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Phagocytosis and leucocyte enzymes in protein-calorie malnutrition
Insights
Protein-calorie malnutrition impairs leucocyte enzyme activity crucial for fighting infection. Nutritional therapy restores these essential enzyme functions, improving immune response in children.
Area of Science:
- Biochemistry
- Immunology
- Pediatric Nutrition
Background:
- Protein-calorie malnutrition (PCM) is associated with increased susceptibility to infections.
- Leucocyte function, particularly bactericidal activity, is critical for host defense.
- Enzyme deficiencies in leucocytes may underlie the impaired immune response in PCM.
Purpose of the Study:
- To investigate the activity of key enzymes involved in leucocyte bactericidal function in children with PCM.
- To determine the effect of nutritional rehabilitation on these enzyme activities.
Main Methods:
- Assay of glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, NADPH oxidase, and acid phosphatase in leucocytes.
- Comparison of enzyme activities between malnourished children and healthy controls.
- Evaluation of enzyme activity changes following dietary intervention.
Main Results:
- Leucocytes from malnourished children showed normal glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activity.
- Significantly reduced NADPH oxidase activity and impaired acid phosphatase release were observed in leucocytes from malnourished children.
- Nutritional therapy led to increased activity of all assayed enzymes and restored acid phosphatase release during phagocytosis.
Conclusions:
- PCM affects specific leucocyte enzymes (NADPH oxidase, acid phosphatase) critical for bactericidal function.
- These enzyme alterations likely contribute to the increased infection risk in malnourished children.
- Nutritional rehabilitation can reverse these detrimental enzyme changes, supporting immune recovery.
Abstract:
1. Enzymes pertinent to bactericidal activities of leucocytes were assayed in children suffering from protein-calorie malnutrition. 2. Leucocytes obtained from malnourished and control children contained similar activities for glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase. Granule-bound NADPH oxidase activity was low in leucocytes isolated from malnourished patients and failed to show the phagocytic stimulation which is normally seen in control leucocytes. Further, leucocytes obtained from malnourished patients did not release the acid phosphatase from lysosomes during phagocytosis, unlike those from controls. 3. Treatment of the malnourishment with a diet high in calories and protein resulted in significant increase in the activities of glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and NADPH oxidase and in releasing the acid phosphatase from the lysosomes into the supernatant fraction during phagocytosis. 4. The significance of these enzyme changes are discussed in relation to the increased susceptibility of these patients to infection.