Background: Rheumatoid arthritis (RA) is a globally prevalent chronic inflammatory disease. Environmental exposures, such as air pollution and smoking, are considered potential risk factors. However, the causal relationships and underlying mechanisms between these factors and RA are not fully understood. Methods: This study utilized large-scale genome-wide association studies (GWASs) from European ethnic backgrounds and employed bidirectional two-sample Mendelian randomization (MR) to investigate the relationships between air pollution, smoking, and RA. Genetic correlations were assessed using linkage disequilibrium score regression (LDSC). Furthermore, mediation analysis was conducted to evaluate the potential mediating roles of iron metabolism and urinary biomarkers in these relationships. Results: The MR analysis revealed that genetically predicted lifetime smoking intensity was associated with an 85% increased risk of RA. Subgroup analysis differentiating between seropositive RA (SPRA) and seronegative RA (SNRA) showed a causal association with SPRA, but not with SNRA. C-reactive protein was identified as a mediator in the relationship between lifetime smoking and both RA and SPRA, mediating 18.23% and 32.45% of the effects, respectively. Genetic correlation analysis further confirmed a positive genetic association between smoking and both RA and SPRA. Conclusions: This study provides significant insights into the genetic and causal connections between air pollution, smoking, and the development of RA, highlighting the mediating role of C-reactive protein. These findings not only offer new perspectives on how smoking might enhance RA risk through inflammatory pathways but also underscore the importance of reducing smoking exposure in public health strategies.

Hypoxia promotes the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), thereby accelerating fracture healing. However, the underlying molecular mechanisms remain unclear. A rat fracture model was established using external force. BMSCs were isolated, identified, and used for in vitro experiments. Flow cytometry was used to assess cell surface markers CD29, CD44, and CD45. Hypoxia-related differentially expressed genes (DEGs) were identified using methylated RNA immunoprecipitation-sequencing (MeRIP-seq) (n = 3, data size: 6G). Functional enrichment analyses (gene ontology and Kyoto encyclopedia of genes and genomes) were performed on the DEGs. SLC2A3 and METTL3 were transfected using the Lipofectamine 2000 kit. Osteogenic capacity was evaluated using Alizarin Red staining, alkaline phosphatase content, glucose uptake, and ATP levels. RNA pull-down and immunoprecipitation analyses were used to verify the interaction between SLC2A3 and METTL3. Western blotting and MeRIP-qPCR were performed to assess the expression levels of these molecules. Hypoxia enhanced the osteogenic capacity of BMSCs. MeRIP-seq analysis revealed that SLC2A3 was differentially expressed in BMSCs under hypoxia treatment. SLC2A3 enhanced osteogenic capacity through the glycolytic pathway by increasing ATP levels, glucose uptake, and the expression of HK2, PKM2, and LDHA. METTL3 demonstrated significantly higher expression in the Hypoxia group than in the Ctrl group. METTL3 further enhanced osteogenesis through the glycolytic pathway by mediating m6A modification of SLC2A3. Results also revealed a binding relationship between METTL3 and SLC2A3. In vivo, SLC2A3 overexpression accelerated fracture healing. Hypoxia promotes METTL3-mediated m6A modification of SLC2A3, thereby enhancing glycolysis and osteogenesis in BMSCs. METTL3–SLC2A3 axis may serve as a therapeutic target for accelerating fracture healing.

Background Currently, the link between cardiovascular diseases and sarcopenia is increasingly garnering attention from researchers. However, studies exploring the association between cardiac structure and sarcopenia are sparse. This study aims to investigate the potential genetic links between cardiac structural features and sarcopenia. Methods During the discovery phase, we employed Linkage Disequilibrium Score Regression (LDSC) and Mendelian Randomization (MR) to assess the genetic correlation and causality between traits related to cardiac structure and sarcopenia, with further validation of the results using validation set data. In the study, we established a scoring system to identify high-confidence trait pairs. For these pairs, we conducted sensitivity analyses to assess their heterogeneity and pleiotropy. Additionally, we undertook follow-up studies of these trait pairs, including using mediation analysis to evaluate the potential mediating effects of lipids, and enrichment analysis to explore possible shared biological pathways linking these characteristics. Results The genetic correlation analyses during the discovery and validation phases identified 5 pairs (in forward analysis) and 16 pairs (in reverse analysis) of high-confidence trait pairs. As a key sarcopenia-related feature, appendicular lean mass (ALM) exhibited positive causal relationships with several cardiac structural features, including the volumes of the left and right atria. Mediation analysis suggested that certain lipids, such as phosphatidylcholine, might mediate these causal relationships. Notably, gene and pathway enrichment analyses revealed that genes associated with significant SNPs in high-confidence trait pairs were enriched in multiple key biological processes and pathways, such as tube morphogenesis, cardiac right ventricle morphogenesis, and muscle system processes in the forward analysis, as well as skeletal system development, heart development, and hemopoiesis in the reverse analysis. Cell-type enrichment analysis pointed to endothelial cells, smooth muscle cells, fibroblasts, and mesenchymal stem cells. Conclusions This study provides evidence for genetic relationships between cardiac structures and sarcopenia-related traits. These findings may enhance our understanding of the biological mechanisms underlying age-related diseases and provide scientific basis for developing future preventive and therapeutic strategies. ### Competing Interest Statement The authors have declared no competing interest.

