Association of circulating inflammatory cells and platelets with gestational diabetes and pregnancy outcomes.
TL;DR: In this article, the authors summarized the studies in this field based on the recent literature and provided evidence for the value of these novel and practical serological markers in early identification of GDM and the prevention and its adverse outcomes.
About: This article is published in Clinica Chimica Acta.The article was published on 2021-12-01. It has received 2 citations till now. The article focuses on the topics: Gestational diabetes & Pregnancy.
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TL;DR: In this paper , the authors investigated the associations of inflammatory blood cell parameters in both early and middle pregnancy and their change patterns from early to middle pregnancy with gestational diabetes mellitus (GDM) risk.
Abstract: CONTEXT
Chronic low-grade inflammation may play a crucial role in the pathogenesis of gestational diabetes mellitus (GDM). However, prospective studies on the relations of inflammatory blood cell parameters during pregnancy with GDM are lacking.
OBJECTIVE
To prospectively investigate the associations of inflammatory blood cell parameters in both early and middle pregnancy and their change patterns from early to middle pregnancy with GDM risk.
METHODS
We used data from the Tongji-Shuangliu Birth Cohort. Inflammatory blood cell parameters (white blood cells, neutrophils, lymphocytes, monocytes, neutrophil to lymphocyte ratio [NLR], and platelets) were assayed before 15 weeks and 16-28 gestational age. Logistic regression was used to evaluate the associations between inflammatory blood cell parameters and GDM.
RESULTS
Of the 6354 pregnant women, 445 were diagnosed with GDM. After adjustment for potential confounders, white blood cells, neutrophils, lymphocytes, monocytes, and NLR in early pregnancy were positively associated with GDM risk (odds ratios [OR] [95% CI] for extreme-quartile comparison were 2.38 [1.76-3.20], 2.47 [1.82-3.36], 1.40 [1.06-1.85], 1.69 [1.27-2.24], and 1.51 [1.12-2.02], respectively, all P for trend ≤.010). Higher level of white blood cells, neutrophils, monocytes, and NLR in middle pregnancy were associated with an increased risk of GDM (all P for trend ≤.014). Stable high levels (≥median in both early and middle pregnancy) of white blood cells, neutrophils, monocytes, and NLR were positively associated with GDM risk (all P ≤.001).
CONCLUSION
Elevated white blood cells, neutrophils, monocytes, and NLR in both early and middle pregnancy and their stable high levels from early to middle pregnancy were associated with a higher GDM risk, highlighting that they might be clinically relevant for identifying individuals at high risk for GDM.
TL;DR: Wang et al. as discussed by the authors developed a visual nomogram model for predicting the probability of preterm delivery in women with GDM at the time of diagnosis, and validated the model on the training and validation cohort.
Abstract: Background The incidence of preterm delivery (<37 weeks’ gestation) is increased due to gestational diabetes mellitus (GDM). The preterm delivery is the leading cause of death in children. If potential preterm delivery can be diagnosed early and then prevented, adverse pregnancy outcomes can be improved. Therefore, effective methods are needed for early prediction of preterm delivery in women with GDM. Methods Patients with GDM defined as the presence of at least 1 plasma glucose abnormality at 24–28 weeks of pregnancy [fasting plasma glucose ≥5.1 mmol/L, 60-min ≥10.0 mmol/L, 120-min ≥8.5 mmol/L by 75 g oral glucose tolerance test (OGTT)] from the First Affiliated Hospital of Wenzhou Medical University were enrolled. The data (564 patients) recorded from January 2017 to June 2020 were named the training cohort, and the data (242 patients) obtained from patients with GDM, from July 2020 to January 2022, were named the validation cohort. Mann-Whitney U test and chi-square test were used to compare the skewed distributed and categorical data, respectively. According to the results of univariate logistic regression analysis, the multivariate logistic regression model was developed in the training cohort. Then, the nomogram was established. The validation of the nomogram was conducted on the training and validation cohort. Results No significant differences in baseline characteristics were detected between the 2 cohorts (all P>0.05). The multivariate analysis suggested that maternal age, insulin use, NLR, and monocyte count were the independent predictors of preterm delivery. A nomogram for predicting the probability of preterm delivery was developed. The model suggested good discrimination [areas under the curve (AUC) =0.885, 95% confidence interval (95% CI): 0.855–0.910, sensitivity =83.0%, specificity =83.1% in the training cohort; AUC =0.919, 95% CI: 0.858–0.980, sensitivity =90.6%, specificity =84.8% in the validation cohort] and good calibration [Hosmer-Lemeshow (HL) test: χ2=3.618, P=0.306 in the training cohort; χ2=6.012, P=0.111 in the validation cohort]. Conclusions The visual nomogram model appears to be a reliable approach for the prediction of preterm delivery, allowing clinicians to take timely measures to prevent the occurrence of preterm delivery in women with GDM at the time of GDM diagnosis, and deserves further investigation.
