Biology subjects

Chen, X.

Publications and source records attributed to Chen, X..

At least 163 records · Page 9Linked to original sources

bioRxiv2026

GPLD1 Regulates the Shedding of IZUMO1R to Block Polyspermy in Porcine Oocyte

Mammalian fertilization commences with the essential interaction between sperm IZUMO1 and its oocyte-surface receptor, JUNO. Following gamete fusion, JUNO is rapidly shed from the oocyte to establish a definitive membrane block to polyspermy, a pathological condition that remains a major hurdle in porcine in vitro fertilization (IVF). Despite its biological importance, the molecular networks driving JUNO cleavage has remained elusive. Here, by integrating proteomics, dual-color live-cell imaging, and functional perturbations, we identify the extended existence of JUNO and the GPI-specific phospholipase D1 (GPLD1) as the requisite enzyme mediating JUNO shedding in porcine oocytes. Targeted knockdown or pharmacological inhibition of GPLD1 stabilizes oocyte JUNO, prolongs the window of oocyte receptivity, and significantly exacerbates polyspermy, ultimately compromising embryonic developmental competence. Conversely, GPLD1 overexpression restricts redundant sperm adherence and enhances the efficiency of monospermic zygote formation and blastocyst development. Live-cell imaging reveals that fertilization triggers a transient, pulsed recruitment of GPLD1 in the oocyte, which precisely coincides with the biphasic kinetics of JUNO depletion. Our findings establish that the enzymatic cleavage of the GPI-anchor by GPLD1 is critical for JUNO release, defining a fundamental mechanism for the membrane-level block to polyspermy. This work provides a molecular framework for ensuring sperm-oocyte recognition and improving in vitro fertilization outcomes in mammals.

developmental biology↗

bioRxiv2026

ProDive reveals pervasive cross-family protein fragment reuse

Cross-family reuse of short protein fragments has been a long-standing mystery whose resolution first demands an algorithm for their systematic detection. Here we introduce ProDive, a closed-form symmetric KL divergence between profile HMMs that enables GPU-accelerated, fragment-level screening across all 25,545 Pfam families. ProDive identifies [~]318,000 cross-family fragment correspondences involving compact cores of 8-13 residues with RMSD values far below random background. Their organisation into diverse graph communities and four-fold enrichment in de novo designed proteins point away from family-specific functions and toward a general biophysical property. Their helix dominance and moderate solvent exposure suggest a role in folding initiation--a link corroborated by overlap with experimentally measured{phi} -values and by a monotonic density gradient across disordered regions. Together, these observations converge on a single explanation: cross-family fragment reuse likely reflects shared requirements for early structure formation during folding, the one biophysical constraint common to all proteins.

bioinformatics↗

bioRxiv2026

Neural cell state modulation by PARK2 and dopaminergic neuroprotection by small molecule Parkin agonism

Parkin, an E3 ubiquitin ligase encoded by PARK2, plays a key role in both hereditary and sporadic Parkinsons disease (PD), yet there are no therapies currently available that can target this important pathway. Here, we show that Parkin is critical for successful neuronal differentiation and survival, and we develop small-molecule Parkin agonists that can protect dopaminergic neurons. Upon differentiation of neural progenitor cells, loss of Parkin results in a reduced capacity to maintain neuronal cell state, dopaminergic neuronal phenotypes, and stress resistance. Moreover, Parkin loss disrupted cell morphology and the stability of neurites. Transcriptional and single-cell analyses reveal that Parkin controls critical pathways regulating stem-like cell transitions and is needed for stable neuronal maturation. We also examined the effects of FB231, a small molecule enhancer of Parkin E3 ligase activity, in models of PD. FB231 reduced pathological -synuclein and enhanced cell survival in human iPSC-derived dopaminergic neurons treated with -synuclein preformed fibrils. Furthermore, FB231 attenuated -synuclein pathology and dopaminergic neurodegeneration in a gut -synuclein murine model of PD. Our findings support that Parkin plays a crucial role in maintaining neuronal homeostasis and that pharmacologic activation of Parkin may be a promising strategy to attenuate neurodegeneration in PD.