This study will evaluate the therapeutic effect of pin distractor assisted reduction of fibular fracture on ankle fracture. A retrospective analysis was performed on 98 patients diagnosed as ankle fracture or pilon fracture. These patients were all combined with fibular fracture. Retrospective analysis included 48 patients in the experimental group (distractor assisted reduction) and 48 patients in the control group (without pin distractor). The statistical indexes include: the time spent in fracture reduction and fixation, the length of surgical incision, the operative blood loss of fracture operation, the incidence of incision skin necrosis, the incidence of fracture end splitting during reduction, the quality of fracture reduction, the time of fracture healing, infection rate, and The American Orthopedic Foot and Ankle Society score at the last follow-up. There were statistical differences between the 2 groups in the time spent in the reduction and fixation of fractures, the incidence of fracture end splitting during reduction, the quality of anatomical reduction of fractures, and the healing time of fractures. The experimental group was better than the control group. In addition, for patients with long spiral fracture, comminuted fracture, osteoporotic fracture and preoperative delay time for operation more than 2 weeks, the time spent in the reduction and fixation of fracture, the operative blood loss of fracture operation, the incidence of fracture end splitting during reduction, the quality of anatomical reduction of fracture, and the healing time of fracture in the experimental group are also better than those in the control group. The pin distractor assisted reduction of fibular fracture has the advantages of simple operation, less trauma, short operation time, less operative blood loss, and fewer complications. It is especially suitable for patients with long spiral fibular fracture, comminuted fracture, osteoporotic fracture, and long preoperative delay time in ankle fracture.

Abstract This study aimed to validate the causal associations of brain structures with osteoarthritis (OA) and then describe key causal genes and proteins in brain related to OA risk. To explore the genetic correlation and causal relationship between brain structures and OA, linkage disequilibrium score regression (LDSC) and mendelian randomization (MR) were employed. Then a transcriptome-wide association study (TWAS), MR and Bayesian colocalization analysis were conducted, integrating human brain transcriptomes (N=2,970) with OA GWAS findings (N=826,690). Concurrently, a proteome-wide association study (PWAS) was carried out, combining GWAS summary data with human brain proteomes (N=152) provided by Banner using the FUSION pipeline. Finally single cell RNA-Seq (scRNA) eQTL data were used to explore the causal genes in brain cells associated with OA. The amalgamation of results from LDSC and MR provides insight into the brain structures majorly associated with OA, including bilateral putamen, amygdala nuclei, thalamic nuclei, insula, superior temporal gyrus, among others. In cortical tissue, seven genes (CLEC18A, CORO7, ERGIC3, EXOSC6, FEZ2, SPPL2A and UQCC1) displayed significant associations with knee OA risk, alongside five genes (COLGALT2, GNL3, OMA1, PPM1M and RAD9A) connected to hip OA risk. Furthermore, proteins related to knee (ICA1L), hip (DGKE), and thumb (SNAP47) OA have been identified. The MR analysis of scRNA found that CPNE1 in excitatory neuronsand EMILIN2 in OPCs/COPs were causally associated with knee OA, along with protein levels identified in the PWAS. This exploration of the genetics of OA associated with the brain-joint axis has advanced our understanding of the pathogenesis of OA.

