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Updated: May 2, 2026

A 3D Human Lung Tissue Model for Functional Studies on Mycobacterium tuberculosis Infection
Published on: October 5, 2015
Effective treatment of pulmonary tuberculosis restores plasma leptin levels
Victoria Perna1, Antonio Pérez-Pérez1, Patricia Fernández-Riejos1
1Department (UGC) of Clinical Biochemistry, Virgen Macarena University Hospital, Seville, Spain.
An impaired immune response in tuberculosis patients seems to be related to weight loss that coexists with an immunoendocrine imbalance. Thus, wasting is well-recognised as a prominent feature of tuberculosis (TB), which may not be reversed even after six months of treatment. Adipokines may play a role in the immune response to M. tuberculosis, and TB may impair the expression of inflammatory adipokines, such as leptin. We aimed to study patients with pulmonary TB before and six months after treatment, by measuring plasma leptin, soluble leptin receptor and adiponectin, weight and body mass index. Nineteen patients with a diagnosis of pulmonary TB were included in the study. Blood samples were obtained before and six months after treatment, to measure plasma adipokine levels. We found an increase in plasma leptin levels after treatment (p<0.05). Even though BMI also increased, the extent was not enough to account for the changes in the leptin levels. On the other hand, plasma soluble leptin receptor and adiponectin levels did not change significantly after treatment. In conclusion, these results suggest that active TB infection may affect the expression of leptin, in addition to the wasting that may occur in these patients, and that effective TB treatment increases circulating leptin levels, probably restoring normal immunological competence.
An impaired immune response in tuberculosis patients seems to be related to weight loss that coexists with an immunoendocrine imbalance. Thus, wasting is well-recognised as a prominent feature of tuberculosis (TB), which may not be reversed even after six months of treatment. Adipokines may play a role in the immune response to M. tuberculosis, and TB may impair the expression of inflammatory adipokines, such as leptin. We aimed to study patients with pulmonary TB before and six months after treatment, by measuring plasma leptin, soluble leptin receptor and adiponectin, weight and body mass index. Nineteen patients with a diagnosis of pulmonary TB were included in the study. Blood samples were obtained before and six months after treatment, to measure plasma adipokine levels. We found an increase in plasma leptin levels after treatment (p<0.05). Even though BMI also increased, the extent was not enough to account for the changes in the leptin levels. On the other hand, plasma soluble leptin receptor and adiponectin levels did not change significantly after treatment. In conclusion, these results suggest that active TB infection may affect the expression of leptin, in addition to the wasting that may occur in these patients, and that effective TB treatment increases circulating leptin levels, probably restoring normal immunological competence.
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