X. Li, L. Lin, X. Duan, J. Dai, T. Hu, and H. Cai, “Efficacy and Mechanism of Action of Ginsenoside Rg3 on Radiation Proctitis in Rats,” Immunity, Inflammation and Disease 12 (2024): e70015, https://doi.org/10.1002/iid3.70015.
In the article, the following errors were identified.
Author Affiliation
Lili Lin's affiliation was originally stated as 2Department of Oncology, Suqian First People's Hospital, Suqian, China. This should be 2Department of Oncology, Suqian First Hospital, Suqian China.
Correspondence:
Lili Lin was inadvertently missed from the original correspondence and should be added. The correspondence should read:
Lili Lin, Department of Oncology, Suqian First People's Hospital, Suqian, China. Email: [email protected]
Hongyi Cai, Department of Radiotherapy, Gansu Provincial Hospital, 204 Donggang West Rd, Lanzhou, Gansu, China. Email: [email protected] and [email protected]
Footnote:
Xuxia Li and Lili Lin did not contribute equally to this paper and this footnote should be removed from the article.
The online version of the article has been corrected.
We apologize for these errors.
Vaccination is one of the effective measures to prevent latent tuberculosis infection (LTBI) from developing into active tuberculosis (TB). Applying bioinformatics methods to pre-evaluate the biological characteristics and immunogenicity of vaccines can improve the efficiency of vaccine development.
To evaluate the immunogenicity of TB vaccine W541 and to explore the application of bioinformatics technology in TB vaccine research.
This study concatenated the immunodominant sequences of Ag85A, Ag85B, Rv3407, and Rv1733c to construct the W541 DNA vaccine. Then, bioinformatics methods were used to analyze the physicochemical properties, antigenicity, allergenicity, toxicity, and population coverage of the vaccine, to identify its epitopes, and to perform molecular docking with MHC alleles and Toll-like receptor 4 (TLR4) of the host. Finally, the immunogenicity of the vaccine was evaluated in animal experiments.
The W541 vaccine protein is a soluble cytoplasmic protein with a half-life of 1.1 h in vivo and an instability index of 45.37. It has good antigenicity and wide population coverage without allergenicity and toxicity. It contains 138 HTL epitopes, 73 CTL epitopes, 8 linear and 14 discontinuous B cell epitopes, and has a strong affinity for TLR4. Immune simulations have shown that it can effectively stimulate innate and adaptive immune responses. Animal experiments confirmed that the W541 DNA vaccine could effectively activate Th1- and Th17-type immune responses, producing high levels of IFN-γ and IL-17A, but could not significantly increase antibody levels.
The W541 DNA vaccine can induce strong cellular immune responses. However, further optimization of the vaccine design is needed to make the expressed protein more stable in vivo. Bioinformatics analysis could reveal the physicochemical and immunological information of vaccines, which is critical for guiding vaccine design and development.
The effectiveness of ultrasound stimulation in treating Alzheimer's disease (AD) has been reported in previous studies, but the underlying mechanisms remain unclear. This study investigated the effects of ultrasound stimulation on the proportion and function of microglia of different phenotypes, as well as on the levels of inflammatory factors. Additionally, it revealed the alterations in proteomic molecules in the mouse hippocampus following ultrasound stimulation treatment, aiming to uncover potential new molecular mechanisms.
Ultrasound stimulation was used to stimulate the hippocampus for 30 min per day for 5 days in the ultrasound stimulation-treated group. Amyloid plaque deposition was measured using immunofluorescence staining. M1 and M2 type microglia were labeled using immunofluorescent double staining, and the ratio was calculated. The levels of Aβ42, IL-10, and TNF-α were determined using ELISA kits. The quantitative proteomics method was employed to explore molecular changes in hippocampal proteins.
Ultrasound stimulation treatment reduced the average fluorescence intensity of amyloid plaques and the concentration of Aβ42. Compared to the AD group, ultrasound stimulation resulted in a 14% reduction in the proportion of M1 microglia and a 12% increase in the proportion of M2 microglia. The concentration of the anti-inflammatory factor IL-10 was significantly increased in the ultrasound stimulation-treated group. Proteomics analysis revealed 753 differentially expressed proteins between the ultrasound stimulation-treated and AD groups, with most being enriched in the oxidative phosphorylation pathway of mitochondria. Additionally, the activity of cytochrome c oxidase, involved in oxidative phosphorylation, was increased after ultrasound stimulation treatment.