OBJECTIVES:Type H blood vessels are a subtype of bone-specific microvessels (CD31hiEmcnhi) that play an important regulatory role in the coupling of angiogenesis and osteogenesis. Despite reports on the distinct roles of type H and L vessels under physiological and pathological bone conditions, their genetic differences remain to be elucidated. This study aims to construct a competitive endogenous RNA (ceRNA) network of key gene for differencial expression (DE) in type H and L vascular endothelial cells (ECs) through integrated bioinformatic methods. METHODS:We downloaded relevant raw data from the ArrayExpress and the Gene Expression Omnibus (GEO) database and used the Limma R-Bioconductor package to screen for DE lncRNAs, DE miRNAs, and DE mRNAs between type H and L vascular ECs. A total ceRNA network was constructed based on their interactions, followed by refinement using protein-protein interaction (PPI) networks to select upregulated and downregulated key genes. Enrichment analysis was performed on these key genes. Random validation was conducted using flow cytometry and real-time RT-PCR. RESULTS:A total of 1 761 DE mRNAs, 187 DE lncRNAs, and 159 DE miRNAs were identified, and a comprehensive ceRNA network was constructed based on their interactions. Six upregulated (Itga5, Kdr, Tjp1, Pecam1, Cdh5, and Ptk2) and 2 downregulated (Csf1r and Il10) key genes were selected via PPI network to construct a subnetwork of ceRNAs related to these key genes. Upregulated key genes were mainly enriched in negative regulation of angiogenesis and vascular apoptosis. Results from flow cytometry and real-time RT-PCR were consistent with bioinformatics analysis. CONCLUSIONS:This study proposes a ceRNA network associated with upregulated and downregulated type H and L vascular ECs based on selected key genes, providing new insights into the regulatory mechanisms of type H and L vascular ECs in bone metabolism.

A wealth of evidence intimates a profound connection between the immune system and osteonecrosis, albeit the specific immune factors underlying this connection remain largely veiled. A bidirectional Mendelian randomization (MR) study was conducted based on genome-wide association study summary data to identify causal links between 731 immune factors and osteonecrosis including drug-induced osteonecrosis. Preliminary MR analysis was accomplished utilizing the inverse-variance weighted method under a multiplicative random effects model, and heterogeneity and potential horizontal pleiotropy were evaluated through Cochrane's Q-test, MR-Egger intercept test, MR-PRESSO global test, and leave-one-out analysis. Upon false discovery rate correction, the gene-predicted level of one immune factor (CD62L − monocyte %monocyte) exhibited a significant positive correlation with osteonecrosis, while eight immune traits associated with monocytes, dendritic cells, and NK cells demonstrated significant causal effects with drug-induced osteonecrosis. Reverse MR revealed no significant correlations. This MR research provides genetic evidence for the causal associations between a broad spectrum of immune factors and osteonecrosis. Such a study aids in unraveling the intricate interaction patterns between the immune and skeletal systems, elucidating the pathogenesis of osteonecrosis, and identifying potential novel therapeutic approaches.

Abstract Background For children with supracondylar humeral fractures (SHFs), iatrogenic ulnar nerve injury resulting from medial pinning remains a challenge for orthopedic surgeons. This study aims to explore a safe medial pinning zone and assess its efficacy. Methods First, the radiographic images of a healthy elbow were reconstructed and mapped by E3d software to display the safe medial pinning zone we summarized. Second, all the pediatric SHF cases treated by our team between May 2014 to May 2020 were retrospectively reviewed to evaluate the safety and efficacy of the pinning zone. Furthermore, we proposed a hand gesture to fast locate the safe medial pin insertion point. Results On the anteroposterior (AP) view, the upper 1/2 part of the slope line segment we defined was safe since the ulnar nerve traversed the ulnar groove at the lower 1/2 part. On the lateral view, the diamond zone we defined was a safe entry zone. In the retrospective study, 134 SHF cases were included and divided into two groups. In group A (74 cases), the medial Kirschner wire (K-wire) was inserted from the safe zone at both AP and lateral views, while in group B (60 cases) the medial pinning point was beyond the safe entry zone. The incidence of iatrogenic ulnar nerve injury in group A was significantly lower than in group B (P < 0.01). Moreover, the exploration and neurolysis of the ulnar nerve were performed in patients involving postoperative ulnar nerve dysfunction. A left-hand gesture by the surgeon during operations could help to fast locate the safe insertion point of medial pins. Conclusion Medial pinning from the safe entry zone based on intraoperative fluoroscopy is an easy, reliable, and reproducible technique to avoid iatrogenic ulnar nerve injury in children with SHFs.