neuroscience↗

bioRxiv2026

DHHC7 palmitoylates KRAS4A and promotes mutant KRAS-driven pancreatic cancers

KRAS mutations underlie many human cancers. While inhibitors such as Sotorasib and Adagrasib targeting KRAS mutants have shown promise, additional strategies are required to address the broader spectrum of KRAS-driven cancers, particularly those displaying drug resistance. Thus, there is a need to better understand KRAS signaling and develop new therapeutic strategies. Here we show that KRAS4A is palmitoylated on Cys180 by a palmitoyl transferase, DHHC7 (gene name ZDHHC7). Palmitoylation promotes KRAS4A plasma membrane localization, and more importantly, nanoclustering. This in turn promotes the activation of ARAF and RAF1, but not BRAF. DHHC7 and KRAS4A Cys180 palmitoylation are important for the normal and anchorage independent growth of pancreatic cancer cell lines. Depletion of ZDHHC7 dramatically inhibits pancreatic tumor growth in mouse xenograft models. These studies provide new understandings about how palmitoylation regulates KRAS4A activity and suggest DHHC7 as a promising new target for KRAS mutant cancers.

cancer biology↗

bioRxiv2026

A Conserved Metabolic Oxidative Axis Underlies Immune Cell Cryo-vulnerability

Immunotherapy has emerged as a transformative approach for treating cancer and other diseases, yet its widespread deployment requires effective cryopreservation strategies to enable scalable global distribution. However, many immune cell types remain acutely vulnerable to freeze-thaw stress, and the underlying mechanisms of this cryo-vulnerability are not well defined. In this study, we combined metabolic flux analysis, ROS quantification, lipidomics, and preclinical xenograft models to investigate how metabolic state influences cryopreservation outcomes. We found that immune cell activation induces a metabolic shift characterized by elevated glucose utilization and excessive ROS production, leading to profound post-thaw loss of viability and function, as demonstrated by a [~]25% survival rate in natural killer (NK) cells. Targeted pretreatments--including inhibitors of glucose metabolism, antioxidants, and suppression of lipid peroxidation--restored post-thaw recovery to nearly 90% while preserving effector activity and antitumor efficacy. Similar protective effects were observed across {beta} T cells, {gamma}{delta} T cells, and macrophages, defining a conserved metabolic-oxidative pathway of cryo-vulnerability and offering applicable strategies to enhance immune cell preservation.

immunology↗

bioRxiv2026

Identification of a somatic H3K23me3 methyltransferase SET-19 in C. elegans

Histone methylation plays essential roles in modulating chromatin organization and gene expression. H3K23 methylation is a conserved histone modification, yet its biological roles and the enzymes responsible for its deposition remain poorly understood. Here, we show that the loss of set-19 leads to a pronounced reduction in H3K23 methylation in C. elegans, as revealed by quantitative mass spectrometry, western blotting, and immunofluorescence staining. In vitro biochemical assays show that recombinant SET-19 proteins purified from E. coli directly catalyze H3K23 methylation. Genome-wide chromatin immunoprecipitation assays reveal that H3K23me3 is enriched at heterochromatic regions and that loss of set-19 alters H3K23me3 levels, accompanied by derepression of gene expression. Genetic analyses indicate that SET-19 is dispensable for both germline and somatic RNAi as well as transgenerational epigenetic inheritance of RNAi. SET-19 is predominantly expressed in somatic cells and specifically mediates H3K23me3 deposition in somatic tissues. The loss of set-19 causes a developmental delay without affecting fertility. Together, our results identify SET-19 as a somatic H3K23 methyltransferase and link H3K23me3 to gene repression in C. elegans.

