Fish oil supplementation in obese rats ameliorates metabolic syndrome response

Accumulation of visceral adipose tissue is associated with metabolic syndrome (MS), insulin resistance, and dyslipidemia. Here we examined several morphometric and biochemical parameters linked to MS in a rodent litter size reduction model, and how a 30-day fish oil (FO) supplementation affected these parameters. On day 3 post-birth, pups were divided into groups of ten or three. On day 22, rats were split into control (C) and small litter (SL) until 60 days old. Then, after metabolic disturbance and obesity were confirmed, FO supplementation started for 30 days and the new groups were named control (C), FO supplemented (FO), obese (Ob), and obese FO supplemented (ObFO). Comparison was performed by Student t-test or 2-way ANOVA followed by Tukey post hoc test. At the end of the 60-day period, SL rats were hyperphagic, obese, hypoinsulinemic, normoglycemic, and had high visceral fat depot and high interleukin (IL)-6 plasma concentration. Obese rats at 90 days of age were fatter, hyperphagic, hyperglycemic, hypertriacylgliceromic, hipoinsulinemic, with low innate immune response. IL-6 production ex vivo was higher, but in plasma it was not different from the control group. FO supplementation brought all biochemical changes to normal values, normalized food intake, and reduced body weight and fat mass in obese rats. The innate immune response was improved but still not as efficient as in lean animals. Our results suggested that as soon MS appears, FO supplementation must be used to ameliorate the morpho- and biochemical effects caused by MS and improve the innate immune response.

Effects of immune exhaustion and senescence of innate immunity in autoimmune disorders

Innate immune system activation is crucial in the inflammatory response, but uncontrolled activation can lead to autoimmune diseases. Cellular exhaustion and senescence are two processes that contribute to innate immune tolerance breakdown. Exhausted immune cells are unable to respond adequately to specific antigens or stimuli, while senescent cells have impaired DNA replication and metabolic changes. These processes can impair immune system function and disrupt homeostasis, leading to the emergence of autoimmunity. However, the influence of innate immune exhaustion and senescence on autoimmune disorders is not well understood. This review aims to describe the current findings on the role of innate immune exhaustion and senescence in autoimmunity, focusing on the cellular and molecular changes involved in each process. Specifically, the article explores the markers and pathways associated with immune exhaustion, such as PD-1 and TIM-3, and senescence, including Β-galactosidase (β-GAL), lamin B1, and p16ink4a, and their impact on autoimmune diseases, namely type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, and immune-mediated myopathies. Understanding the mechanisms underlying innate immune exhaustion and senescence in autoimmunity may provide insights for the development of novel therapeutic strategies.

Mechanism of Helicobacter pylori metabolites antagonizing host innate immunity / 中国免疫学杂志

