The interrelationships between various components of the non-immune inflammatory response (white cell count, plasma lactoferrin, C-reactive protein, ferritin, iron and iron-binding capacity), were studied serially in a variety of inflammatory conditions including acute lobar pneumonia, active pulmonary tuberculosis, rheumatoid arthritis on gold therapy and sepsis in the face of marrow hypoplasia induced by chemotherapy. Lactoferrin concentrations paralleled the white count in all groups. They were highest in pneumonia and tuberculosis, mildly elevated in rheumatoid arthritis and markedly decreased in neutropenic sepsis. Very high initial lactoferrin concentrations were associated with a poor prognosis in acute pneumonia. C-reactive protein and ferritin concentrations remained elevated through the period of study in acute pneumonia and neutropenic sepsis, while they gradually normalised over weeks in subjects with tuberculosis or rheumatoid arthritis on therapy. In pneumonia and tuberculosis moderate hypoferraemia and a reduced iron-binding capacity were evident. In contrast, a raised percentage saturation was present in neutropenic sepsis, probably related to erythroid marrow suppression. Comparisons between ferritin, lactoferrin and C-reactive protein in the various groups supported the concept that ferritin behaves in part as an acute phase reactant and that hypoferraemia in inflammation is due to deviation of iron into ferritin stores. The suggestion that lactoferrin is responsible for the hypoferraemia and hyperferritinaemia was not supported by the present data. Iron deficiency appeared to limit the hyperferritinaemic response in rheumatoid arthritis, while erythropoietic inhibition by chemotherapy dampened the hypoferraemic response in neutropenic sepsis.

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The effect of parenteral hydrocortisone on plasma lactoferrin concentration, neutrophil count and 1actoferrin:neutrophil ratio was assessed in 10 volunteer subjects.Administration of a single dose of corticosteroid was followed by a significant rise in the circulating neutrophil count, a significant but proportionately smaller rise in the plasma lactoferrin concentration and a significant fall in the 1actoferrin:neutrophil ratio. Acute viral infections were found to be associated with a disproportionately low plasma lactoferrin concentration relative to the circulating neutrophil count. The relatively low lactoferrin concentrations in both these situations could be of significance in regard to the propensity to bacterial infection and superinfection which these 2 groups of subjects display. Compared to patients with viral infection, those suffering from plasmodium falciparum malaria showed a significantly elevated lactoferrin:neutrophil ratio, although this ratio was not significantly different when malarial patients were compared to normal individuals. These findings suggest that the pathogenesis of relative neutropenia in viral and protozoal illnesses is fundamentally different. Finally, it was found that the temperature at which specimen collection takes place does not appear to be a significant variable determining the plasma lactoferrin concentration.

Plasma concentrations of lactoferrin were measured in immediately separated EDTA samples from 5 subjects who had received HLA identical bone marrow transplants for leukaemia or aplastic anaemia and from 7 subjects who were leucopenic as a consequence of chemotherapy for a variety of malignant conditions. Plasma lactoferrin concentrations were found to closely parallel the leucocyte count and were not found to either predict or to antedate leucocyte regeneration. Serial measurements of plasma lactoferrin in a subject with no circulating neutrophils who received a bone marrow graft revealed that the clearance of lactoferrin followed an exponential pattern and had an initial half time of 2.2 h.

The effect of low density lipoproteins on esterification of cholesterol was studied in lymphocytes from patients with familial hypercholesterolaemia; results were compared with those obtained using cells from normal individuals. Freshly isolated lymphocytes were maintained in lipoprotein-deficient medium for 48 h and the rate of formation of [3H] cholesteryl oleate from [3H] oleate was then determined in the presence or absence of low density lipoproteins. In the absence of low density lipoproteins, incorporation of [3H] oleate was higher in heterozygote and homozygote cells than in normal lymphocytes. Incorporation in the presence of low density lipoproteins was increased relative to that measured in their absence for all of the subjects studied; heterozygotes and homozygotes showed marked changes in some cases but not in others.