genetics↗

bioRxiv2026

Motor Cortical Computations Underlying Natural Dexterous Movement in Freely Flying Bats

Elucidating the neural computations underlying natural, complex movement remains a fundamental challenge in neuroscience. Bat flight presents a formidable motor control challenge, requiring the use of hand-like wings whose many degrees of freedom must be precisely coordinated to enable rapid three-dimensional maneuvers. Here we performed large-scale wireless recordings of neuronal ensembles from the wing motor cortex of freely flying bats using Neuropixels probes, alongside detailed 3D pose tracking of wing kinematics. Despite the complexity of flight control, bats repeatedly executed highly accurate flights through precise adjustments of individual wingbeats. Surprisingly, motor cortical activity was not dominated by the global wingbeat cycle. Instead, individual neurons were sparsely active, exhibiting mixed selectivity for specific flight kinematics combined with variable entrainment to the wingbeat phase reaching millisecond-scale precision. This yielded a high-dimensional population regime driven by low shared variance across wingbeats, with successive wingbeats occupying distinct neural population states. Our findings reveal that during complex natural behavior the mammalian motor cortex operates in a high-dimensional computational regime that challenges prevailing views of motor cortical computation and underscores the importance of studying ethologically relevant behaviors to uncover neural principles governing brain function.

neuroscience↗

bioRxiv2026

The mechanism of Hsa_circ_0000629 in bronchial asthma through sponge adsorption of miR-212-5p/NLRP3

To explore the mechanism of Hsa_circ_0000629 adsorbing miR-212-5p/ nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) through sponge in bronchial asthma. Twenty BALB/C mice were randomly divided into a normal control group and an asthma group. Pathological changes in lung tissue were observed via HE staining. Human bronchial epithelial cells (16HBE) were transfected with Hsa_circ_0000629 overexpression group (Hsa_circ_0000629-over), Hsa_circ_0000629 siRNA (Hsa_circ_0000629-si), mimic NC, miR-212-5p mimic, inhibitor NC, miR-212-5p inhibitor, and LPS+Hsa_circ_0000629 si. LPS-induced asthmatic cell models (LPS group) and untransfected 16HBE cells (NC group) served as controls. qRT-PCR was used to measure Hsa_circ_0000629, miR-212-5p and NLRP3 expression. ELISA assessed interleukin 18 (IL-18), interleukin 1{beta} (IL-1{beta}), interleukin 6 (IL-6) and tumor necrosis factor - (TNF-) levels. Cell proliferation and the apoptosis were evaluated by EDU assay and flow cytometry, respectively. Western blot analyzed Cleaved-caspase 1, 3 and 9 proteins expression. Dual-luciferase assay verified the binding sites of Hsa_circ_0000629 to miR-212-5p and NLRP3 to miR-212-5p. HE staining revealed inflammatory cell infiltration, bronchial wall thickening, smooth muscle hyperplasia, and alveolar destruction in asthmatic mice. Compared with the controls, Hsa_circ_0000629 and NLRP3 expression were significantly increased, while miR-212-5p expression was decreased in asthmatic lung tissues. In 16HBE cells, Hsa_circ_0000629-over and LPS groups showed elevated Hsa_circ_0000629 and NLRP3 expression but reduced miR-212-5p levels. Silencing Hsa_circ_0000629 in LPS-treated cells (LPS+Hsa_circ_0000629-si) reversed these effects. Overexpression of miR-212-5p counteracted Hsa_circ_0000629-induced NLRP3 upregulation, while miR-212-5p inhibition enhanced NLRP3 expression. LPS exposure increased TNF-, IL-18, IL-6, and IL-1{beta} levels, reduced cell proliferation, and promoted apoptosis. These changes were attenuated by Hsa_circ_0000629 silencing or miR-212-5p overexpression. Western blot confirmed that Hsa_circ_0000629 overexpression upregulated Cleaved-Caspase 1, 3, and 9, whereas miR-212-5p mimic or Hsa_circ_0000629-si reversed this trend. Dual-luciferase assays demonstrated targeted interactions among Hsa_circ_0000629, miR-212-5p, and NLRP3. Interference with Hsa_circ_0000629 expression can alleviate LPS induced apoptosis in 16HBE cells and inhibit the expression of inflammatory factors by targeting the miR-212-5p/NLRP pathway, which may be a new target for the treatment of asthma.