Objective:To investigate potential mechanism of Helicobacter pylori metabolites antagonizing host innate immunity.Methods:RNA sequencing and pathway enrichment analysis were used to analyze only LPS-stimulated gastric mucosal cells GES-1,GES-1 cells co-treated with LPS and Helicobacter pylori culture supernatant,and untreated GES-1 cells.The culture supernatant of He-licobacter pylori was filtered by a 3KD ultrafiltration tube,and the filtered filtrate(metabolite part)and the retained solution(protein part)were treated with LPS-stimulated GES-1 cells to detect activity of NF-κB pathway,phosphorylation level of NF-κB,secretion levels of NF-κB pathway effectors TNF-α,IL-6 and IL-8.Identification of key metabolites by untargeted metabolic mass spectrometry.Results:Compared with GES-1 cells stimulated only by LPS,after co-treated with LPS and Helicobacter pylori culture supernatant,expression levels of various genes were regulated and tended to the level of GES-1 in untreated gastric mucosal cells,mainly in the NF-κB pathway.After co-treatment with LPS and culture supernatant of Helicobacter pylori,activity of NF-κB pathway was inhibited(P<0.05).Helicobacter pylori metabolites could inhibit the activity of NF-κB pathway,inhibit phosphorylation of NF-κB,and inhibit the secretion of NF-κB pathway effectors TNF-α,IL-6 and IL-8(P<0.05).1,5 and 25 μmol/L of Helicobacter pylori metabolite 2-D-Glu-copyranose(2DG)treatment inhibited activity of NF-κB pathway and phosphorylation of NF-κB in GES-1 cells,and secretion of NF-κB pathway effectors TNF-α,IL-6 and IL-8 were inhibited(P<0.05).After 2DG treatment,activity of NF-κB in GES-1 cells with TLR3,TLR4,TLR5,TLR6,TLR7,TLR8,TLR9 and TLR10 knockout were significantly decreased(P<0.05);while there was no significant changes in activity of NF-κB in TLR1 and TLR2 knockout GES-1 cells.Both TLR1 and TLR2 interactions were attenuated in GES-1 cells after 2DG treatment.Molecular docking showed that 2DG could bind to TLR2 amino acid disabled R321,K347 and F349,the binding energy was-12 kcal/mol.TLR2 wild-type and mutant plasmids(R321K,K347R,F349A)were constructed,and TLR2-knockout GES-1 cells were respectively transfected.It was found that 2DG treatment did not reduce NF-κB activity in GES-1 cells transfected with TLR2 mutant.Conclusion:Helicobacter pylori metabolite 2DG can interact with TLR2,reduce the formation of het-erodimers between TLR2 and TLR1,and inhibit the activity of innate immune NF-κB pathway.

Type 2 inflammatory diseases: a new pattern of Group 2 innate lymphoid cells-dendritic cells-T helper 2 cells and advances in targeted drug therapies / 中华实用儿科临床杂志

In recent years, the discovery of Group 2 innate lymphoid cells(ILC2) has expanded the understanding of type 2 immunity and promoted the birth of the concept of type 2 inflammation.Type 2 inflammation is an inflammatory reaction mediated by both innate and adaptive immunity.It is mainly involved by ILC2 cells and T helper 2 cells and is characterized by upregulation of type 2 cytokines and IgE-mediated release of inflammatory mediators and barrier dysfunction.Due to the common intrinsic mechanism, several kinds of type 2 inflammatory diseases always coexist in the same person, and their prevalence rate and severity continue to rise among children and adolescents, placing a heavy burden on them and their families.This review summarizes the recent development in understanding the mechanism of type 2 immune response and the pathophysiological mechanism of type 2 inflammatory diseases, emphasize the importance of ILC2 and summarize some targeted biologics used in the treatment of related diseases, so as to have a more systematic, comprehensive and in-depth understanding of type 2 inflammation.

Research progress on immunomodulatory properties of periodontal ligament stem cells / 口腔疾病防治

@#Periodontal ligament stem cells (PDLSCs) have the potential for multidirectional differentiation and are the preferred seed cells for periodontal tissue regeneration. In recent years, a large number of studies have confirmed that PDLSCs also possess broad immunomodulatory properties. Therefore, in-depth exploration of their specific molecular mechanisms is of great significance for the treatment of periodontitis. The aim of this paper is to summarize the research progress on the regulation of PDLSCs on various immune cells and the effect of the inflammatory environment on the immune characteristics of PDLSCs to provide an important theoretical basis for the allotransplantation of PDLSCs and improve the therapeutic effect of periodontal tissue regeneration. Studies have shown that PDLSCs possess a certain degree of immunosuppressive effect on both innate and acquired immune cells, and inflammatory stimulation may lead to the impairment of the immunoregulatory properties of PDLSCs. However, current studies are mainly limited to in vitro cell tests and lack in-depth studies on the immunomodulatory effects of PDLSCs in vivo. In vivo studies based on cell lineage tracing and conditional gene knockout technology may become the main directions for future research.

