Two-dimensional metal-organic framework for post-synthetic immobilization of graphene quantum dots for photoluminescent sensing.

Immobilization of graphene quantum dots (GQDs) on a solid support is crucial to prevent GQDs from aggregation in the form of solid powder and facilitate the separation and recycling of GQDs after use. Herein, spatially dispersed GQDs are post-synthetically coordinated within a two-dimensional (2D) and water-stable zirconium-based metal-organic framework (MOF). Unlike pristine GQDs, the obtained GQDs immobilized on 2D MOF sheets show photoluminescence in both suspension and dry powder. Chemical and photoluminescent stabilities of MOF-immobilized GQDs in water are investigated, and the use of immobilized GQDs in the photoluminescent detection of copper ions is demonstrated. Findings here shed the light on the use of 2D MOFs as a platform to further immobilize GQDs with various sizes and distinct chemical functionalities for a range of applications.

Epidemiological characteristics of common respiratory infectious diseases in children before and during the COVID-19 epidemic.

Background: Since the outbreak of coronavirus disease 2019 (COVID-19), public's awareness of infection prevention and control has increased overall, and various prevention and control measures have been adopted. These measures may also have a certain impact on the occurrence of other infectious diseases. Therefore, we collected information on children with several respiratory infectious diseases in Jinan Children's Hospital in China from 2016 to 2022 and analyzed their changes. Method: We collected data on age, sex and number of cases of pertussis, measles, scarlet fever, pulmonary tuberculosis, mumps and influenza, which were diagnosed by clinical and laboratory criteria, from 1 January 2016 to 31 December 2022 in Jinan Children's Hospital in Jinan, Shandong Province, China. Data on the number of people affected by these diseases in China from the Chinese Center for Disease Control and Prevention were compared. Then, we processed the data by using WPS Excel 2019 and SPSS. Results: A total of 12,225 cases were included in this study in Jinan Children's Hospital, which consisted of 3,688 cases of pertussis (2,200 cases before COVID-19 and 1,488 during COVID-19), 680 cases of measles (650 cases before COVID-19 and 30 during COVID-19), 4,688 cases of scarlet fever (4,001 cases before COVID-19 and 687 during COVID-19), 114 cases of tuberculosis (86 cases before COVID-19 and 28 during COVID-19), 449 cases of mumps (340 cases before COVID-19 and 109 during COVID-19) and 2,606 cases of influenza (1,051 cases before COVID-19 and 1,555 during COVID-19). The numbers of children in the hospital with pertussis, measles, scarlet fever, mumps and influenza decreased substantially during COVID-19 in 2020-2022 compared with numbers in 2016-2019, while numbers of patients in China with all six respiratory infectious diseases, including pulmonary tuberculosis, declined during the pandemic. A rebound of pertussis, scarlet fever and influenza was observed in 2021 and 2022. Conclusions: The study found that viral pathogens such as those causing measles, mumps and influenza all decreased during the pandemic, after which influenza rebounded. Infection diseases caused by bacteria such as scarlet fever and pertussis also decreased during COVID-19, and then a rebound occurred. However, tuberculosis stayed relatively constant.

Expression of circulating angiotensin-converting enzyme 2 in children with asthma and the effects of inhaled corticosteroids.

BACKGROUND: The global spread of coronavirus disease 2019 (COVID-19) has resulted in a significant disease burden, yet asthma patients do not have the expected high morbidity and mortality rates in the pandemics of COVID-19. OBJECTIVE: To find the difference of angiotensin-converting enzyme 2 (ACE2) in asthma and nonasthma children and evaluate the effect of inhaled corticosteroids (ICS) on its expression. METHODS: The ACE2, immunoglobulin E (IgE), and eosinophils were tested in different children. RESULTS: A total of 157 children aged 3-16 years were enrolled. The expression of ACE2 in asthma children were lower than nonasthma children (T = -2.512, p = .013). Allergic nonasthma children had a significant higher ACE2 expression than children with allergic asthma (p = .013) and nonallergic asthma (p = .029). The expression of ACE2 had no significant difference between first-diagnosed asthma children and that had been treated with ICS for ≥6 months (F = 0.028, p = .598). The allergic asthma children showed a significantly higher eosinophils cells (EC) count than the allergic nonasthma (W = 200, p < .001) and nonallergic nonasthma children (W = 1089, p < .001). Nonallergic asthma children also had a significant higher EC count than the allergic non-asthma (W = 182.5, p < .001) and nonallergic non-asthma (W = 200.5, p < .001) children. There was no significant difference in IgE levels between asthmatic children and non-asthmatic children (W = 2792.5, p = .18). CONCLUSION: Circulating ACE2 levels in asthmatic children were lower than those in non-asthmatic children and ICS treatment for ≥6 months did not affect the expression of ACE2 in peripheral blood in the asthma children.

