Atopic dermatitis (AD) and psoriasis are chronic skin diseases with a global impact, posing significant challenges to public health systems and severely affecting patients\' quality of life. This review delves into the key role of the gut microbiota in these diseases, emphasizing the importance of the gut-skin axis in inflammatory mediators and immune regulation and revealing a complex bidirectional communication system. We comprehensively assessed the pathogenesis, clinical manifestations, and treatment strategies for AD and psoriasis, with a particular focus on how the gut microbiota and their metabolites influence disease progression via the gut-skin axis. In addition, personalized treatment plans based on individual patient microbiome characteristics have been proposed, offering new perspectives for future treatment approaches. We call for enhanced interdisciplinary cooperation to further explore the interactions between gut microbiota and skin diseases and to assess the potential of drugs and natural products in modulating the gut-skin axis, aiming to advance the treatment of skin diseases.

Allergic rhinitis (AR) is a prevalent inflammatory disorder of the nasal mucosa, triggered by allergen exposure and characterized by symptoms such as sneezing, nasal congestion, itching, and rhinorrhea. This comprehensive review aims to unravel the molecular mechanisms underpinning AR, exploring the pathogenesis from allergen recognition to chronic inflammation and tissue remodelling. Central to the disease are immunoglobulin E (IgE)-mediated hypersensitivity reactions, involving key inflammatory mediators and cellular players such as mast cells, eosinophils, and T cells. Genetic predisposition and environmental factors also play significant roles in susceptibility and disease progression. Therapeutic strategies for AR are varied, ranging from symptomatic relief through antihistamines and nasal corticosteroids to more targeted approaches like allergen-specific immunotherapy. Emerging treatments focus on novel molecular pathways, with a growing emphasis on personalized medicine to optimize patient outcomes. Despite advancements, challenges remain in fully understanding the heterogeneity of AR and developing universally effective treatments. This review synthesizes current knowledge, highlighting critical insights into the molecular basis of AR and their implications for clinical practice. It underscores the need for integrated, multidisciplinary approaches to enhance therapeutic efficacy and calls for ongoing research to address unresolved questions and explore new frontiers in AR management. Through this comprehensive synthesis, the review aims to inform and inspire future research and clinical strategies, ultimately improving the quality of life for individuals affected by AR.

BACKGROUND: According to the theory of traditional Chinese medicine (TCM), the spleen and stomach are the basis of acquired nature and the source of qi and blood biochemistry. After surgery and chemotherapy, patients with colorectal cancer often develop spleen and stomach qi deficiency syndrome, leading to decreased immune function. Buzhong Yiqi decoction, a classic TCM prescription, has the effect of tonifying middle-jiao and invigorating qi, boosting Yang, and suppressing immune-related inflammation. Moreover, it is widely used in the treatment of spleen and stomach qi deficiency syndrome.
OBJECTIVE: To investigate the effect of Buzhong Yiqi decoction on spleen and stomach qi deficiency in patients with colorectal cancer.
METHODS: One hundred patients with colorectal cancer who underwent preoperative chemotherapy and laparoscopy at The First TCM Hospital of Changde from January 2022 to October 2023 were retrospectively analyzed. The patients were divided equally into control and observation groups. Both groups underwent conventional rehabilitation surgery, and the observation group was supplemented with Buzhong Yiqi decoction. SPSS 26.0 was used for statistical analyses. The χ 2 test was used for univariate analysis; independent sample t-tests were used in all cases.
RESULTS: No significant differences were observed preoperatively in the general characteristics of the two groups. Fourteen days post-surgery, the abdominal distension, emaciation, loose stool, loss of appetite, and vomiting scores were significantly lower in the observation group than in the control group (P < 0.05). Immune function and interleukin (IL)-10 levels in the observation group were significantly higher than those of the control group, whereas IL-6, tumor necrosis factor-α, and C-reactive protein levels, tumor biological indexes, and adverse reactions in the observation group were significantly lower than those of the control group (P < 0.05). One month after surgery, the patients\' quality of life in the observation group was significantly higher than that of the patients in the control group (P < 0.05).
CONCLUSIONS: Buzhong Yiqi decoction can regulate inflammatory responses and metabolic processes by enhancing immune function, thereby promoting overall immune nutrition and restoring the body\'s balance.