Pathogenesis of Diabetes from Theory of Spleen Deficiency Causing Diabetes Based on Intestinal Innate Immunity / 中国实验方剂学杂志

In western medicine， the small intestine anatomically belongs to the digestive system and is also an important immune organ of the body. The innate immune system of the small intestine consists of a tissue barrier， innate immune cells， and innate immune molecules. The dysfunction of any part can cause metabolic disorders and eventually lead to diabetes. In the pathogenesis of diabetes， traditional Chinese medicine （TCM） has the theory of ''spleen deficiency causing diabetes''， which points out that the impaired spleen function results in inadequate transformation， impaired essence spread， and turbidity by essence accumulation， which is the core pathological link of blood glucose metabolism disorder in diabetes. In terms of the relationship between the small intestine and the spleen， the theory of TCM holds that the small intestine is located in the abdomen and the abdomen is dominated by the spleen. The digestion， absorption， and endocrine functions of the small intestine are also similar to the functions of spleen in governing movement and transformation and spreading essence by virtue of spleen Qi. Therefore， the anatomical and physiological functions of the small intestine in western medicine are closely related to the spleen in TCM. At the same time， the spleen is closely related to the innate immune function of the small intestine in TCM. The spleen participates in the generation and distribution of defense Qi， and the process of defense Qi playing the external function is similar to the process of the activation of the innate immune response. The spleen is also an important organ involved in fluid metabolism， which can cooperate with the lung and kidney to timely remove turbid fluid from the body. It can also work with the stomach as the hub of Qi ascending and descending and regulate the physiological activities of "clear Yang" and "turbid Yin"， so as to ensure the homeostasis of the internal environment of the body， which is the basis for maintaining the normal function of the innate immunity of the small intestine. Therefore， taking "spleen deficiency causing diabetes" as a bridge， the theory of TCM and western medicine were combined to explain the relationship between small intestinal innate immunity imbalance and the pathogenesis of diabetes from the perspective of TCM， which is helpful to understand the pathogenesis of diabetes in a deeper level and also provide a new perspective and new way for the prevention and treatment of this disease with TCM.

Initiation and maintenance of acquired immunity in dry eye / 国际眼科杂志(Guoji Yanke Zazhi)

Dry eye(DE)is a multifactorial ocular surface disorder arising from numerous pathologies. The pathogenesis of DE includes immune inflammation, oxidative stress, changes in tear film composition, corneal nerve abnormalities, and meibomian gland dysfunction. Among them, the immune inflammatory response is the most crucial in the pathogenesis of DE, which is regulated by both innate and acquired immune responses on the ocular surface. Multiple environmental stresses trigger the ocular surface innate immune response leading to corneal epithelial cell damage and inflammation and activate acquired immunity to participate in the ocular surface immune inflammatory response. Currently, multiple immune cells and inflammatory factors have been shown to be involved in the occurrence and development of DE. This article reviewed the immune progress and focused on the initiation and maintenance of acquired immunity in DE. Through the analysis of the latest viewpoints and research hot spots, we systematically introduced the immunomodulating mechanism underlying the mechanisms of the pathogenesis of DE and provided references for the prevention and treatment of DE.

Research progress on the role and changes of natural killer cells in sepsis / 中国小儿急救医学

Sepsis is the organ dysfunction caused by infection.It is one of the most common critical diseases in clinic.Its morbidity and mortality are increasing year by year，which has seriously threatened human health.Innate immunity is the first line of defense against pathogens.Nature killer（NK）cells are important cells involved in the regulation of innate immunity in sepsis，and can play an important role on the progression of sepsis by secreting cytokines，inducing apoptosis and mediating cytotoxic effects.It has been found that the changes of NK cells in the early stage of sepsis are related to the prognosis of the disease.Therefore，further study on the role of NK cells in sepsis can provide a new idea for the clinical diagnosis and treatment of sepsis，and contribute to the early identification of sepsis and the improvement of prognosis.This review summarized the role and changes of NK cell in sepsis.

