Type 2 diabetes mellitus metabolic control correlates with the phenotype of human monocytes and monocyte-derived macrophages

Valtierra-Alvarado, Monica Alejandra; Castañeda-Delgado, Julio Enrique; Ramírez-Talavera, S.I.; Lugo‐Villarino, Geanncarlo; Dueñas-Arteaga, F.; Lugo-Sánchez, Anahí; Adame-Villalpando, M.S.; Rivas-Santiago, Bruno; Enciso-Moreno, José Antonio; Serrano, Carmen

doi:10.1016/j.jdiacomp.2020.107708

Cited by 17 publications

(10 citation statements)

References 45 publications

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“…First, we showed the effect of T2D on the expression of activation markers on MDM in response to mock and Mtb infection, and on MDM differentiated through a bystander effect generated in the context of TB. Previously, we reported the basal expression of some markers in MDM from patients with T2D 15 . In this study, we extended this phenotypic analysis using a battery of cell‐surface markers characteristic representative of the two ends of macrophage activation program spectrum (M1 and M2), and a recently proposed metabolic‐oriented program (MMe).…”

Section: Discussionmentioning

confidence: 94%

“…Recently, our group reported that T2D impacts the activation status of circulating monocytes that is conserved even after differentiation towards MDM 15 . However, we ignore whether this effect enacted by T2D on monocyte activation plays a role in the susceptibility to TB.…”

Section: Resultsmentioning

confidence: 99%

“…The buffy coats from healthy donors were obtained at the H.G.Z.1, IMSS blood bank. Monocytes from HC and T2D were isolated by negative magnetic labeling (130‐096‐537; Miltenyi, Bergisch Gladbach, Germany) and differentiated to macrophages (MDM) with M‐CSF (130‐096‐489; Miltenyi, Bergisch Gladbach, Germany) and autologous serum, as previously described 15 …”

Section: Methodsmentioning

confidence: 99%

“…We have previously reported that T2D influences blood monocyte subsets in terms of frequency and cell‐surface markers yielding a phenotype that is preserved during their differentiation towards monocyte‐derived macrophages (MDM) 15 . This phenotype is distinguished by the lower expression of activation markers, such as HLA‐DR and CD86, along with the macrophage marker CD163 15 . However, we did not determine whether this effect enacted by T2D on monocytes has any consequences in the context of TB infection.…”

Section: Introductionmentioning

confidence: 99%

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Impact of type 2 diabetes on the capacity of human macrophages infected with Mycobacterium tuberculosis to modulate monocyte differentiation through a bystander effect

et al. 2021

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Type 2 diabetes mellitus (T2D) is a risk factor for the development of tuberculosis (TB) through mechanisms poorly understood. Monocytes and macrophages are key effector cells to control TB, but they are also subverted by Mycobacterium tuberculosis (Mtb). Specifically, Mtb can induce a bystander effect that skews monocyte differentiation towards macrophages with a permissive phenotype to infection. Here, we evaluated whether T2D impacts this TB aspect. Our approach was to differentiate monocytes from healthy control (HC) subjects and T2D patients into macrophages (MDM), and then assess their response to Mtb infection, including their secretome content and bystander effect capacity. Through flow cytometric analyses, we found a lower level of activation markers in MDM from T2D patients than from HC in response to mock (HLA‐DR, CD86 and CD163) or Mtb challenge (CD14 and CD80). In spite of high TGF‐β1 levels in mock‐infected MDM from T2D patients, cytometric bead arrays indicated that there were no major differences in the secretome cytokine content in these cells relative to HC‐MDM, even in response to Mtb. Mimicking a bystander effect, the secretome of Mtb‐infected HC‐MDM drove HC monocytes towards MDM with a permissive phenotype for Mtb intracellular growth. However, the secretome from Mtb‐infected T2D‐MDM did not exacerbate the Mtb load compared to secretome from Mtb‐infected HC‐MDM, possibly due to the high IL‐1β production relative to Mtb‐infected HC‐MDM. Collectively, despite T2D affecting the basal MDM activation, our approach revealed that it has no major consequence on their response to Mtb or capacity to generate a bystander effect influencing monocyte differentiation.