UNASSIGNED: This study aimed to explore the levels of circulating inflammatory factors CRP, IL-6, IL-10 and TNF- α based on the literature review. This study also examined the influence of single nucleotide polymorphism (SNP) sites on the susceptibility of abdominal aortic aneurysm (AAA) using meta-analysis and intended to provide additional information on pathogenesis of AAA research.
UNASSIGNED: Electronic databases including PubMed and Web of Science were systemically searched to collect the information on AAA, inflammatory factors such as CRP, IL-6, IL-10, TNF- α and the SNP sites for data extraction. Altogether six SNPs in four genes (rs3091244, CRP; rs1800947, CRP; rs1205, CRP; rs1800795, IL-6; rs1800896, IL-10; and rs1800629, TNF) were assessed.
UNASSIGNED: This study enrolled altogether 41 relevant investigations involving 9,007 AAA patients to carry out meta-analysis. According to pooled analysis, circulating CRP and IL-6 levels were shown to be related to the AAA, while plasma IL-10 and TNF- α levels were not associated with AAA. The circulating CRP level standard mean difference (SMD) was 0.30 (95% confidence interval (CI): 0.17-0.43), the IL-6 level SMD was 0.34 (95% CI: 0.20-0.49), the IL-10 level SMD was -0.01 (95% CI: -0.09-0.06), and the TNF- α level SMD was 0.09 (95% CI: 0.00-0.19). Similarly, the odds ratio (OR) of rs3091244 (CRP) under the recessive gene model was 1.70 (95% CI: 1.13-2.57). In addition, individuals with A and T mutant genes at locus rs3091244 might have a higher tendency of AAA susceptibility than those with C allele. Consecutively, the OR was 0.91 (95% CI: 0.51-0.97) for rs1800795 (IL-6) locus in the allele model, and individuals with G mutant gene at locus rs1800795 (IL-6) might be less susceptible to AAA than those with C allele. Meanwhile, the rs1800896 (IL-10) locus had a positive association under the five statistical models, and individuals with A mutant gene at locus rs1800896 might have a higher susceptibility to AAA than those with G allele. Nevertheless, the rs1800947 (CRP), rs1205 (CRP), and rs1800629 (TNF) loci did not have positive correlation under the five statistical models, with no statistical significance. The results indicate that the gene polymorphisms at rs1800629, rs1800947, and rs1205 loci were not related to the AAA susceptibility.
UNASSIGNED: Gene polymorphisms in certain known inflammatory mediators related to AAA susceptibility might serve as potential predictive biomarkers for clinical applications. Moreover, SNP of inflammatory mediators relevant to abdominal aortic aneurysmal formation and progression need extensive investigations to confirm these results.

UNASSIGNED: Degradation of host proteins by bacterial proteases leads to the subversion of the host response and disruption of oral epithelial integrity, which is considered an essential factor in the progression of periodontitis. High-temperature requirement A (HtrA) protease, which is critical for bacterial survival and environmental adaptation, is found in several oral bacteria, including the periodontal pathogen Tannerella forsythia. This study investigated the proteolytic activity of HtrA from T. forsythia and its ability to modulate the host response.
UNASSIGNED: HtrA of T. forsythia was identified bioinformatically and produced as a recombinant protein. T. forsythia mutants with depleted and restored HtrA production were constructed. The effect of T. forsythia wild-type, mutants and recombinant HtrA on the degradation of casein and E-cadherin was tested in vitro. Additionally, the responses of human gingival fibroblasts and U937 macrophages to the different HtrA-stimuli were investigated and compared to those triggered by the HtrA-deficient mutant.
UNASSIGNED: T. forsythia wild-type producing HtrA as well as the recombinant enzyme exhibited proteolytic activity towards casein and E-cadherin. No cytotoxic effect of either the wild-type, T. forsythia mutants or rHtrA on the viability of host cells was found. In hGFB and U937 macrophages, both T. forsythia species induced an inflammatory response of similar magnitude, as indicated by gene and protein expression of interleukin (IL)-1β, IL-6, IL-8, tumour necrosis factor α and monocyte chemoattractant protein (MCP)-1. Recombinant HtrA had no significant effect on the inflammatory response in hGFBs, whereas in U937 macrophages, it induced a transient inflammatory response at the early stage of infection.
UNASSIGNED: HtrA of T. forsythia exhibit proteolytic activity towards the host adhesion molecule E-cadherin and has the potential to influence the host response. Its role in the progression of periodontitis needs further clarification.

BACKGROUND: This study investigated the combination of venous stasis and inflammation in varicose vein development.
METHODS: The study included patients with primary varicose veins operated using high ligation and stripping of greater saphenous vein. All of them showed reflux at sapheno-femoral junction on preoperative Doppler ultrasound. Mesenteric veins from early or advanced gastric cancer specimens were used as control group. Inflammatory mediators expressed in the venous wall were measured via immunohistochemistry and compared between the two groups.
RESULTS: Thirty-five (59.3%) men and 24 women with a mean age of 52.8 years (range, 23-77 years) were included and 29 (49.2%) patients had edema or skin changes according to Clinical-Etiology-Anatomy-Pathophysiology (CEAP) classification and reporting standards for chronic venous disorders. The expression of interleukin 6 (IL-6) and transforming growth factor β1 (TGF-β1) in intima and those of IL-6 in media of greater saphenous veins increased, with statistically significant differences between the two groups (p < 0.001). IL-6 in media and TGF-β1 levels in intima were independent predictors of varicose veins (adjusted odds ratios 74.62 and 66.69, respectively).
CONCLUSIONS: Elevated venous pressure represented by reflux on Doppler ultrasound and increased expression of inflammatory cytokines including IL-6 in media and TGF-β1 in intima are associated with the development of varicose veins.

