BackgroundAedes albopictus, commonly known as the tiger mosquito, has attracted global attention because its bite can transmit several viruses, such as dengue virus. With the absence of an effective therapy and vaccine, mosquito control is the sole method for dengue fever control. However, Ae. albopictus has developed resistance to most insecticides, especially pyrethroids. Many scholars have conducted thorough research for the target-site of pyrethroids. The main target-site is the voltage-gated sodium channel gene (VGSC) whose mutation causes knockdown resistance (kdr). The spatial distribution of three locus kdr mutations in Ae. albopictus has not been comprehensively analyzed nationwide in China. In addition, the relationship between the frequency of kdr mutations and dengue fever has not yet been explored.MethodsA total of 2,241 Ae. albopictus samples from 49 populations from 11 provinces of mainland China were collected in 2020 and analyzed for mutations in the VGSC gene. DNAstar 7.1. Seqman and Mega-X were used to compare the sequences and read the peak map to confirm the genotypes and alleles of each mutation. ArcGIS 10.6 software was used to make interpolation and extract meteorological data of collection sites and to conduct spatial autocorrelation analysis. R 4.1.2 software was used to conduct a chi-square test for kdr mutations and dengue area and to analyze the correlation between meteorological factors and kdr mutations.ResultsThe overall frequencies of mutant alleles at 1016G, 1532T, and 1534S/C/L were 13.19%, 4.89%, and 46.90%, respectively. Mutations at the three loci were found at 89.80% (44/49), 44.90% (22/49), and 97.96% (48/49) of the field populations. At each of the loci V1016 and I1532, only one allele was detected, which was GGA(G) and ACC(T), respectively. Five mutant alleles were found at codon 1534: TCC/S (33.49%), TGC/C (11.96%), TTG/L (0.60%), CTC/L (0.49%), and TTA/L (0.58%). In total, 31 triple-locus genotype combinations were found, and the single locus mutation was the most common. We also found firstly triple-locus mutant individuals, whose genotypes were V/G+I/T+F/S and V/G+I/T+S/S. The 1016 and 1532 mutation rates were significantly negatively related to the annual average temperature (AAT), but the 1534 mutation rate was significantly positively related to AAT. The 1532 mutation rate was significantly positively related to the 1016 mutation rate but negatively related to the 1534 mutation rate. A relationship was observed between the 1534 codon mutation rate and dengue epidemic areas in this study. Furthermore, spatial autocorrelation analysis results showed that the mutation rates of different codons in different geographical areas had spatial aggregation and positive spatial correlation.ConclusionThis study showed that the multiple kdr mutations at codon 1016, 1532 and 1534 of Ae. albopictus were found in most areas of China. Two novel triple-locus genotype combinations, V/G+I/T+F/S and V/G+I/T+S/S, were detected in this study. In addition, the relationship between mosquito resistance and dengue fever outbreak should be further explored, especially considering the insecticide-usage history in different areas. The characteristic of spatial aggregation of VGSC gene mutation rates reminds us to notice the gene exchange and similarity of insecticide usage in the adjacent areas. The use of pyrethroids should be restricted to delay resistance development. New-type insecticides should be developed to adjust the changes in the resistance spectrum. Our study provides abundant data on the Ae. albopictuskdr gene mutation in China; these findings will be useful for the correlation analysis of molecular mechanism of insecticide resistance.

BackgroundPreeclampsia (PE) is a common pregnancy-related disorder characterized by disrupted maternal-fetal immune tolerance, involving diffuse inflammatory responses and vascular endothelial damage. Alterations in the gut microbiota (GM) during pregnancy can affect intestinal barrier function and immune balance.Aims and purposeThis comprehensive review aims to investigate the potential role of short-chain fatty acids (SCFAs), essential metabolites produced by the GM, in the development of PE. The purpose is to examine their impact on colonic peripheral regulatory T (Treg) cells, the pathogenic potential of antigen-specific helper T (Th) cells, and the inflammatory pathways associated with immune homeostasis.Key insightsAn increasing body of evidence suggests that dysbiosis in the GM can lead to alterations in SCFA levels, which may significantly contribute to the development of PE. SCFAs enhance the number and function of colonic Treg cells, mitigate the pathogenic potential of GM-specific Th cells, and inhibit inflammatory progression, thereby maintaining immune homeostasis. These insights highlight the potential significance of GM dysregulation and SCFAs produced by GM in the pathogenesis of PE. While the exact causes of PE remain elusive, and definitive clinical treatments are lacking, the GM and SCFAs present promising avenues for future clinical applications related to PE, offering a novel approach for prophylaxis and therapy.

Stroke, a serious systemic inflammatory disease, features neurological deficits and cardiovascular dysfunction. Neuroinflammation is characterized by the activation of microglia after stroke, which disrupts the cardiovascular-related neural network and the blood–brain barrier. Neural networks activate the autonomic nervous system to regulate the cardiac and blood vessels. Increased permeability of the blood–brain barrier and the lymphatic pathways promote the transfer of the central immune components to the peripheral immune organs and the recruitment of specific immune cells or cytokines, produced by the peripheral immune system, and thus modulate microglia in the brain. In addition, the spleen will also be stimulated by central inflammation to further mobilize the peripheral immune system. Both NK cells and Treg cells will be generated to enter the central nervous system to suppress further inflammation, while activated monocytes infiltrate the myocardium and cause cardiovascular dysfunction. In this review, we will focus on microglia-mediated inflammation in neural networks that result in cardiovascular dysfunction. Furthermore, we will discuss neuroimmune regulation in the central–peripheral crosstalk, in which the spleen is a vital part. Hopefully, this will benefit in anchoring another therapeutic target for neuro-cardiovascular dysfunction.

BackgroundPreeclampsia (PE) is a common pregnancy-related disorder characterized by disrupted maternal-fetal immune tolerance, involving diffuse inflammatory responses and vascular endothelial damage. Alterations in the gut microbiota (GM) during pregnancy can affect intestinal barrier function and immune balance.Aims and purposeThis comprehensive review aims to investigate the potential role of short-chain fatty acids (SCFAs), essential metabolites produced by the GM, in the development of PE. The purpose is to examine their impact on colonic peripheral regulatory T (Treg) cells, the pathogenic potential of antigen-specific helper T (Th) cells, and the inflammatory pathways associated with immune homeostasis.Key insightsAn increasing body of evidence suggests that dysbiosis in the GM can lead to alterations in SCFA levels, which may significantly contribute to the development of PE. SCFAs enhance the number and function of colonic Treg cells, mitigate the pathogenic potential of GM-specific Th cells, and inhibit inflammatory progression, thereby maintaining immune homeostasis. These insights highlight the potential significance of GM dysregulation and SCFAs produced by GM in the pathogenesis of PE. While the exact causes of PE remain elusive, and definitive clinical treatments are lacking, the GM and SCFAs present promising avenues for future clinical applications related to PE, offering a novel approach for prophylaxis and therapy.