Interfacial modification in perovskite-based tandem solar cells.

With photovoltaic performance of metal halide perovskite-based solar cells skyrocketing to approximately 26% and approaching the theoretical Shockley-Queisser limit of single junction solar cells, researchers are now exploring multi-junction tandem solar cells that use perovskite materials to achieve high efficiency next-generation photovoltaics. Various types of bottom subcells, including silicon solar cells used commercially in industry, chalcogenide thin film cells, and perovskite cells, have been combined with perovskite top subcells on the strength of facile fabrication methods based on solution processes. However, owing to the nature that photovoltages of the subcells are added up and the structure containing numerous layers, interfacial issues that cause open-circuit voltage (VOC) deficit need to be handled carefully. In addition, morphological issues or process compatibility make it difficult to fabricate solution-processed perovskite top cells. In this paper, we summarize and review the fundamentals and strategies to overcome interfacial issues in tandem solar cells for high efficiency and stability confronting this field.

OASL1-Mediated Inhibition of Type I IFN Reduces Influenza A Infection-Induced Airway Inflammation by Regulating ILC2s.

PURPOSE: Three observations drove this study. First, 2'-5'-oligoadenylate synthetase-like protein (OASL) is a negative regulator of type I interferon (IFN). Second, type I IFN plays a central role during virus infections and the pathogenesis of various diseases, including asthma. Third, influenza A virus (IAV) causes non-eosinophilic asthma. To evaluate the potential relationships between OASL, type I IFN, and pulmonary innate immune cells in IAV-induced acute airway inflammation by using Oasl1-/- mice. METHODS: Asthma was induced in wild-type (WT) and Oasl1-/- mice with IAV or ovalbumin (OVA). Airway hyperreactivity (AHR) and immune cell infiltration in the bronchoalveolar lavage (BAL) fluids were measured. The immune cells in the lungs were analyzed by flow cytometry. To investigate the ability of type I IFN to shape the response of lung type 2 innate lymphoid cells (ILC2s), IFN-α was treated intratracheally. Plasmacytoid dendritic cells (pDCs) sorted from bone marrow and ILC2s sorted from lungs of naive mice were co-cultured with/without interferon-alpha receptor subunit 1 (IFNAR-1)-blocking antibodies. RESULTS: In the IAV-induced asthma model, Oasl1-/- mice developed greater AHR and immune cell infiltration in the BAL fluids than WT mice. This was not observed in OVA-induced asthma, a standard model of allergen-induced asthma. The lungs of infected Oasl1-/- mice also had elevated DC numbers and Ifna expression and depressed IAV-induced ILC2 responses, namely, proliferation and type 2 cytokine and amphiregulin production. Intratracheal administration of type I IFN in naïve mice suppressed lung ILC2 production of type 2 cytokines and amphiregulin. Co-culture of ILC2s with pDCs showed that pDCs inhibit the function of ILC2s by secreting type I IFN. CONCLUSIONS: OASL1 may impede the IAV-induced acute airway inflammation that drives AHR by inhibiting IAV-induced type I IFN production from lung DCs, thereby preserving the functions of lung ILC2s, including their amphiregulin production.

Increased GM-CSF-producing NCR- ILC3s and neutrophils in the intestinal mucosa exacerbate inflammatory bowel disease.

