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Introduction: Upon infection, insect hosts simultaneously express a cocktail of antimicrobial peptides (AMPs) which can impede pathogen colonization and increase host fitness. It has been proposed that such a cocktail might be adaptive if the effects of co-expressed AMPs are greater than the sum of individual activities. This could potentially prevent the evolution of bacterial resistance. However, studies on AMPs in combination are scarce. Attacins are one of the relatively large AMP families, which show anti-Gram-negative activity .
Material And Methods: Here, we used RNA interference (RNAi) to silence three members of the Attacin family genes in the mealworm beetle, : ( (), (), and 2 () both individually and in combination. We then infected with the Gram negative entomopathogen .
Results: We found that survival of the beetles was only affected by the knockdown of , and the knockdown of all three Attacins together. Triple knockdown, rather than individual or double knockdowns of AMPs, changes the temporal dynamics of their efficiency in controlling the colonization of in the insect body.
Discussion: More precisely, AMP gene expression influences load early in the infection process, resulting in differences in host survival. Our results highlight the importance of studying AMP-interactions .
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http://dx.doi.org/10.3389/fimmu.2023.1140627 | DOI Listing |
J Ethnopharmacol
September 2025
Ethnopharmacological Relevance: Fujian Tablet (FJT), a traditional Chinese herbal compound formulation developed under the theoretical framework of "nourishing the liver and kidney, replenishing essence and marrow" , has been clinically applied for over two decades to treat post-stroke neurological deficits. Preliminary studies demonstrated its efficacy in improving motor function and promoting cervical spinal cord neuroaxonal growth in a middle cerebral artery occlusion (MCAO) rat model. Building upon these findings, this study integrates metabolomic evidence of Foxo3a-GPX4 axis activation to systematically elucidate Fujian Tablet's neurorestorative mechanisms through three interconnected pathways: regulation of ferroptosis, promotion of oligodendrocyte proliferation, and remyelination.
View Article and Find Full Text PDFRedox Biol
September 2025
Department of Spine Surgery, The Second Affiliated Hospital of Nantong University, Nantong First People's Hospital, Medical School of Nantong University, Nantong, Jiangsu, 226000, China; Research Institute for Spine and Spinal Cord Disease of Nantong University, Nantong, Jiangsu, 226000, China. Elec
Spinal cord injury (SCI) is a devastating condition characterized by the accumulation of myelin debris (MD), persistent neuroinflammation, and impaired neural regeneration. Although macrophages are pivotal for MD clearance, the impact of excessive MD phagocytosis on macrophage phenotype and function remains poorly understood. Building upon our prior evidence that exendin-4 (Ex-4), a glucagon-like peptide-1 receptor (GLP-1R) agonist, mitigates microglia-driven neuroinflammation post-SCI, this study elucidates the therapeutic efficacy and underlying mechanisms of Ex-4 in alleviating macrophage senescence, restoring efferocytotic capacity, and facilitating neural repair.
View Article and Find Full Text PDFMicrobes Infect
September 2025
Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530007, P.R. China. Electronic address:
Background: While autophagy is pivotal in antimicrobial defense, its regulatory role in Talaromyces marneffei (TM) infected bronchial epithelium remains elusive.
Objective: To elucidate the impact of TM infection on autophagy in bronchial epithelial cells and to identify the key molecular regulators involved in this process.
Methods: Primary computational screening identified core autophagy modulators.
Immunology
September 2025
Department of the Fifth Ward of Medical Oncology, Anyang Tumor Hospital, Anyang, China.
With 1 in every 20 women afflicted, breast cancer is the most frequent malignant tumour in women and a significant health burden on women. Drug resistance in cancer is the key problem limiting current therapy approaches. Cyclooxygenase-2 (COX-2, namely PTGS2) is linked to immune evasion and chemoresistance in tumour cells, and it is frequently overexpressed in many forms of cancer.
View Article and Find Full Text PDFJ Biol Chem
September 2025
Department of Biological Chemistry, University of Michigan, Ann Arbor, MI 48109. Electronic address:
Hydrogen sulfide (HS) is a respiratory poison and also a product of our own metabolism. The toxicity of HS is mitigated by the activity of mitochondrial sulfide quinone oxidoreductase (SQOR), which oxidizes HS while concomitantly reducing coenzyme Q. An unusual cysteine trisulfide cofactor distinguishes SQOR from other members of the flavin disulfide reductase superfamily.
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