Ultrasound stimulation affects microglial polarization, reduces amyloid plaque load, and enhances levels of anti-inflammatory factors in APP/PS1 mice. Proteomics analysis reveals molecular changes in hippocampal proteins after ultrasound stimulation treatment. The mechanism behind ultrasound stimulation-induced modulation of microglial polarization may be related to changes in mitochondrial oxidative phosphorylation.
Cancer is still regarded as a major worldwide health issue due to its high health and socioeconomic burden. Currently, lung cancer is the most common cause of cancer-related fatalities globally. Additionally, mesotheliomas and other cancers of the respiratory system, including those of the trachea, larynx, and bronchi, are also posing a significant health threat. Natural killer (NK) cells are lymphocytes of the innate immune system involved in response against cancer.
This review discussed recent findings in the context of NK cell activity in the immune surveillance of respiratory system cancers and NK cell-based treatments to combat those malignancies.
The presence of natural killer cells in the tumor microenvironment is shown to be associated with a higher survival rate in patients with various malignancies. However, cancerous cells benefit from several mechanisms to evade natural killer cell-mediated cytotoxicity, including reduced major histocompatibility complex I expression, shedding of ligands, upregulation of inhibitory receptors, and release of soluble factors. Using NK cells to design therapeutic approaches may enhance antitumor immunity and improve clinical outcomes. Clinical trials investigating the use of natural killer cells in combination with cytokine stimulation or immune checkpoint inhibitors have exhibited promising results in various respiratory system malignancies.
Respiratory system cancers present significant health challenges worldwide, and while NK cells play a crucial role in tumor surveillance, tumors often evade NK cell responses through various mechanisms. Advances in NK cell-based therapies, including CAR-NK cells, immune checkpoint inhibitors, and cytokine stimulation, have shown promising outcomes in tackling these tactics. However, challenges such as the immunosuppressive tumor microenvironment persist. Ongoing research is crucial to improve NK cell therapies by targeting autophagy, modulating miRNAs, and developing combinatorial approaches to enhance treatment efficacy for respiratory cancers.
Some changes in nasal mucus and paranasal sinuses may occur due to zinc deficiency, which can cause chronic rhinosinusitis with nasal polyps (CRSwNP). The current study was designed to compare the serum zinc concentration between patients with chronic rhinosinusitis complicated with eosinophilic or neutrophilic nasal polyps and a control group.
A total of 105 patients participated in the study. Patients in three different groups were evaluated for CRSwNP (35 in the eosinophilia group and 35 in the neutrophil group), and 35 patients underwent surgery for reasons other than polyposis (control group). The serum zinc level was determined.
The mean age of the patients was 39.4 ± 12.61 years. Forty-one patients (39%) were female. Based on the enzyme linked immunosorbent assay results, the average serum zinc level in the control group was 137.01 ± 19.42 (μgm/100 mL), and in all patients with CRSwNP, it was 127.27 ± 21.7 (μgm/100 mL). The serum zinc concentration in patients with CRSwNP was significantly lower than that in the control group (p = .027). Among the CRSwNP patients with eosinophilic polyps and neutrophilic polyps, 130.42 ± 21.92 (μgm/100 mL) and 127.27 ± 21.7 (μgm/100 mL), respectively, were detected. Based on the statistical analysis, the neutrophilic and eosinophilic groups were homogenous according to the average serum zinc concentration (p = .631), and the same conditions prevailed for the eosinophilic and control groups (p = .574). There was a noticeable distinction between the neutrophilic group and the control group (p = .034).
Serum zinc concentrations were significantly lower in patients with neutrophilic polyps than in the general population. This difference may be due to the essential role of zinc in the inflammatory process in patients with neutrophilic polyposis.
Smoke inhalation lung injury (SILI) is a common complication in fires and wars, characterized by acute onset and severe condition. Pirfenidone (PFD), a new small-molecule drug, has been shown to improve lung function and inhibit pulmonary fibrosis and inflammation. This study aimed to elucidate the effect and underlying mechanism of PFD on SILI in rats.