References
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TL;DR: It is described that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria, which degrade virulence factors and kill bacteria.
Abstract: Neutrophils engulf and kill bacteria when their antimicrobial granules fuse with the phagosome. Here, we describe that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria. These neutrophil extracellular traps (NETs) degrade virulence factors and kill bacteria. NETs are abundant in vivo in experimental dysentery and spontaneous human appendicitis, two examples of acute inflammation. NETs appear to be a form of innate response that binds microorganisms, prevents them from spreading, and ensures a high local concentration of antimicrobial agents to degrade virulence factors and kill bacteria.
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TL;DR: This review focuses on the functions of PRRs in innate immunity and their downstream signaling cascades and identifies cytoplasmic PRRs to detect pathogens that have invaded cytosols.
Abstract: The innate immune system is an evolutionally conserved host defense mechanism against pathogens. Innate immune responses are initiated by pattern recognition receptors (PRRs), which recognize specific structures of microorganisms. Among them, Toll-like receptors (TLRs) are capable of sensing organisms ranging from bacteria to fungi, protozoa, and viruses, and play a major role in innate immunity. However, TLRs recognize pathogens either on the cell surface or in the lysosome/endosome compartment. Recently, cytoplasmic PRRs have been identified to detect pathogens that have invaded cytosols. In this review, we focus on the functions of PRRs in innate immunity and their downstream signaling cascades.
2,049 citations
TL;DR: Research defining the signal transduction pathways induced by IL-17R family cytokines has lagged behind that of other cytokine families, but studies in the past 2 years have begun to delineate unusual functional motifs and new proximal signalling mediators used by the IL- 17R family to mediate downstream events.
Abstract: Interleukin-17A (IL-17A), the hallmark cytokine of the newly defined T helper 17 (T(H)17) cell subset, has important roles in protecting the host against extracellular pathogens, but also promotes inflammatory pathology in autoimmune disease. IL-17A and its receptor (IL-17RA) are the founding members of a newly described family of cytokines and receptors that have unique structural features which distinguish them from other cytokine families. Research defining the signal transduction pathways induced by IL-17R family cytokines has lagged behind that of other cytokine families, but studies in the past 2 years have begun to delineate unusual functional motifs and new proximal signalling mediators used by the IL-17R family to mediate downstream events.
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TL;DR: The mechanisms and consequences of TLR-mediated signal transduction are described with a focus on themes identified in the TLR pathways that also explain the operation of other immune signaling pathways.
867 citations
TL;DR: It is shown that neutrophils can be added to the extensive repertoire of immune cells that participate in inflammation-induced metabolic disease and that deletion of neutrophil elastase in high-fat-diet–induced obese (DIO) mice leads to less tissue inflammation that is associated with lower adipose tissue neutrophile and macrophage content.
Abstract: Chronic low-grade adipose tissue and liver inflammation is a major cause of systemic insulin resistance and is a key component of the low degree of insulin sensitivity that exists in obesity and type 2 diabetes. Immune cells, such as macrophages, T cells, B cells, mast cells and eosinophils, have all been implicated as having a role in this process. Neutrophils are typically the first immune cells to respond to inflammation and can exacerbate the chronic inflammatory state by helping to recruit macrophages and by interacting with antigen-presenting cells. Neutrophils secrete several proteases, one of which is neutrophil elastase, which can promote inflammatory responses in several disease models. Here we show that treatment of hepatocytes with neutrophil elastase causes cellular insulin resistance and that deletion of neutrophil elastase in high-fat-diet–induced obese (DIO) mice leads to less tissue inflammation that is associated with lower adipose tissue neutrophil and macrophage content. These changes are accompanied by improved glucose tolerance and increased insulin sensitivity. Taken together, we show that neutrophils can be added to the extensive repertoire of immune cells that participate in inflammation-induced metabolic disease.
761 citations