The role of innate immunity in diabetic nephropathy and their therapeutic consequences / 药物分析学报

Diabetic nephropathy(DN)is an enduring condition that leads to inflammation and affects a substantial number of individuals with diabetes worldwide.A gradual reduction in glomerular filtration and emergence of proteins in the urine are typical aspects of DN,ultimately resulting in renal failure.Mounting evidence suggests that immunological and inflammatory factors are crucial for the develop-ment of DN.Therefore,the activation of innate immunity by resident renal and immune cells is critical for initiating and perpetuating inflammation.Toll-like receptors(TLRs)are an important group of re-ceptors that identify patterns and activate immune responses and inflammation.Meanwhile,inflam-matory responses in the liver,pancreatic islets,and kidneys involve inflammasomes and chemokines that generate pro-inflammatory cytokines.Moreover,the activation of the complement cascade can be triggered by glycated proteins.This review highlights recent findings elucidating how the innate immune system contributes to tissue fibrosis and organ dysfunction,ultimately leading to renal failure.This re-view also discusses innovative approaches that can be utilized to modulate the innate immune responses in DN for therapeutic purposes.

The association of blood biomarkers with cerebral white matter and myelin content in bipolar disorder: a systematic review

Objectives: Evidence from diffusion tensor imaging (DTI) and postmortem studies has demonstrated white-matter (WM) deficits in bipolar disorder (BD). Changes in peripheral blood biomarkers have also been observed; however, studies evaluating the potential relationship between brain alterations and the periphery are scarce. The objective of this systematic review is to investigate the relationship between blood-based biomarkers and WM in BD. Methods: PubMed, Embase, and PsycINFO were used to conduct literature searches. Cross-sectional or longitudinal studies reporting original data which investigated both a blood-based biomarker and WM (by neuroimaging) in BD were included. Results: Of 3,750 studies retrieved, 23 were included. Several classes of biomarkers were found to have a significant relationship with WM in BD. These included cytokines and growth factors (interleukin-8 [IL-8], tumor necrosis factor alpha [TNF-α], and insulin-like growth factor binding protein 3 [IGFBP-3]), innate immune system (natural killer cells [NK]), metabolic markers (lipid hydroperoxidase, cholesterol, triglycerides), the kynurenine (Kyn) pathway (5-hydroxyindoleacetic acid, kynurenic acid [Kyna]), and various gene polymorphisms (serotonin-transporter-linked promoter region). Conclusion: This systematic review revealed that blood-based biomarkers are associated with markers of WM deficits observed in BD. Longitudinal studies investigating the potential clinical utility of these specific biomarkers are encouraged. Systematic review registration: PROSPERO CRD42021279246.

Innate immune receptors are differentially expressed in mice during experimental Schistosoma mansoni early infection

BACKGROUND The impact of Schistosoma mansoni infection over the immune response and the mechanisms involved in pathogenesis are not yet completely understood. OBJECTIVES This study aimed to evaluate the expression of innate immune receptors in three distinct mouse lineages (BALB/c, C57BL/6 and Swiss) during experimental S. mansoni infection with LE strain. METHODS The parasite burden, intestinal tissue oogram and presence of hepatic granulomas were evaluated at 7- and 12-weeks post infection (wpi). The mRNA expression for innate Toll-like receptors, Nod-like receptors, their adaptor molecules, and cytokines were determined at 2, 7 and 12 wpi in the hepatic tissue by real-time quantitative polymerase chain reaction (qPCR). FINDINGS Swiss mice showed 100% of survival, had lower parasite burden and intestinal eggs, while infected BALB/c and C57BL/6 presented 80% and 90% of survival, respectively, higher parasite burden and intestinal eggs. The three mouse lineages displayed distinct patterns in the expression of innate immune receptors, their adaptor molecules and cytokines, at 2 and 7 wpi. MAIN CONCLUSIONS Our results suggest that the pathogenesis of S. mansoni infection is related to a dynamic early activation of innate immunity receptors and cytokines important for the control of developing worms.