OBJECTIVES: Inflammatory bowel disease (IBD) is characterised by dysregulated mucosal immune responses associated with genetic, environmental and microbial factors. Recent therapies targeting key inflammatory mediators such as tumor necrosis factor (TNF)-α emphasise the importance of innate immunity in the development of IBD. METHODS: We examined the distribution of innate immune cells such as innate lymphoid cells (ILCs) and myeloid cells in the intestinal epithelium from children diagnosed as IBD and murine models of colitis induced by dextran sulphate sodium (DSS) or an anti-CD40 antibodies. RESULTS: We found an increased number of type 3 ILCs (ILC3s) that do not express the natural cytotoxicity receptor (NCR) and neutrophils, in both human IBD patients and colitis-induced mice. A co-culture experiment of neutrophils with NCR- ILC3s revealed that NCR- ILC3s stimulate neutrophils by producing granulocyte-macrophage colony-stimulating factor (GM-CSF). Furthermore, a blockade of GM-CSF could inhibit the development of IBD by inhibiting neutrophil activity. CONCLUSION: The NCR- ILC3: GM-CSF: neutrophil axis could contribute to the development of IBD.

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11cintermediate macrophages.

BACKGROUND: Chlorine is widely used in daily life as disinfectant. However, chronic exposure to chlorine products aggravates allergic TH 2 inflammation and airway hyperresponsiveness (AHR). Innate lymphoid cells (ILCs) in airways contribute to the inception of asthma in association with virus infection, pollution, and excess of nutrient, but it is not known whether chronic chlorine exposure can activate innate immune cells. The aim of this study was to evaluate the impact of chlorine inhalation on the innate immunity such as ILCs and macrophages in relation with the development of asthma by using murine ovalbumin (OVA) sensitization/challenge model. METHODS: Six-week-old female BALB/c mice were sensitized and challenged with OVA in the presence and absence of chronic low-dose chlorine exposure by inhalation of naturally vaporized gas of 5% sodium hypochlorite solution. AHR, airway inflammatory cells, from BALF and the population of ILCs and macrophages in the lung were evaluated. RESULTS: The mice exposed to chlorine with OVA (Cl + OVA group) showed enhanced AHR and eosinophilic inflammation compared to OVA-treated mice (OVA group). The population of TH 2 cells, ILC2s, and ILC3s increased in Cl + OVA group compared with OVA group. CD11cint macrophages also remarkably increased in Cl + OVA group compared with OVA group. The deletion of macrophages by clodronate resulted in reduction of ILC2s and ILC3s population which was restored by adoptive transfer of CD11cint macrophages. CONCLUSIONS: Chronic chlorine inhalation contributes to the exacerbation of airway inflammation in asthmatic airway by mobilizing pro-inflammatory macrophage into the lung as well as stimulating group 2 and 3 ILCs.

Invariant NKT Cells Functionally Link Microbiota-Induced Butyrate Production and Joint Inflammation.

Emerging evidence indicates that the gut microbiota contributes to the regulation of joint inflammation by modulating the function of immune cells. However, the mechanism by which the microbiota regulates joint inflammation is unclear. To address this, we investigated the effect of the gut microbiota on Ab-induced arthritis (AIA). Feeding mice a high-fiber diet attenuated AIA in a microbiota-dependent manner. Among the short-chain fatty acids produced by the microbiota, butyrate suppressed cytokine production by invariant NKT (iNKT) cells by inhibiting class I histone deacetylases. Furthermore, butyrate alleviated AIA in wild-type, but not iNKT cell-deficient Jα18 knockout (KO), mice. Adoptive transfer of butyrate-pretreated iNKT cells had no effect on AIA in Jα18 KO mice, whereas transfer of untreated iNKT cells into Jα18 KO mice restored AIA. In conclusion, our data indicate that gut microbiota-induced butyrate production attenuates AIA by inhibiting cytokine production by iNKT cells. Thus, the microbiota/butyrate/iNKT cell axis may be a therapeutic target for joint inflammation.

Innate immune crosstalk in asthmatic airways: Innate lymphoid cells coordinate polarization of lung macrophages.