immunology↗

bioRxiv2026

Hyperactive STAT1 Promotes T Follicular Helper Type 1 Cell Differentiation to Trigger Autoimmunity

ABSTRACTSHeterozygous gain-of-function (GOF) mutations in signal transducer and activator of transcription 1 (STAT1) cause an inborn error of immunity characterized by immune dysregulation, recurrent infections and various autoimmune manifestations. However, the precise pathogenic mechanism by which STAT1 GOF contributes to autoimmunity remains elusive. In our cohort, STAT1-GOF patients exhibit biased circulating follicular helper T (cTfh) populations with CXCR3+ Tfh1-like features. Using a Stat1 GOF mouse model that spontaneously developed autoimmunity, we found that overactivated STAT1 promotes Tfh differentiation and disrupted T cell-dependent humoral responses with skewed immunoglobulin class switching towards IgG2. Furthermore, STAT1 GOF directly targets to Tfh and Th1 cell signature genes and thereby drives the development of Tfh1 cells with excessive IFN-{gamma} production, which implicated in autoantibody production and the development of autoimmunity. Notably, IFN-{gamma} neutralization significantly alleviated autoimmune cellular responses and autoantibody levels in mutant mice, highlighting IFN-{gamma} blockade as a promising targeted therapy for the STAT1-GOF patients with autoimmunity. Our findings suggest that proper regulation of STAT1 activity within a reasonable magnitude is crucial for ensuring optimal host-protective humoral immunity. One-sentence summaryOveractivated STAT1 promotes Tfh1 differentiation to drive autoimmunity.

immunology↗

bioRxiv2026

Trem2hi macrophages bridge inflammation resolution and fibrosis initiation after ischemia-reperfusion injury in the kidney

Maladaptive repair of acute kidney injury (AKI) may lead to the development of chronic kidney disease (CKD) characterized by renal fibrosis. Macrophages play roles in AKI-to-CKD progression; however, the interplay between inflammation and fibrosis after AKI remains controversial and the precise role of the distinct macrophage subsets remains elusive. In the present study we identified a unique population of Trem2hi macrophages derived from the bone marrow as a mediator bridging inflammation resolution and fibrosis establishment after kidney injury. Trem2 deficient mice exhibited mitigated renal fibrosis after ischemia-reperfusion injury (IRI) while the renal injury and inflammation persisted. Mechanistically, Trem2 promoted renal inflammation resolution by facilitating macrophage efferocytosis to remove apoptotic tubule cells and reshaping the macrophage cytokine production profile. Loss of Trem2 expression led to excessive cholesterol accumulation in macrophages via Lxr-Abca1/Abcg1 axis and thus sustained pro-inflammatory cytokines production. Moreover, Trem2hi macrophages orchestrated the pro-fibrotic tubular epithelial cells and the activation of myofibroblasts through SPP1 to promote the establishment of renal fibrotic niche. Based on our findings, Trem2hi macrophages may serve as a potential therapeutic target for AKI-to-CKD in combination with anti-inflammatory remedies.