La Viabilidad y Funcionalidad de Leucocitos Humanos en presencia de un Extracto Hidro-alcohólico de E. coca / The Viability and Functionality of Human Leukocytes in the presence of a Hydro-alcoholic Extract of E. coca.

Introducción : Para estudiar el efecto de cualquier producto natural, aunque sea de uso habitual de la medicina tradicional, es necesario establecer previamente los márgenes de seguridad para su utilización en humanos. En el caso de Erythroxylum coca, para trazar sus perspectivas de uso como fitofármaco o de producto industrial, es necesario conocer si tiene algún grado de toxicidad o si es completamente inocuo, no obstante, su larga tradición de consumo. Objetivo : Explorar el efecto de un extracto hidro-alcohólico de E. coca sobre granulocitos y mononucleares de voluntarios donadores humanos, en condiciones de cultivo celular. Se examinó, por un lado, el efecto sobre la viabilidad celular y la actividad del sistema mitocondrial/citoplasmático de óxido-reductasas y, por otra parte, se exploró su efecto sobre la funcionalidad celular a través de la determinación de la capacidad fagocítica, la quimiotaxis, la endocitosis y la actividad microbicida, en el ámbito de la inmunidad innata, y la capacidad de liberación o estimulación de citoquinas en el ámbito de la respuesta inflamatoria. Materiales y Métodos : Se evaluó la viabilidad por Azul Tripan, la actividad de oxido reductasas por reducción de MTT, la capacidad endocitica de levaduras, quimiotaxis en gel de agarosa hacia el péptido Fmlp y actividad microbicida sobre S.aureus. Las liberaciones de citoquinas se evaluaron por ELISA. Resultados : Se encontró que a las dosis equivalentes a la del consumo habitual humano, los leucocitos conservan su viabilidad (0,13µg/ml), la que se mantiene hasta dosis relativamente altas (130µg/ml). En esta franja de seguridad se encontró que E. coca no altera la capacidad de las enzimas mitocondriales y citoplasmáticas de óxido- reducción, al contrario, en dosis bajas es capaz de estimular dicha actividad. La actividad quimiotactica no es afectada por el extracto hidroalcoholico de coca por el contrario a dosis intermedias esta actividad se eleva de manera ostensible. La capacidad endocitica no se ve afectada y por el contrario se pudo observar un estímulo de la misma; en la actividad microbicida no existe cambios significativos. Conclusiones : Se concluye que, este producto a las dosis equivalentes a las recomendadas por la medicina tradicional no tiene efectos deletéreos sobre la viabilidad y funcionalidad de los leucocitos humanos. En lo que respecta a la actividad del extracto sobre la producción de citoquinas, se encontró que E. coca tiene efecto de estimulación en la liberación de TNF e inhibición de IL-10 modulando así mayor actividad proinflamatoria.

Introduction : In order to study the effect of any natural product, even if it is commonly used in traditional medicine, it is necessary to previously establish the safety margins for its use in humans. In the case of Erythroxylum coca, in order to trace its prospects of use as a phytopharmaceutical or industrial product, it is necessary to know if it has any degree of toxicity or if it is completely innocuous, despite its long tradition of consumption. Objective : To explore the effect of a hydro-alcoholic extract of E. coca on granulocytes and mononuclear cells of human donor volunteers, under cell culture conditions. We examined, on the one hand, the effect on cell viability and the activity of the mitochondrial/cytoplasmic oxidoreductase system and, on the other hand, it was explored its effect on cellular functionality through the determination of phagocytic capacity, chemotaxis, endocytosis and microbicidal activity, in the field of innate immunity, and the capacity of release or stimulation of cytokines in the field of inflammatory response. Materials and Methods : Viability by Trypan Blue, oxidoreductase activity by MTT reduction, endocytic capacity of yeast, chemotaxis in agarose gel towards Fmlp peptide and microbicidal activity on S.aureus were evaluated. Cytokine release was evaluated by ELISA. Results : It was found that at doses equivalent to the usual human consumption, leukocytes retain their viability (0.13µg/ml), which is maintained up to relatively high doses (130µg/ml). In this safety range it was found that E. coca does not alter the capacity of mitochondrial and cytoplasmic oxidation-reduction enzymes, on the contrary, at low doses it is able to stimulate such activity. The chemotactic activity is not affected by the hydroalcoholic extract of coca, on the contrary, at intermediate doses this activity is ostensibly elevated. The endocytic capacity is not affected and, on the contrary, a stimulus of the same was observed; in the microbicidal activity there are no significant changes. Conclusions : It is concluded that this product, at doses equivalent to those recommended by traditional medicine, has no deleterious effects on the viability and functionality of human leukocytes. Regarding the activity of the extract on the production of cytokines, it was found that E. coca has a stimulating effect on the release of TNF and inhibition of IL-10, thus modulating greater proinflammatory activity.