SILI rats were constructed using a homemade smoking device, which was then treated with PFD. The blood was collected from the abdominal aorta, and the arterial blood gas was detected. The productions of oxidative stress markers and inflammatory cytokines in plasma were measured by enzyme linked immunosorbent assay assay. Moreover, the alveolar surface area, wet:dry weight ratio of the lung tissues, and bronchoalveolar lavage fluid (BALF) were determined as well. The pulmonary histopathology, cell apoptosis, and the related proteins of nuclear factor kappa B (NF-κB) pathway were determined by hematoxylin-eosin staining, TdT-mediated dUTP-biotin nick end labeling, and western blot assays, respectively.
PFD had a significant protective effect on SILI via inhibiting oxidative stress, inflammation, and apoptosis. Mechanistically, PFD inhibited the activation of NF-κB pathway in vivo. Moreover, activation of NF-κB pathway attenuated the PFD-mediated protective effect against SILI.
These data demonstrate that PFD alleviates SILI of rats via the NF-κB signaling pathway, which provides an attractive therapeutic option for SILI treatment.
Atopic dermatitis (AD) is a type of chronic inflammatory disorder that affects all age groups including children. AD is characterized by elevated inflammatory marker levels.
To assess the safety and effectiveness of topical tacrolimus ointment versus topical hydrocortisone cream in the treatment of pediatric AD by comparing the two treatments' ability to reduce serum cytokines.
One hundred AD patients who fulfilled the eligibility criteria completed this clinical study. Two groups of 50 AD patients each were selected from Tanta University's Dermatology Department., Group 1 (the hydrocortisone group) was administered topical hydrocortisone cream for a duration of 4 months. For 4 months, Group 2 was administered tacrolimus topically. Serum levels of thymus and activation regulated chemokine (TARC), cutaneous T cell attractant chemokine (CTAC), interleukin-10 (IL-10), interleukin-6 (IL-6), E selectin (E-selectin), and thymic stromal lymphopoietin (TSLP) were measured during an evaluation of the patients by a dermatologist at the beginning and 4 months after the treatment had been started. Children's Dermatology Life Quality Index was used to assess quality of life in these patients.
With the exception of E-selectin, IL-6, and IL-10 (p > .05), the tacrolimus group had a significant reduction in TARC, CTACK, TSLP (p < .05) when compared to its baseline and when compared to the hydrocortisone group. Both groups showed a significant improvement in quality of life but no significant changes between groups were observed.
In children with AD, tacrolimus reduces inflammatory biomarkers better than hydrocortisone.
Eosinophil activation is associated with asthma. Whether air pollution affects the activation of blood eosinophils in patients with asthma remains unknown. In this study, we investigated the correlation between transcriptional activity in eosinophils and air pollutant exposure in patients receiving different levels of Global Initiative for Asthma (GINA) treatment.
We evaluated the expression levels of activation- and function-related genes in eosinophils from patients with GINA 4 or 5 (n = 20), those with GINA 3 (n = 12), and normal individuals (n = 7); the eosinophils were activated with interleukin (IL)−5 or IL-17. A land use regression model was used to estimate air pollutant exposure. The correlations between mRNA expression, lung function, and air pollutant exposure were investigated.
The expression levels of TGFB1, IL7R, and TLR3 were significantly higher for patients with GINA 4 or 5 than for those with GINA 3 or normal individuals. The expression of certain genes, particularly in IL-17-activated eosinophils, was correlated with lung function decline in patients with GINA 4 or 5. For patients with GINA 4 or 5, NO2 exposure was correlated with upregulated TGFB1 expression in IL-5-activated eosinophils. For patients with GINA 3, O3 exposure was correlated with upregulated CCR5, IL5RA, IL7R, and TGFB1 expression in IL-17-activated eosinophils and upregulated IL7R expression in IL-5-activated eosinophils.
Patients with GINA 4 or 5 may exhibit elevated transcriptional activity in eosinophils; this elevation is correlated with lung function decline. Air pollution may affect eosinophil mRNA expression in patients with asthma.
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：