Heber Biotec · CSF3 · 重组蛋白
granulocyte colony stimulating factor 是一种重组蛋白，由Heber Biotec研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)。
| 商品名 | Hebervital |
| 公司 | Heber Biotec |
| 药物类别 | 重组蛋白 |
| 分子靶点 | CSF3 |
| 给药途径 | Injectable (Others) |
| 状态 | Approved |
granulocyte colony stimulating factor 作用于 1 个分子靶点：
| CSF3 | colony stimulating factor 3 (GCSF, CSF3OS) |
granulocyte colony stimulating factor 针对 2 个适应症，涉及 1 个治疗领域。
| 治疗领域 | 疾病/病症 | 分期 |
|---|---|---|
| Blood and lymphatic system disorders | Neutropenia | ✓ Approved |
| Blood and lymphatic system disorders | Bone marrow disorder | ✓ Approved |
International Journal Of Molecular Sciences Editorial Office
With this notice, the IJMS Editorial Office alerts readers to concerns regarding this article [...].
Wang Xun X, Liao Shi-Han SH, Wang Nan N, Chen Ya-Ting YT et al.
Microglia, the brain's resident immune cells, are increasingly recognized as key regulators of brain physiology and behavior. However, their specific role in affective states remains controversial, with studies reporting conflicting depression-like outcomes following their removal. Using the colony stimulating factor-1 receptor (CSF1R) inhibitor PLX5622 in adult mice of both sexes, we found that microglial deletion selectively induced despair-like behavior (increased immobility in the forced swim test and the tail suspension test) in either sex, without affecting locomotion, anxiety, sociability, anhedonia, or cognition. This effect was accompanied by reactive astrogliosis in the medial prefrontal cortex (mPFC). Unexpectedly, microglial deletion induced a predominant A2-like astrocyte reactivity. Notably, both the despair-like and A2-like phenotypes resolved upon microglia repopulation. Critically, pharmacological inhibition of these hyperactive mPFC astrocytes with fluorocitrate reversed the despair-like phenotype, indicating that microglial loss triggers maladaptive astrocyte reactivity that drives behavioral despair. Our results reveal an essential role for microglia in maintaining emotional homeostasis, possibly through interaction with astrocytes.
Zhou Yifan Y, Wu Jianfeng J, Gong Lihao L, Zhu Xinyi X et al.
DC development requires balanced signaling from cytokines, such as Fms-like tyrosine kinase 3 ligand (Flt3L) and macrophage colony-stimulating factor (M-CSF), but how these pathways are integrated to control lineage fate is not fully understood. Using a murine genetic model, we identified the kinase p38α as a central node that orchestrates this balance. We demonstrated that p38α, which acts as a critical effector downstream of Flt3L, is indispensable for plasmacytoid DC (pDC) differentiation. Mechanistically, the Flt3L-p38α pathway sustains the expression of the E3 ubiquitin ligase Nedd4, which mediates the degradation of the M-CSF receptor (CD115). Consequently, genetic deletion of p38α disrupts this primary Flt3L signaling cascade, leading to Nedd4 downregulation and triggering compensatory upregulation of surface CD115 expression on hematopoietic progenitors. This paradoxically enhanced their differentiation potential, leading to a numerical compensation of pDCs and increased overall myeloid repopulation; the resulting DCs were functionally impaired and exhibited defective production of type I/III interferons and IL-12. Crucially, this functional collapse abrogated their ability to orchestrate antitumor immunity. As a direct consequence, mice with p38α-deficient hematopoiesis failed to mount effective IFN-γ+CD8+ T-cell responses and were unable to control tumor growth. Our study reveals a novel p38α-Nedd4 molecular switch that integrates signaling from Flt3L and M-CSF to balance the quantity and functional quality of DCs, highlighting p38α as a key determinant of effective cancer immunosurveillance in a murine system.
Zhang Lei L, Liu Chennan C, Li Xiaodong X, Wang Bin B et al.
The growing prevalence of multidrug-resistant Mycobacterium tuberculosis complicates tuberculosis control efforts. We discovered that Rv1453, as a new transcription factor, is crucial for lipid metabolism in bacteria. Rv1453 suppresses expression of genes related to fatty acid β-oxidation (fadD18, fadE5, fadE12, fadE13, fadE18, fadE30, fadE31, echA7) and genes for lipid synthesis (accA2, accD2). Furthermore, acyl-Coenzyme A influences signals regulated by Rv1453. Removing Rv1453 boosts expression of these genes, alters cell wall lipid composition, changes colony morphology, thickens the cell wall, and contributes to the reduced multidrug susceptibility. These findings point to an association between Rv1453-mediated lipid metabolism and multidrug sensitivity in Mycobacterium tuberculosis.
Li Xue X, Wang Jing J, Xiao Meng M, Jia Peiyao P et al.
Microbial colony analysis is routinely used in clinical microbiology, pharmaceutical quality control, food safety, and environmental monitoring. Colony enumeration remains challenging because real-world plates frequently show crowding, size variation, background debris, and plate-rim interference. Low contrast on membrane or filter media, weak colony boundaries, and ultra-dense or too-numerous-to-count (TNTC) growth further complicate analysis. These conditions increase counting variability and limit rule-based counters. This review examines artificial intelligence (AI)-enabled colony analysis and links recurrent plate-reading challenges to method selection and validation requirements. We examine traditional threshold- and morphology-based pipelines, object detection, semantic segmentation, instance segmentation, and density- or keypoint-based estimation. Current evidence is stronger for plate-level triage and semi-quantitative interpretation than for direct colony enumeration. However, evidence supporting routine quantitative colony-forming unit (CFU) reporting across laboratories remains limited. Reliable deployment requires methods suited to plate format, organism, imaging conditions, and intended use, with validation in the target workflow.
Xiong Ting T, Hu Zongwen Z, Yang Zhiyue Z, Yang Minghua M et al.
Honey bees provide a tractable model for studying the gut-brain axis in social insects. Unlike mammalian systems, the gut-brain axis in honey bees is jointly shaped by a relatively simple yet functionally specialized microbiota, physiological traits determined by caste differentiation and division of labor, and social interactions within the colony. Accumulating evidence indicates that gut microbes can influence neural function in honey bees through metabolic, immune, and neuroendocrine pathways, thereby affecting cognition, social behavior, immune homeostasis, and other host traits, and ultimately influences colony performance. Conversely, changes in host physiological state and environmental exposures can also reshape the gut microbiota, forming a dynamic feedback circuit between gut status and brain function. Given the high sociality of honey bees, microbial transmission and behavioral interactions among individuals may further amplify gut-brain axis effects and influence overall health of the colony. This review summarizes the establishment and temporal dynamic of the honey bee gut microbiome, the information transfer mechanisms between gut microbes and the host nervous system, and the effects of these interactions on key behaviors (learning, memory, foraging) and colony performance. It also examines major perturbing agents-pesticides, antibiotics, and pathogens-and explores strategies for colony health maintenance from the perspective of the gut-brain axis. Finally, the potential of microbiome-targeted interventions for improving colony health is critically evaluated. This review proposes an integrative framework from microbial dynamics to behavioral regulation and colony health, serving as a reference to promote basic research on the honey bee gut-brain axis and its applied translation for sustainable colony health management. These findings may also provide heuristic value for the study of human gut-brain interactions, neurobehavioral disorders related to microbial dysbiosis, and the development of microbiome-targeted health intervention strategies.
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