In this study,we aimed to investigate the causal associations of brain structure with bone mineral density(BMD).Based on the genome-wide association study(GWAS)summary statistics of 1 325 brain imaging-derived phenotypes(BIDPs)of brain structure from the UK Biobank and GWAS summary datasets of 5 BMD locations,including the total body,femoral neck,lumbar spine,forearm,and heel from the GEFOS Consortium,linkage disequilibrium score regression(LDSC)was conducted to determine the genetic correlations,and Mendelian randomization(MR)was then performed to explore the causal relationship between the BIDPs and BMD.Several sensitivity analyses were performed to verify the strength and stability of the present MR outcomes.To increase confidence in our findings,we also performed confirmatory MR between BIDPs and osteoporosis.LDSC revealed that 1.93%of BIDPs,with a false discovery rate(FDR)<0.01,were genetically correlated with BMD.Additionally,we observed that 1.31%of BIDPs exhibited a significant causal relationship with BMD(FDR<0.01)through MR.Both the LDSC and MR results demonstrated that the BIDPs"Volume of normalized brain,""Volume of gray matter in Left Inferior Frontal Gyrus,pars opercularis,""Volume of Estimated Total Intra Cranial"and"Volume-ratio of brain segmentation/estimated total intracranial"had strong associations with BMD.Interestingly,our results showed that more left BIDPs were causally associated with BMD,especially within and around the left frontal region.In conclusion,a part of the brain structure causally influences BMD,which may provide important perspectives for the prevention of osteoporosis and offer valuable insights for further research on the brain-bone axis.

Due to increasing morbidity worldwide, fractures are becoming an emerging public health concern. This study aimed to investigate the effect of metformin on the healing of osteoporotic as well as normal fractures. Type H vessels have recently been identified as a bone-specific vascular subtype that supports osteogenesis. Here, we show that metformin accelerated fracture healing in both osteoporotic and normal mice. Moreover, metformin promoted angiogenesis in vitro under hypoxia as well as type H vessel formation throughout fracture healing. Mechanistically, metformin increased the expression of HIF-1α, an important positive regulator of type H vessel formation, by inhibiting the expression of YAP1/TAZ in calluses and hypoxia-cultured human microvascular endothelial cells (HMECs). The results of HIF-1α or YAP1/TAZ interference in hypoxia-cultured HMECs using siRNA further suggested that the enhancement of HIF-1α and its target genes by metformin is primarily through YAP1/TAZ inhibition. Finally, overexpression of YAP1/TAZ partially counteracted the effect of metformin in promoting type H vessel-induced angiogenesis-osteogenesis coupling during fracture repair. In summary, our findings suggest that metformin has the potential to be a therapeutic agent for fractures by promoting type H vessel formation through YAP1/TAZ inhibition.

BackgroundGaleazzi fracture dislocation is a compound injury that encompasses fractures of the distal third of the radius and dislocation of the distal radial ulnar joint (DRUJ). Clinically, this condition is rare and often leads to distal ulnar bifurcation. In previous similar reports, patients were effectively managed through surgery.Case presentationIn this case report, we describe an 11-year-old male child who presented with an ulnar bifida following trauma to the hand, and was treated with manipulation and conservative treatment without surgery. A follow-up performed over the years demonstrated that the patient recovered well, and had normal wrist movements without significant pain, and the patient expressed great satisfaction.ConclusionsUlnar diaphyseal fracture may occur in children or adolescents due to injuries, and may be accompanied with manipulation and repositioning. Conservative treatment can be applied to avoid the trauma associated with surgery especially in the absence of severe joint mobility impairment with good outcomes.