Effect of Antiretroviral Therapy on Neutrophil Oxidative Burst in Children

Objective To ascertain the efect of human immunodefciency virus (HIV) infection, as well as, antiretroviral therapy (ART) on neutrophil oxidative burst in children. Methods Fifty-fve children living with HIV infection (30 receiving ART for?2 y, 25 treatment-naïve) and 30 healthy controls, aged 18 mo–18 y, were assessed for hemogram and neutrophil oxidative burst. The treatment-naïve children were followed up and the above tests were repeated after 6 mo of ART. Results Mean (SD) serum MPO activity at 6 mo after ART [32.1 (±19.9) U/L] was comparable to that at disease onset [17.2 (±23.0) U/L], although it was signifcantly higher compared to that in children on ART?2 y [13.3 (±15.8) U/L] and controls [12.1 (±11.9) U/L]. Median fuorescence intensity (MFI) of unstimulated DHR was highest at 6 mo after ART and in the treatment-naïve group, which was signifcantly higher than in the controls, as well as, children receiving ART?2 y. Stimulation index was highest in the control group [442.4 (341.9–562.9)], which was comparable to that in children on ART?2 y [304.2 (153.2–664.8)], but was signifcantly higher than the treatment-naïve cohort [266.1 (148.2–339.4)] and children on ART for 6 mo [318.8 (154.9–395.6)]. Conclusion A hyperinfammatory state caused by an increased serum myeloperoxidase enzyme activity and increased basal neutrophil oxidative burst was seen in untreated HIV infection and during initial 6 mo of ART. ART given for?2 y normalized the impaired neutrophilic phagocytic functions.

Advances in the study of congenital immune mechanisms mediated by modifiable cardiovascular risk factors for atherosclerosis / 中国胸心血管外科临床杂志

@#Obesity, sleep disorders, psychological stress, sedentary are modifiable cardiovascular risk factors. There is growing evidence that these risk factors may accelerate the chronic inflammatory process of atherosclerosis and lead to myocardial infarction. Studies on the role of immune cells and their related immune mechanisms in atherosclerosis have shown that the above modifiable risk factors can affect the hematopoiesis of the bone marrow system, affect the production of immune cells and phenotypes, and then affect the progress of atherosclerosis. This review will focus on the effects of modifiable cardiovascular risk factors on the progression of atherosclerosis through the role of the innate immune system.

Study on inhibitory effects of Wubao capsule on airway inflammation in asthmatic model mice by regulating the upstream and downstream cytokines of type Ⅱ innate lymphoid cells / 中国药房