Although Down syndrome (DS) is considered a risk factor for hemodynamic instabilities (mainly pulmonary hypertension-PH) following surgery for congenital cardiac communications, many DS patients do surprising well postoperatively. We prospectively analyzed perioperative factors for a possible correlation with post-cardiopulmonary bypass (CPB) inflammatory reaction and postoperative PH in pediatric subjects. Sixty patients were enrolled (age 3 to 35 months), 39 of them with DS. Clinical and echocardiographic parameters (anatomical and hemodynamic) were computed preoperatively. Pulmonary and systemic mean arterial pressures (PAP and SAP) were assessed invasively intra and postoperatively. Immediate postoperative PAP/SAP ratio (PAP/SAPIPO) and the behavior of pressure curves were selected as primary outcome. Serum levels of 36 inflammatory proteins were measured by chemiluminescence preoperatively and 4 h post CPB. Of all factors analyzed, peripheral oxygen saturation (O2Sat, bedside assessment) was the only preoperative predictor of PAP/SAPIPO at multivariate analysis (p = 0.007). Respective values in non-DS, DS/O2Sat ≥ 95% and DS/O2Sat < 95% subgroups were 0.34 (0.017), 0.40 (0.027) and 0.45 (0.026), mean (SE), p = 0.004. The difference between non-DS and DS groups regarding postoperative PAP curves (upward shift in DS patients, p = 0.015) became nonsignificant (p = 0.114) after adjustment for preoperative O2Sat. Post-CPB levels of at least 5 cytokines were higher in patients with O2Sat < 95% versus those at or above this level, even within the DS group (p < 0.05). Thus, a baseline O2Sat < 95% representing pathophysiological phenomena in the airways and the distal lung, rather than DS in a broad sense, seems to be associated with post-CPB inflammation and postoperative PH in these patients.

Acute kidney injury (AKI) is a critical medical condition characterized by high morbidity and mortality rates. The pathogenesis of AKI potentially involves bursts of reactive oxygen species (ROS) bursts and elevated levels of inflammatory mediators. Developing nanoparticles (NPs) that downregulate ROS and inflammatory mediators is a promising approach to treat AKI. However, such NPs would be affected by the glomerular filtration barrier (GFB). Typically, NPs are too large to penetrate the glomerular system and reach the renal tubules─the primary site of AKI injury. Herein, we report the development of ultrasmall carbon dots-gallic acid (CDs-GA) NPs (∼5 nm). These NPs exhibited outstanding biocompatibility and were shown not only to efficiently eliminate ROS and alleviate oxidative stress but also to suppress the activation of the NF-κB signaling pathway, leading to a reduction in the release of inflammatory factors. Importantly, CDs-GA NPs were shown to be able to rapidly accumulate rapidly in the renal tissues without the need for intricate targeting strategies. In vivo studies demonstrated that CDs-GA NPs significantly reduced the incidence of cisplatin (CDDP)-induced AKI in mice, surpassing the efficacy of the small molecular drug, N-acetylcysteine. This research provides an innovative strategy for the treatment of AKI.

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UNASSIGNED: According to data from several observational studies, there is a strong association between circulating inflammatory cytokines and postherpetic neuralgia (PHN), but it is not clear whether this association is causal or confounding; therefore, the main aim of the present study was to analyze whether circulating inflammatory proteins have a bidirectional relationship with PHN at the genetic inheritance level using a Mendelian randomization (MR) study.
UNASSIGNED: The Genome-Wide Association Study (GWAS) database was used for our analysis. We gathered data on inflammation-related genetic variation from three GWASs of human cytokines. These proteins included 91 circulating inflammatory proteins, tumor necrosis factor-alpha (TNF-α), macrophage inflammatory protein 1b (MIP-1b), and CXC chemokine 13 (CXCL13). The PHN dataset was obtained from the FinnGen biobank analysis round 5, and consisted of 1,413 cases and 275,212 controls. We conducted a two-sample bidirectional MR study using the TwoSampleMR and MRPRESSO R packages (version R.4.3.1). Our main analytical method was inverse variance weighting (IVW), and we performed sensitivity analyses to assess heterogeneity and pleiotropy, as well as the potential influence of individual SNPs, to validate our findings.
UNASSIGNED: According to our forward analysis, five circulating inflammatory proteins were causally associated with the development of PHN: interleukin (IL)-18 was positively associated with PHN, and IL-13, fibroblast growth factor 19 (FGF-19), MIP-1b, and stem cell growth factor (SCF) showed reverse causality with PHN. Conversely, we found that PHN was closely associated with 12 inflammatory cytokines, but no significant correlation was found among the other inflammatory factors. Among them, only IL-18 had a bidirectional causal relationship with PHN.
UNASSIGNED: Our research advances the current understanding of the role of certain inflammatory biomarker pathways in the development of PHN. Additional verification is required to evaluate the viability of these proteins as targeted inflammatory factors for PHN-based treatments.