compared to 18 mg of hexose for liver of uninfected rats with a 23-day-old deficiency. The maximum difference observed was 6 mg of hexose. Kidney homogenates from infected rats and thiamine-deficient formed 2–4 mg more of hexose per gram of tissue than uninfected controls. The results of this study imply that T. lewisi cells stimulate growth of rats by increasing metabolic activities of host cells. Inasmuch as the lack of thiamine induced biochemical defects in rat tissue, and the presence of T. lewisi cells moderated the defects that thiamine alone can correct, theoretically T. lewisi supplies thiamine to the deficient host. This is considered evidence supporting the view that a dependent trypanosome cell exchanges molecular substances with its environment.