ObjectivesPrevious research has indicated a potential association between immune factors and osteoarthritis (OA), but the causal relationship between CD25 expression on immune cells and hip OA remains enigmatic. To shed light on this relationship, this study utilized the two-sample Mendelian Randomization (MR) method.MethodsLeveraging genome-wide association studies (GWAS) data from the UK Biobank and arcOGEN, the investigation encompasses a substantial European cohort comprising 15,704 hip OA cases and 378,169 controls. Genetic insights into CD25 stem from a subgroup of 3,757 individuals with European ancestry, encompassing 77 CD25-related traits. Several MR methods were applied, and robustness was assessed through heterogeneity and sensitivity analysis.ResultsAmong the 77 traits examined, 66 shared the same single nucleotide polymorphisms (SNPs) with hip OA. Of these, 7 CD25-related traits were found to be causally associated with hip OA (adjusted P><0.05), with F-statistics ranging from 33 to 122. These traits are specifically related to CD4+CD25+ T cells, exhibiting odds ratios (OR) and 95% confidence intervals (CI) less than 1. Notably, no causal link was discerned with the CD8+CD25+ T cell subset. Within absolute count (AC) and relative count (RC) trait types, a significant causal relationship was observed solely between CD4+CD25+ T cells and hip OA, without subtype localization. A more intricate examination of CD25 expression levels within the CD4+CD25+ T cell subset revealed a correlation with the CD39+ regulatory T (Treg) subset and hip OA, particularly within the CD39+ activated Treg subset. Furthermore, a notable causal relationship emerged between CD25 expression levels in the CD45RA- not Treg subset and hip OA. However, no significant causal link was established with any subsets of B cells.ConclusionThe genetic prediction suggests that CD25, particularly within the realm of CD4+CD25+ T cells, may exert a protective influence against the development of hip OA. These findings provide a novel therapeutic approach for the prevention and treatment of hip OA.

Dimethoate (DMT) is an organophosphorus pesticide which is widely used to prevent and control agricultural diseases and pests. But it also remains in crops and the environment, affecting other non-target organisms. Existing research mainly focuses on aquatic invertebrates, and research on terrestrial invertebrates is still relatively weak. This study selected the lepidopteran model insect silkworm (Bombyx mori) as the research object and revealed the influence of DMT on the reproduction of silkworms. This study used digital gene expression (DGE) and RT-qPCR analysis to compare gene expression changes in eggs laid by silkworms under the exposure of DMT (200 mg/L). A total of 320 differential genes were detected, of which 211 genes were up-regulated and 109 genes were down-regulated. The GO enrichment analysis bar graph shows those differential genes enriched in the BP's metabolic process, cellular process, CC's membrane part, cell, MF's catalytic activity, binding. KEGG enrichment analysis showed more differential genes enriched in signal transduction, endocrine system, cancers: Overview pathway. The results showed that the differential genes were mainly concentrated on promoting trehalase transporter genes, stress response-related genes, zinc finger protein genes, epidermal protein genes, and 5-HT pathway-related genes. The results of this study will provide important gene sequence information for insect toxicology studies, and also clarify the mechanism of influence of DMT on silkworm reproduction at the transcription level.

Fluoride is a serious health risk to animals and humans. The microbiota-gut-blood barrier (MGBB) plays an indispensable role in maintaining the systematic homeostasis of host organisms. However, the toxic effects of fluoride on MGBB of organisms have not been extensively investigated. Here, we used the silkworm interspecies model to explore the adverse effects of fluoride on the gut microbiota and intestinal tissue and circulating metabolites of organisms. Results showed that fluoride exposure significantly declined the body weight gain and survival rate of organisms and evidently damaged intestinal epithelial cells. In addition, fluoride altered the composition and abundance of intestinal microbiota, which was accompanied by changing gene expression levels of antimicrobial peptides in intestinal tissue. Shifts in the relative abundance of Enterococcus, Aquabacterium, Aureimonas and Methylobacterium in the gut had significant correlations with the concentrations of certain differential metabolites (e.g., amino acids, nucleotides, and nucleotide derivatives) in the bloodstream. Moreover, most circulating metabolites in related nucleotide metabolism pathways were upregulated, whereas those in the pathways of amino acid metabolism were downregulated. This study deepens our understanding of the disruptive effect of fluoride on the MGBB of host organisms and may provide a new insight into the preventive therapy of fluoride-induced diseases.

The symbiotic association between bacterial symbionts and insect hosts is a complicated process that is not completely understood. Herein, we used a silkworm model to study the association between symbiotic Bacillus and lepidopteran insect by investigating the changes in intestinal microbiota and hemolymph circulating metabolites of silkworm after symbiotic Bacillus subtilis treatment. Results showed that B. subtilis can generate a variety of primary and secondary metabolites, such as B vitamins and antimicrobial compounds, to provide micronutrients and enhance the pathogen resistance of their insect host. Shifts in the relative abundance of Enterococcus, Brevibacterium, Buttiauxella, Pseudomonas, Brevundimonas and Limnobacter had significant correlations with the concentrations of differential metabolites (e.g. phospholipids and certain amino acids) in insect hemolymph. The antimicrobial compounds secreted by B. subtilis were the primary driving force for the reconstruction of intestinal microbiota. Meanwhile, the altered levels of circulating metabolites in multiple metabolic pathways were potential adaptive mechanism of insect hosts in response to the shifts of intestinal microbiota. Our findings provided concrete evidence that bacterial intestinal symbiont can alter the physiological state of insects and highlighted the importance of the compositional alterations of intestinal microbiota as a source of variation in circulating metabolites of insect hosts.

