Effective treatment of pulmonary tuberculosis restores plasma leptin levels

Perna, Victoria; Pérez-Pérez, Antonio; Fernández‐Riejos, Patricia; Polo-Padillo, Juan; Batista, Nínive; Domínguez-Castellano, Ángel; Sánchez-Margalet, Vı́ctor

doi:10.1684/ecn.2014.0346

Cited by 9 publications

(9 citation statements)

References 29 publications

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“…Our results were explained by Perna et al (6), she measured plasma leptin, soluble leptin receptor and adiponectin, weight and body mass index in nineteen patients with diagnosed pulmonary TB before and six months after treatment and suggested that impaired immune response in tuberculosis patients seems to be related to weight loss that coexists with an immunoendocrine imbalance suggesting that wasting is well-recognized prominent feature of tuberculosis (TB), which may not be reversed even after six months of treatment, concluding 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.…”

Section: Discussionsupporting

confidence: 85%

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Assessment of Adiponectin as a Marker for Severity of Pulmonary Tuberculosis

El-Margoushy¹,

Nashar²,

Shadab³

et al. 2014

EJHM

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Background:To evaluate the serum levels of adiponectin in patients with both active and old pulmonary Tuberculosis (TB) and their possible relation with the severity of the disease, forty patients of both sexes suffering from pulmonary TB (20 cases active and 20 cases old) were matched with 20 healthy control volunteers in this study from February 2014 to June 2014. Body mass index (BMI) and serum levels of adiponectin were measured in all subjects. Results: Both BMI and serum levels of adiponectin were significantly different between active TB patients and control. Comparing old TB patients with controls also have the same results. No correlation between BMI and serum adiponectin level in old TB patients was found, while adiponectin levels in active TB patients show a significant negative correlation. Conclusion: Increased adiponectin in serum of TB patients may be a promising marker for severity of the disease independent of BMI.

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Section: Discussionsupporting

confidence: 85%

“…Adipokines may play a role in the immune response to M. tuberculosis, and TB may impair the expression of inflammatory adipokines, such as leptin and adiponectin. (6)…”

Section: Introductionmentioning

confidence: 99%

Assessment of Adiponectin as a Marker for Severity of Pulmonary Tuberculosis

El-Margoushy¹,

Nashar²,

Shadab³

et al. 2014

EJHM

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“…75 Significantly, leptin deficiency resulted in impaired Th1 acute immune responses with ob/ob deficient mice developing higher mycobacterial burdens associated with defective granuloma formation. 19 Although anti-TB therapy may restore leptin levels, 76 it does not result in complete bacillus clearance with adipocytes acting as depots for bacilli persistence. 72 GLIAL AND NEURONAL CELLS M. tuberculosis has been reported to invade the CNS through the phagocyte-facilitated or trans-cellular routes.…”

Section: Adipocytesmentioning

confidence: 99%

Mycobacterium tuberculosis infection of the ‘non‐classical immune cell’

et al. 2015

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Mycobacterium tuberculosis can infect 'non-classical immune cells', which comprise a significant constituency of cells that reside outside of those defined as 'classical immune cells' from myeloid or lymphoid origin. Here we address the influence of specific 'non-classical immune cells' in host responses and their effects in controlling mycobacterial growth or enabling an environment conducive for bacilli persistence. The interaction of M. tuberculosis with epithelial cells, endothelial cells, fibroblasts, adipocytes, glia and neurons and downstream cellular responses that often dictate immune regulation and disease outcome are discussed. Functional integration and synergy between 'classical' and 'non-classical immune cells' are highlighted as critical for determining optimal immune outcomes that favour the host.

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“…На этом фоне системное введение грелина мышам, получающим обогащенный жирами рацион, способствовало увеличению сывороточного VEGF (фактор роста эндотелия) и снижению сывороточных концентраций лептина и NO (окись азота II) [19]. Лептин и грелин, наравне с цитокинами, обладают плейотропной активностью и участвуют в механизмах регуляции воспаления, как одного из компонентов метаболического синдрома [23,25,33]. Корреляционная зависимость L/Gh, показателей абсолютной и относительной массы органов и тканей с рядом достоверно изменяющихся концентраций цитокинов в плазме мышей -достаточно интересная и закономерная находка.…”

Section: биомаркеры гиперлипидемииunclassified

“…Подобная структурная особенность лептина свидетельствует о его роли, наравне с перечисленными цитокинами, в регуляции иммунного ответа [32]. У мышей при отсутствии секреции лептина (ob/ob mice) и рецепторов к лептину (db/db mice) наблюдаются не только эндокринная недостаточность и избыток жировых отложений, но и различные иммунодефицитные состояния, сопровождающиеся аутоиммунными процессами [12,15,33]. Цитокины: IL-12(p40), IL-2, IL-9, IL-13, RANTES, IL-3 и G-CSF, для которых выявлена прямая или опосредованная зависимость с изменениями L/Gh, принимают непосредственное участие в механизмах регуляции воспаления и инсулинорезистентности при метаболическом синдроме [24,32].…”

Section: биомаркеры гиперлипидемииunclassified