immunology↗

bioRxiv2026

Principles of subclonal gene dosage across human cancer

Intratumor heterogeneity drives disease progression, but even though subclonal copy number variation (CNV) is a major contributor to this heterogeneity1, its impact on cell phenotype is not fully understood. Here, by applying high-quality joint whole genome sequencing and mRNA profiling in single cells (DNTR-seq2) to solid tumors and leukemias from 57 patients, we have analyzed the in vivo transcriptional effect of subclonal CNVs within a tumor. We found that gene dosage is generally additive in low and moderate copy states, but that cancer-type-specific compensation is common, and core promoter elements are associated with reduced additivity. We find that different classes of subclonal CNV impose varying degrees of transcriptional constraints on a cell, with highly amplified megabase-size regions associated with a strong effect both in cis and trans, while arm level CNVs generally exert a milder effect. We also describe a previously unappreciated class of tumors with transient clonality, where every cell is genetically highly distinct. We find that transient clonality is common in ovarian cancer and soft tissue sarcoma, that it is preceded by a whole genome duplication event, and that gene dosage in these tumors affects transcript abundance to a similar degree as in cancer with stable subclones.

cancer biology↗

bioRxiv2026

TRIM21 is a molecular rheostat for influenza A virus replication

TRIM21 is a multifunctional E3 ubiquitin ligase and intracellular antibody receptor, yet its role during viral infection remains unclear, with reports describing both antiviral and proviral activities. Here, we show that TRIM21 regulates influenza infection in an expression-dependent manner by functioning as a molecular rheostat rather than a binary restriction factor. This graded activity of TRIM21, which leads to both suppression and promotion of influenza replication, couples linkage-specific ubiquitination of viral nucleoprotein with modulation of innate immune signaling. Additionally, loss of TRIM21 unmasks a compensatory antiviral program centered on PRKDC, which is a ubiquitination target of TRIM21. This positions PRKDC as a latent restriction factor selectively engaged when primary TRIM21 control is lost. Together, these findings reveal a hierarchical and plastic antiviral network in which TRIM21 sets an adjustable threshold for host defense while restraining secondary restriction pathways. This framework highlights the sophisticated layers of regulation of the host ubiquitin-mediated antiviral immunity.

cell biology↗

bioRxiv2026

Genetically Engineered Biomimetic Nanozymes Reprogram Immune Niches to Intercept Colitis-Carcinoma Transition

Colitis-associated colorectal cancer (CAC) arises from chronic inflammatory niches characterized by persistent oxidative stress and dysregulated immune cell recruitment. Current anti-inflammatory therapies provide only transient symptom relief and fail to prevent malignant progression due to their inability to simultaneously mitigate oxidative injury and immune chemotaxis. Our analysis of clinical samples revealed markedly elevated C-X-C motif chemokine ligand 2 (CXCL2) in intestinal tissues from patients with inflammatory bowel disease (IBD) and CAC, implicating the CXCL2-CXCR2 axis in driving excessive neutrophil and macrophage infiltration and fostering tumorigenesis. Herein, we report a biomimetic nanozymes (PB@ECM) that reprogram inflammatory immune niches to intercept CAC progression. PB@ECM integrates a Prussian blue nanozyme core with genetically engineered macrophage membranes, enabling concurrent scavenging of reactive oxygen species through superoxide dismutase- and catalase-like activities and sequestration of CXCL2 via membrane-displayed CXCR2 receptors. In murine models of colitis and CAC, PB@ECM significantly alleviated intestinal inflammation, suppressed neutrophil and macrophage infiltration, and effectively inhibited colitis-carcinoma transition. By disrupting the pathological crosstalk between oxidative stress and immune chemotaxis, this work establishes a biomimetic nanozyme strategy for preventing inflammation-driven carcinogenesis.

bioengineering↗

bioRxiv2026

Meaning-based guidance of attention in rhesus monkeys during naturalistic scene viewing