OBJECTIVE To study the effects of Wubao capsule on airway inflammation in asthmatic model mice by regulating upstream and downstream cytokines of type Ⅱ innate lymphoid cells （ILC2s）. METHODS Totally 40 female BABL/c mice were randomly divided into normal group， model group， positive control group （dexamethasone 1 mg/kg）， Wubao capsule low-dose and high-dose groups （0.5， 1 g/kg）， with 8 mice in each group. Asthma models were induced by ovalbumin （OVA） sensitization and nebulization. Each group was given normal saline or drug intragastrically for 7 consecutive days. The contents of IgE and OVA-IgE in serum， the contents of interleukin 5 （IL-5）， IL-9， IL-13， IL-25， IL-33， thymic stromal lymphopoietin （TSLP） and mucin 5AC （MUC5AC） in bronchoalveolar lavage fluid （BALF） were determined by ELISA. HE staining was used to observe the pathological changes of lung tissues in mice. PAS staining was used to observe the changes of goblet cell proliferation in each group. The number of ILC2s in lung tissue was determined by flow cytometry （except for Wubao capsule low-dose group）. RESULTS Compared with model group， the contents of IgE and OVA-IgE in serum and the contents of IL-5， IL-9， IL-13， IL-25， IL-33， TSLP and MUC5AC in BALF were significantly reduced in Wubao capsule high-dose and low-dose groups （P＜0.01）. The infiltration of inflammatory cells and the thickening of basement membrane in lung tissue was alleviated to varying degrees， and the proliferation of goblet cells was inhibited； the number of ILC2s in lung tissues of mice in Wubao capsule high-dose group was significantly reduced （P＜0.01）. CONCLUSIONS Wubao capsule could effectively reduce the number of ILC2s in lung tissue， the contents of upstream and downstream cytokines of ILC2s in BALF of asthmatic model mice， so as to inhibit the airway inflammation and improve asthma.

Changes and significance of type 2 innate lymphoid cells and their related factors in bronchopulmonary dysplasia / 中国当代儿科杂志

OBJECTIVES@#To investigate the changes and significance of type 2 innate lymphoid cells (ILC2), interleukin-33 (IL-33), interleukin-25 (IL-25), thymic stromal lymphopoietin (TSLP), interleukin-5 (IL-5), and interleukin-13 (IL-13) in peripheral blood of preterm infants with bronchopulmonary dysplasia (BPD).@*METHODS@#A total of 76 preterm infants with a gestational age of <32 weeks and a length of hospital stay of ≥14 days who were admitted to the Department of Pediatrics of the Affiliated Hospital of Jiangsu University from September 2020 to December 2021 were enrolled. According to the diagnostic criteria for BPD, they were divided into a BPD group with 30 infants and a non-BPD group with 46 infants. The two groups were compared in terms of the percentage of ILC2 and the levels of IL-33, IL-25, TSLP, IL-5, and IL-13 in peripheral blood on days 1, 7, and 14 after birth.@*RESULTS@#The BPD group had significantly lower birth weight and gestational age than the non-BPD group (P<0.05). On days 7 and 14 after birth, the BPD group had significantly higher levels of ILC2, IL-33, TSLP, and IL-5 than the non-BPD group (P<0.05), and these indices had an area under the curve of >0.7 in predicting the devolpment of BPD (P<0.05). Multivariate logistic regression analysis showed that after adjusting for gestational age and birth weight, peripheral blood IL-33, TSLP and IL-5 on days 7 and 14 after birth were closely related to the devolpment of BPD (P<0.05).@*CONCLUSIONS@#Early innate immune activation and upregulated expression of related factors may be observed in preterm infants with BPD. ILC2, IL-33, TSLP, and IL-5 may be used as biological indicators for early diagnosis of BPD.

Somatostatin-Positive Neurons in the Rostral Zona Incerta Modulate Innate Fear-Induced Defensive Response in Mice / 神经科学通报·英文版