BACKGROUND: Recent studies have emphasized the role of innate lymphoid cells (ILCs) in the development of asthma. The involvement of group 2 innate lymphoid cells (ILC2s) in asthma is well studied: however, the participation of other types of ILCs in the development of asthma remains unclear. OBJECTIVE: This study aims to understand the role of various ILCs in patients with asthma, especially their effect on macrophage polarization. METHODS: Each subset of ILCs and macrophages in induced sputum from 51 steroid-naive patients with asthma and 18 healthy donors was analyzed by using flow cytometry. Alveolar macrophages (AM) were sorted and cocultured with each subset of ILCs to determine whether the polarization of macrophages could be regulated by ILCs. RESULTS: In addition to ILC2s, numbers of group 1 innate lymphoid cells (ILC1s) and group 3 innate lymphoid cells (ILC3s) were increased in induced sputum from asthmatic patients when compared with those in healthy control subjects. The dominance of macrophages in induced sputum was more prominent in asthmatic patients than in healthy control subjects. A positive correlation between numbers of ILC2s and numbers of M2 macrophages and those of ILC1s/ILC3s and M1 macrophages was observed. Coculture of ILC2s with AMs induced expression of M2 macrophage-related genes, whereas coculture of ILC1s and ILC3s with AMs induced expression of M1 macrophage-related genes through cytokine secretion, as well as cell-cell contact. According to the inflammatory signature, patients with eosinophilic asthma have more ILC2s and M2 macrophages, and those with noneosinophilic asthma have an M1 macrophage-dominant profile. CONCLUSION: A different subset of ILCs regulates macrophage polarization, contributing to developing the distinct phenotype of asthma.

Functional Defects in Type 3 Innate Lymphoid Cells and Classical Monocytes in a Patient with Hyper-IgE Syndrome.

Hyper-IgE syndrome (HIES) is a very rare primary immune deficiency characterized by elevated serum IgE levels, recurrent bacterial infections, chronic dermatitis, and connective tissue abnormalities. Autosomal dominant (AD) HIES involves a mutation in signal transducer and activator of transcription 3 (STAT3) that leads to an impaired TH17 response. STAT3 signaling is also involved in the function of RORγt+ type 3 innate lymphoid cells (ILC3s) and RORγt+TH17 cells. The aim of this study was to investigate the role of innate immune cells such as innate lymphoid cells (ILCs), granulocytes, and monocytes in a patient with HIES. Peripheral blood mononuclear cells (PBMCs) from a patient with HIES and three age-matched healthy controls were obtained for the analysis of the innate and adaptive immune cells. The frequencies of ILCs in PBMCs were lower in the patient with HIES than in the controls. Moreover, granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-17A produced by ILC3s in PBMCs were lower in the patient with HIES than the controls. Compared with the controls, classical monocytes (CD14+CD16low), which have a high antimicrobial capability, were also lower in the patient with HIES, while non-classical monocytes (CD14lowCD16+) as well as intermediate monocytes (CD14+CD16intermediate) were higher. Taken together, these results indicate that the impaired immune defense against pathogenic microbes in the patient with HIES might be partially explained by functional defects in ILC3s and inflammatory monocytes.

IL-23 secreted by bronchial epithelial cells contributes to allergic sensitization in asthma model: role of IL-23 secreted by bronchial epithelial cells.

IL-23 has been postulated to be a critical mediator contributing to various inflammatory diseases. Dermatophagoides pteronyssinus (Der p) is one of the most common inhalant allergens. However, the role of IL-23 in Der p-induced mouse asthma model is not well understood, particularly with regard to the development of allergic sensitization in the airways. The objective of this study was to evaluate roles of IL-23 in Der p sensitization and asthma development. BALB/c mice were repeatedly administered Der p intranasally to develop Der p allergic sensitization and asthma. After Der p local administration, changes in IL-23 expression were examined in lung tissues and primary epithelial cells. Anti-IL-23p19 antibody was given during the Der p sensitization period, and its effects were examined. Effects of anti-IL-23p19 antibody at bronchial epithelial levels were also examined in vitro. The expression of IL-23 at bronchial epithelial layers was increased after Der p local administration in mouse. In Der p-induced mouse models, anti-IL-23p19 antibody treatment during allergen sensitization significantly diminished Der p allergic sensitization and several features of allergic asthma including the production of Th2 cytokines and the population of type 2 innate lymphoid cells in lungs. The activation of dendritic cells in lung-draining lymph nodes was also reduced by anti-IL-23 treatment. In murine lung alveolar type II-like epithelial cell line (MLE-12) cells, IL-23 blockade prevented cytokine responses to Der p stimulation, such as IL-1α, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-33, and also bone marrow-derived dendritic cell activation. In conclusion, IL-23 is another important bronchial epithelial cell-driven cytokine which may contribute to the development of house dust mite allergic sensitization and asthma.