In humans and other primates, high-acuity vision is restricted to the fovea, requiring frequent saccadic eye movements to sample visual information, a process known as overt attention. Classical visual salience theory explains how low-level image features guide these movements, but recent human studies have shown that overt attention is also strongly guided by scene meaning--the spatial distribution of semantic informativeness. Whether this form of attentional guidance is uniquely human or shared across primate vision remains unknown. Here, we addressed this question by recording eye movements from two rhesus macaques freely viewing naturalistic indoor scenes. Fixation selection was modeled using meaning maps alongside image-based salience maps and center proximity. In both monkeys, meaning robustly predicted fixation selection after controlling for visual salience and center bias. Moreover, high-meaning regions captured attention independently of visual salience, whereas salience played an increasingly important role as meaning decreased. While this prioritization of meaningful regions remained robust across environments, familiarity broadened visual exploration by increasing the likelihood of fixating less meaningful areas. Finally, the influence of meaning on fixation selection strengthened with attentional engagement. These findings suggest that meaning-based attention is an evolutionarily conserved component of primate vision and establish a behavioral foundation for investigating its neural mechanisms.

animal behavior and cognition↗

bioRxiv2026

HitAnno: Atlas-level cell type annotation based on scATAC-seq data via a hierarchical language model

The single-cell assay for transposase-accessible chromatin using sequencing (scATAC-seq) has emerged as a core technology for dissecting cellular epigenomic heterogeneity and gene regulatory programs. With the emergence of atlas-level scATAC-seq datasets, cell type annotation increasingly faces challenges arising from unprecedented data scale and increased cell-type diversity, which together place stringent demands on model reliability and robustness. Here, we introduce HitAnno, a hierarchical language model capable of accurate and scalable cell type annotation in atlas-level scATAC-seq data. Leveraging selected cell-type-specific peaks to construct "cell sentences", HitAnno employs a two-level attention mechanism that captures accessibility profiles hierarchically. Extensive evaluations show that HitAnno robustly annotates both major and rare cell types across multiple settings, including intra-dataset, cross-donor and inter-dataset annotation. The hierarchical attention mechanisms of the model reveal co-accessibility patterns among peaks and dependencies across higher-order peak sets, ensuring an interpretable annotation process. Training on a 31-cell-type human atlas, HitAnno can directly annotate new query datasets without retraining and is accessible through an online interface. Our model identifies heterogeneous subgroups within mixed labeled cells from unseen datasets, demonstrating its potential to assist researchers in refining existing cell atlases.

bioinformatics↗

bioRxiv2026

A Genetic Tool for Specific Tracking of Mature Neutrophils

Tracking mature neutrophils remains challenging due to the lack of reliable cell surface markers. Although CD101 is a promising candidate for mature neutrophils, its stability under pathological conditions is unclear. Using a CD101-tdTomato reporter mouse model, we confirmed that the reporting system does not alter CD101 expression, and tdTomato fluorescence is predominantly expressed in mature neutrophils across peripheral tissues. Further analysis revealed that CD101+ and tdTomato+ neutrophils display identical characteristics of mature neutrophil, including poly-segmented nuclei, cell size, and key functions under homeostasis. By comparing tdTomato fluorescence with CD101 protein levels, we demonstrate that reduced CD101 expression under pathological states was not attributed to shedding or degradation. Our finding enhances CD101 as a robust and reliable marker of neutrophil maturity, providing a foundation for future applications in spatial transcriptomics and lineage tracing studies to dissect neutrophil heterogeneity and function. Highlights of the studyO_LIIn CD101-tdTomato homozygous mice, tdTomato is predominantly expressed in neutrophils and labels nearly 100% of mature neutrophils, aligning with the phenotype of CD101+ mature neutrophils; C_LIO_LIThe CD101-tdTomato reporting system does not interrupt CD101 expression or neutrophil functions; C_LIO_LICD101 remains a stable and reliable cell surface marker for labeling mature neutrophils, even under pathological conditions. C_LI

immunology↗

bioRxiv2026

c-Fos enhances influenza virus replication by stabilizing the M2 protein and promoting autophagosome accumulation