Defensive behaviors induced by innate fear or Pavlovian fear conditioning are crucial for animals to avoid threats and ensure survival. The zona incerta (ZI) has been demonstrated to play important roles in fear learning and fear memory, as well as modulating auditory-induced innate defensive behavior. However, whether the neuronal subtypes in the ZI and specific circuits can mediate the innate fear response is largely unknown. Here, we found that somatostatin (SST)-positive neurons in the rostral ZI of mice were activated by a visual innate fear stimulus. Optogenetic inhibition of SST-positive neurons in the rostral ZI resulted in reduced flight responses to an overhead looming stimulus. Optogenetic activation of SST-positive neurons in the rostral ZI induced fear-like defensive behavior including increased immobility and bradycardia. In addition, we demonstrated that manipulation of the GABAergic projections from SST-positive neurons in the rostral ZI to the downstream nucleus reuniens (Re) mediated fear-like defensive behavior. Retrograde trans-synaptic tracing also revealed looming stimulus-activated neurons in the superior colliculus (SC) that projected to the Re-projecting SST-positive neurons in the rostral ZI (SC-ZIrSST-Re pathway). Together, our study elucidates the function of SST-positive neurons in the rostral ZI and the SC-ZIrSST-Re tri-synaptic circuit in mediating the innate fear response.

Role of type 2 innate lymphoid cells in helminth infections: a review / 中国血吸虫病防治杂志

Helminth infections may trigger host innate and adaptive immune responses. Group 2 innate lymphoid cells (ILC2) are an important factor involved in type 2 immune responses, and produce a large number of T helper 2 cell (Th2) cytokines following stimulation by interleukin (IL)-25, IL-33 and thymic stromal lymphopoietin (TSLP), which play a critical role in parasite clearance and tissue repair. Following helminth infections, autocrine factors, mast cells, enteric nervous system and Th2 cells have been recently found to be involved in regulation of ILC2. Unraveling the role of ILC2 in immune response against helminth infections is of great value for basic research and drug development. This review summarizes the research progress on ILC2 and its role in helminth infections.

Research progress of interaction between peste des petits ruminants virus and host cells / 中国生物制品学杂志

@#Peste des petits ruminants(PPR)is a highly contagious disease with high mortality which is caused by peste des petits ruminants virus(PPRV)infection and leads to enormous economic losses for sheep husbandry both at home and abroad. The knowledge of interactions between PPRV and host cells is the basis of understanding of the pathogenesis and the prerequisite of disease prevention and control. This paper reviews the studies on the activation of host innate immune response by PPRV infection,the immune evasion of PPRV mediated by viral protein products,and the induction of apoptosis,autophagy and inflammasome resistance to virus,which provides a reference for further discussion on the immune evasion of PPRV and the key nodes involved in the interaction between PPRV and the host,thus providing theoretical guidance for effective prevention and control of PPR transmission.

Potentiating effect and mechanism of extract of Jingfang Granules on activation of macrophages / 中国中药杂志

This study aimed to explore the potentiating effect and mechanism of the extract of Jingfang Granules(JFG) on the activation of macrophages. The RAW264.7 cells were treated with JFG extract and then stimulated by multiple agents. Subsequently, mRNA was extracted, and reverse transcription-polymerase chain reaction(RT-PCR) was used to measure the mRNA transcription of multiple cytokines in RAW264.7 cells. The levels of cytokines in the cell supernatant were detected by enzyme-linked immunosorbent assay(ELISA). In addition, the intracellular proteins were extracted and the activation of signaling pathways was determined by Western blot. The results showed that JFG extract alone could not promote or slightly promote the mRNA transcription of TNF-α, IL-6, IL-1β, MIP-1α, MCP-1, CCL5, IP-10, and IFN-β, and significantly enhance the mRNA transcription of these cytokines in RAW264.7 cells induced by R848 and CpG in a dose-dependent manner. Furthermore, JFG extract also potentiated the secretion of TNF-α, IL-6, MCP-1, and IFN-β by RAW264.7 cells stimulated with R848 and CpG. As revealed by mechanism analysis, JFG extract enhanced the phosphorylation of p38, ERK1/2, IRF3, STAT1, and STAT3 in RAW264.7 cells induced by CpG. The findings of this study indicate that JFG extract can selectively potentiate the activation of macrophages induced by R848 and CpG, which may be attributed to the promotion of the activation of MAPKs, IRF3, and STAT1/3 signaling pathways.