Phagocytic Activity Is Impaired in Type 2 Diabetes Mellitus and Increases after Metabolic Improvement

Lecube, Albert; Pachón, Gisela; Pétriz, Jordi; Hernández, Cristina; Simó, Rafael

doi:10.1371/journal.pone.0023366

Cited by 181 publications

(147 citation statements)

References 27 publications

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“…Hyperglycemia in diabetes has been shown to affect phagocytosis (11). This defect is partially corrected by control of hyperglycemia [12].…”

Section: Discussion:-mentioning

confidence: 99%

Invitro Study of Role of Vitamin D on Macrophages Dysfunction in Patients With Diabetic Foot Infection.

Gupta¹,

Singh²

2016

IJAR

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In addition to macro and micro vascular complication, hyperglycemia also causes dysfunction of immune system that protects the individuals against infection. Vitamin D deficiency, which has very high prevalence among the diabetic population, might contribute to impairment of macrophage dysfunction. The present study aimed to accesses the effect of vitamin D on phagocytic activity of macrophages in patients with diabetic foot infection in an in-vitro experimental model. The subjects included in the study were divided in to three groups. Serum vitamin D level of all groups was measured by Radioimmunoassay methods. Human PBMC were isolated by densitygradient centrifugation and cultured for 5 days in presence and absence of vitamin D. Phagocytosis was assessed by Confocal and fluorescent microscopy. Comparisons were performed using ANOVA and data were expressed as mean ± SD. The increased percentage of phagocytosis was observed in macrophages treated with 1X10 -7 M concentration of vitamin D3 in comparison to untreated sample among the diabetic foot group. In conclusion this study demonstrated that vitamin D deficiency lead to impaired phagocytosis of macrophages from diabetic subjects. Addition of vitamin D in culture medium of the macrophages improves phagocytosis significantly. This remarkable observation strengthens the concept of vitamin D supplementation to the diabetic foot for improving innate immunity.Copy Right, IJAR, 2016,. All rights reserved.

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“…Hyperglycemia in diabetes has been shown to affect phagocytosis (11). This defect is partially corrected by control of hyperglycemia [12].…”

Section: Discussion:-mentioning

confidence: 99%

Invitro Study of Role of Vitamin D on Macrophages Dysfunction in Patients With Diabetic Foot Infection.

Gupta¹,

Singh²

2016

IJAR

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“…Chronic treatment with insulin strongly depressed the macrophage phagocytosis in rats [70]. The phagocytic activity is low in type 2 diabetes and improves after metabolic improvement [71]. Insulin inhibits phagocytosis of normal human neutrophils [72].…”

Section: Peptide Hormonesmentioning

confidence: 99%

Is there a hormonal regulation of phagocytosis at unicellular and multicellular levels? A critical review

Csaba

2017

AMicr

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Phagocytosis is an ancient cell function, which is similar at unicellular and multicellular levels. Unicells synthesize, store, and secrete multicellular (mammalian) hormones, which influence their phagocytosis. Amino acid hormones, such as histamine, serotonin, epinephrine, and melatonin stimulate phagocytosis, whereas peptide hormones, such as adrenocorticotropic hormone (ACTH), insulin, opioids, arginine vasopressin, and atrial natriuretic peptide decreased it, independently on their chemical structure or function in multicellulars. Macrophage phagocytosis of multicellulars is also stimulated by amino acid hormones, such as histamine, epinephrine, melatonin, and thyroid hormones, however, the effect of peptide hormones is not uniform: prolactin, insulin, glucagon, somatostatin, and leptin have positive effects, whereas ACTH, human chorionic gonadotropin, opioids, and ghrelin have negative ones. Steroid hormones, such as estrogen, hydrocortisone, and dexamethasone are stimulating macrophage phagocytosis, whereas progesterone, aldosterone, and testosterone are depressing it. Considering the data and observations there is not a specific phagocytosis hormone, or a hormonal regulation of phagocytosis neither unicellular, nor multicellular level, however, hormones having specific functions in multicellulars also influence phagocytosis at both levels universally (in unicellulars) or individually (in macrophages). Nevertheless, the hormonal influence cannot be neglected, as phagocytosis (as a function) is rather sensitive to minute dose of hormones and endocrine disruptors. The hormonal influence of phagocytosis by macrophages can be deduced to the events at unicellular level.

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“…Like myeloid cells from db patients (35), Gr-1 + cells from Lepr db/db mice have an impaired capacity for phagocytosis (36). To examine whether Cebpa induction by G-CSF could rescue this defect, we compared phagocytosis of Alexa Fluor 488-labeled zymosan particles by db-derived Gr-1 + cells cultured for 24 h in the presence and absence of G-CSF.…”

Section: G-csf Treatment Rescues Ccr2 and Cxcr2mentioning

confidence: 99%

Diabetes Inhibits Gr-1+ Myeloid Cell Maturation viaCebpaDeregulation

et al. 2015

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Recruitment of innate immune cells from the bone marrow (BM) to an injury site is required for effective repair. In diabetes, this process is altered, leading to excessive recruitment and retention of dysfunctional myeloid cells that fail to promote angiogenesis, prolong inflammation, and block healing. The aberrant myeloid phenotype is partially mediated by stable intrinsic changes to developing cells in the BM that are induced by the diabetic (db) environment, but the exact mechanisms remain largely unknown. Here, we show that the db-derived Gr-1+CD11b+ immature myeloid population has widespread misexpression of chromatin-remodeling enzymes and myeloid differentiation factors. Crucially, diabetes represses transcription of the key myeloid transcription factor CEBPA via diminished H3 Lys 27 promoter acetylation, leading to a failure in monocyte and granulocyte maturation. Restoring Cebpa expression by granulocyte colony-stimulating factor reverses the db phenotype and rescues myeloid maturation. Importantly, our data demonstrate a possible link between myeloid cell maturation and chronic inflammation.

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Phagocytic Activity Is Impaired in Type 2 Diabetes Mellitus and Increases after Metabolic Improvement

Cited by 181 publications

References 27 publications

Invitro Study of Role of Vitamin D on Macrophages Dysfunction in Patients With Diabetic Foot Infection.

Invitro Study of Role of Vitamin D on Macrophages Dysfunction in Patients With Diabetic Foot Infection.

Is there a hormonal regulation of phagocytosis at unicellular and multicellular levels? A critical review

Diabetes Inhibits Gr-1+ Myeloid Cell Maturation viaCebpaDeregulation

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