Eicosanoids are crucial downstream signals in the insect immune responses. Phospholipase A2 (PLA2) catalyzes phospholipids, the initial step in eicosanoid biosynthesis. In mammals, the biological roles of Ca2+-independent Phospholipase A2 (iPLA2) have been extensively studied; however, only a few studies have attempted to explore iPLA2 functions in insects. In this study, we identified two iPLA2 genes (designated as BmiPLA2A and BmiPLA2B) in the silkworm, Bombyx mori. BmiPLA2A had a 2427 base pair (bp) open reading frame (ORF) that coded for a protein with 808 amino acids. In contrast, BmiPLA2B had a 1731 bp ORF that coded for a protein with 576 amino acids. Domain analysis revealed that BmiPLA2A had six ankyrin repeat domains, but BmiPLA2B lacks these domains. BmiPLA2A and BmiPLA2B were transcribed widely in various tissues and developmental stages with different expression patterns. The administration of 20-hydroxyecdysone increased their expression levels in the epidermis and hemocytes. Furthermore, challenged with virus, fungus, Gram-negative bacteria, and Gram-positive bacteria induced the expression of BmiPLA2A and BmiPLA2B with variable degrees along with different time points. Our findings imply that BmiPLA2A and BmiPLA2B may have important biological roles in the development and innate immunity of B. mori.

Abstract Background None of the existing classifications of heterotopic ossification (HO) of the elbow is based on anatomy, therefore they cannot accurately guide or predict excision. This study was to evaluate the anatomical morphology of HO of the elbow resulting from different etiologies and to propose a new HO classification system based on three-dimensional (3D) mapping technology. Methods We retrospectively included 76 cases of HO of the elbow from 2014 to 2021. All their demographic and etiologic information were collected and imported into medical imaging software. The distribution of the HO of the elbows and the 3D heat map was then created to evaluate the location and pattern of the HO. The volume of each HO based on mapping model and the length of the HO were measured to better analyze the characteristics of different types of HO. Results From the aggregated 3D image of the 76 HO cases, 85.53% have affected the dorsal side of the elbow, especially on the humeroulnar side (81.58%). And 26.32% have involved the anterior part of elbow, few cases were distributed among the radial head (10.53%) and olecranon fossa (1.32%). Subsequently, in accordance with the anatomical and morphological characteristics, a new HO classification of the elbow was proposed. The kappa score for inter- and intra-observer agreement of this classification system was 0.86 (95% CI, 0.72 -1.00) and 0.90 (95% CI, 0.78 -1.00), respectively. Conclusion This new HO classification system of the elbow may help surgeons to speculate the possible pathological anatomy and to design the best preoperative plan for excision.

The insect egg surface can serve as a vehicle for vertical symbiont transmission from the maternal parent to its offspring. Hypochlorite and formaldehyde are two common disinfectants used for insect egg surface sterilization. Here, we explored the intestinal microecology and immune response profile of the silkworm Bombyx mori strain Dazao after disinfectant exposure by using high-throughput sequencing technology and real-time PCR analysis. After egg surface sterilization, no significant difference ( P > 0.05) in overall body weight was observed among the control, sodium hypochlorite, and formaldehyde groups. 16S rRNA metagenomic sequencing revealed that the main abundant intestinal bacteria were Enterococcus , Burkholderia , Phenylobacterium , Ralstonia , Chitinophaga , Bradyrhizobium , Herbaspirillum , and two unclassified Bacteroidetes species. Egg surface sterilization evidently altered the composition and abundance of intestinal microbiota but did not significantly change its alpha diversity. The dysbiosis of intestinal microbiota resulted in the perturbation of the immune response profile of the silkworm intestine. Our findings reveal that hypochlorite has a blocking effect on the symbiont transmission compared with formaldehyde. More importantly, egg surface sterilization exerts substantial effects on the ecophysiological traits of insects. The present study contributes to the scientific and reasonable application of disinfectants for insect egg surface sterilization during industrial silk production and laboratory-scale insect rearing.