The influenza A virus (IAV) employs multiple strategies to hijack host cellular machinery for efficient replication. While autophagosome accumulation is known to promote IAV replication, and the viral matrix protein 2 (M2) ion channel protein plays essential roles in viral uncoating, assembly, and autophagy induction, the mechanisms regulating M2 stability remain incompletely understood. Furthermore, although c-Fos participates in the replication of various viruses, its function in IAV infection has not been characterized. Here, we identify c-Fos as a critical proviral host factor that enhances IAV replication through stabilizing M2 protein and promoting autophagosome accumulation. We demonstrate that IAV infection triggers M2-mediated cytosolic calcium elevation, which upregulates c-Fos expression. The induced c-Fos physically interacts with M2 and prevents its proteasome and lysosomal degradation, thereby increasing M2 accumulation. This stabilized M2 protein as a viral protein directly facilitates viral replication while simultaneously promoting autophagosome accumulation to further enhance the process. Our findings reveal a novel positive feedback loop in IAV infection, establishing c-Fos as a key regulator of IAV replication through M2 stabilization, and highlighting these interactions as potential therapeutic targets for antiviral intervention. IMPORTANCEInfluenza A virus (IAV) remains a significant global health threat, causing substantial morbidity and mortality. Understanding virus-host interactions is crucial for developing antiviral strategies. Here, we uncover a previously unrecognized positive feedback loop in which IAV exploits the host transcription factor c-Fos to enhance its own replication. We demonstrate that IAV infection upregulates c-Fos through M2-mediated calcium signaling, and the induced c-Fos in turn stabilizes the viral M2 protein. This stabilized M2 not only directly supports viral replication but also promotes autophagosome accumulation, further facilitating virus production. Our findings establish c-Fos as a critical proviral host factor and reveal a mechanism by which IAV hijacks host cellular machinery to create a favorable environment for efficient replication. The identification of this c-Fos-M2 axis not only advances our understanding of IAV-host interactions but also opens new avenues for therapeutic intervention targeting this vulnerability in the viral life cycle.

cell biology↗

bioRxiv2026

Comparative study on the inhibition of copper oxide, nickel, and sodium tungstate on microbially induced concrete corrosion under sewer conditions

Microbially induced concrete corrosion (MICC) is a significant issue that reduces the service life of sewer systems. Bacteriostatic agent in concrete can inhibit microbial activity and the process of MICC to some extent. However, a systematic comparison of the inhibition effects of various bacteriostatic agents on MICC remains lacking. In this study, three bacteriostatic agents (copper oxide, nickel, and sodium tungstate) were investigated for their inhibitory effects on MICC. For each inhibitor, the cement mortar coupons with 0.05 wt%, 0.1 wt%, and 0.2 wt% of the inhibitor were prepared. The coupons were partially submerged in sewage of a controlled laboratory corrosion chamber (20 {+/-} 5 ppm H2S) to simulate the tidal region of gravity sewer. During the 56 days of exposure, the intensification of pores, cracks, surface erosion, and spalling was observed on all coupons. After 56 days of exposure, the sulfate concentration and adenosine triphosphate (ATP) content of coupons without inhibitor were 10.65 mg/cm2 and 30.17 {+/-} 3.87 mol/cm2, respectively. They were higher than those of coupons containing 0.05 wt%, 0.1 wt%, and 0.2 wt% of copper oxide and 0.05wt% of nickel. The temporal profiles of ATP of coupons without inhibitor was similar to those of coupons containing sodium tungstate. After exposure for 28 days, the surface pH of coupons without inhibitor was 7.45, meanwhile of those coupons containing 0.2 wt% of copper oxide and 0.05 wt% of nickel were 9.42 and 9.93, respectively. Those results indicated that the bacteriostatic effect of copper oxide and nickel (0.05 wt %) was found to be the most prominent. The findings indicate that a single bacteriostatic agent is only effective during specific corrosion stages, suggesting that a combination of multiple agents may be a promising strategy to combat the multi-stage MICC process over the long term. This study provides a theoretical basis for the selection and development of protective materials against concrete corrosion in sewer networks.

microbiology↗