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Section: Discussionmentioning

confidence: 94%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Impact of type 2 diabetes on the capacity of human macrophages infected with Mycobacterium tuberculosis to modulate monocyte differentiation through a bystander effect

et al. 2021

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“…Valtierra-Alvarado et al observed a lower expression of HLA-DR and CD68 on both human monocytes and MDMs from T2D patients. HLA-DR expression in monocytes correlated negatively with HbA1c, VLDL-C and triglyceride concentrations, but HLA-DR and CD68 correlated positively with HDL-C [54]. Restrepo et al demonstrated reduced HLA-DR expression in diabetic monocytes, even after controlling for BMI and HDL-C. [55].…”

Section: T2d-related Chronic Hyperglycemiamentioning

confidence: 99%

Diabetes-Associated Susceptibility to Tuberculosis: Contribution of Hyperglycemia vs. Dyslipidemia

2021

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Diabetes is a major risk factor for tuberculosis (TB). Diabetes increases the risk of the progression from latent tuberculosis infection (LTBI) to active pulmonary TB and TB patients with diabetes are at greater risk of more severe disease and adverse TB treatment outcomes compared to TB patients without co-morbidities. Diabetes is a complex disease, characterised not only by hyperglycemia but also by various forms of dyslipidemia. However, the relative contribution of these underlying metabolic factors to increased susceptibility to TB are poorly understood. This review summarises our current knowledge on the epidemiology and clinical manifestation of TB and diabetes comorbidity. We subsequently dissect the relative contributions of body mass index, hyperglycemia, elevated cholesterol and triglycerides on TB disease severity and treatment outcomes. Lastly, we discuss the impact of selected glucose and cholesterol-lowering treatments frequently used in the management of diabetes on TB treatment outcomes.

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Bioactive poly(salicylic acid)‐poly(citric acid) scaffolds improve diabetic wound repair via regulating HIF‐1α, Nrf2 and macrophage

Xie,

Ma,

Luo

et al. 2024

J Biomedical Materials Res

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Diabetic wounds environment is over‐oxidized, over‐inflammatory, leading to difficulties in regenerating blood vessels, and retardation of healing in diabetic wounds. Therefore, diabetic wounds can be treated from the perspective of scavenging oxidative free radicals and reducing the level of inflammation. Herein, we report a bioactive poly(salicylic acid)‐poly(citric acid) (FPSa‐PCG) hydrogel for diabetic wound repair. The FPSa‐PCG hydrogel shows abilities of antioxidation, anti‐inflammation, and regulation of macrophage phenotype. The FPSa‐PCG hydrogel showed good biocompatibility, and obtain the abilities of promotion of macrophages migration, reduction of ROS generation, suppression of the M1‐type macrophage polarization. FPSa and PCG could synergistically enhance the angiogenesis through upregulating the mRNA expression of HIF1Α, VEGF, and CD31 in endothelial cells and reduce the ROS level of macrophages through upregulating the mRNA expression of Nrf2. The in vivo diabetic wound model confirmed the promoting effect of FPSa‐PCG hydrogel on wound closure in diabetes. The further studies found that FPSa‐PCG hydrogel could induce the CD31 protein expression in the subcutaneous tissue and inhibit the TNF‐a protein expression. This work shows that the simple composition FPSa‐PCG hydrogel has a promising therapeutic potential in the treatment of diabetic wounds.

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Type 2 diabetes mellitus metabolic control correlates with the phenotype of human monocytes and monocyte-derived macrophages

Cited by 17 publications

References 45 publications

Impact of type 2 diabetes on the capacity of human macrophages infected with Mycobacterium tuberculosis to modulate monocyte differentiation through a bystander effect

Impact of type 2 diabetes on the capacity of human macrophages infected with Mycobacterium tuberculosis to modulate monocyte differentiation through a bystander effect

Diabetes-Associated Susceptibility to Tuberculosis: Contribution of Hyperglycemia vs. Dyslipidemia

Bioactive poly(salicylic acid)‐poly(citric acid) scaffolds improve diabetic wound repair via regulating HIF‐1α, Nrf2 and macrophage

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