In Stock Cell Lines
Mus musculus (Mouse)
Lung
Adherent and suspension
The S100a8 Knockout MH-S Cell Line is a CRISPR/Cas9-edited knockout line derived from mouse alveolar macrophages, featuring disruption of the gene encoding the pro-inflammatory calcium-binding protein S100A8. Loss of S100A8 eliminates S100A8/A9-mediated activation of TLR4 and RAGE, reducing MyD88-dependent NF-??B and MAPK signaling and impairing production of IL-6, CXCL8, and other mediators. Hosted in the MH-S alveolar macrophage cell line, which retains phagocytic and immune surveillance functions, this model is suited for investigating lung inflammation, calprotectin signaling, and innate immunity. Key applications include anti-inflammatory drug screening, cytokine profiling, and pathway analysis using ELISA, western blotting, and NF-??B reporter assays.
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The S100a8 Knockout MH-S Cell Line is a CRISPR/Cas9-edited knockout cell line derived from MH-S mouse alveolar macrophages. This cell line features targeted disruption of the S100a8 gene, which encodes the pro-inflammatory calcium-binding protein S100A8. By eliminating functional S100A8, researchers can study the loss of S100A8/A9-mediated signaling in a stable macrophage model, facilitating dissection of TLR4/RAGE-dependent pathways without confounding transient effects.
The MH-S host cell line originates from mouse alveolar macrophages and retains key primary cell functions, including phagocytosis, Toll-like receptor responsiveness, and cytokine secretion. Alveolar macrophages are central to lung immune defense, surfactant clearance, and immune surveillance. The MH-S line is a widely accepted model for pulmonary immunology, enabling genetic manipulation while preserving physiologically relevant phenotypes. The S100a8 knockout in this background permits focused investigation of calprotectin-dependent processes in a respiratory-relevant context.
S100A8 forms the S100A8/A9 heterodimer (calprotectin), a DAMP that activates TLR4 and RAGE. This engagement triggers MyD88-dependent NF-??B and MAPK signaling, leading to expression of pro-inflammatory mediators such as IL-6, CXCL8, MMP9, and ROS. The S100a8 knockout disrupts this axis, abolishing S100A8/A9-mediated receptor activation and downstream signaling. S100a8 expression is induced by IL-1??, TNF-??, and LPS via NF-??B and AP-1, and is repressed by glucocorticoids. S100A8 also interacts with CD14, NADPH oxidase, and ANO1, underscoring its multifaceted role in inflammation.
In alveolar macrophages, S100A8-mediated signaling is implicated in pulmonary inflammatory diseases such as asthma, COPD, and acute lung injury. The knockout line allows researchers to dissect S100A8-specific contributions to macrophage chemotaxis, phagocytosis, and respiratory burst in response to LPS or other stimuli. It is thus a valuable tool for understanding calprotectin-driven pathology in the airway and for evaluating therapeutic interventions targeting the TLR4/RAGE?CNF-??B pathway.
This S100a8 knockout cell line supports diverse experimental applications, including macrophage inflammation modeling, innate immune signaling studies, and anti-inflammatory compound screening. Compatible assays encompass ELISA, western blotting for NF-??B phosphorylation, RT-qPCR, flow cytometry, NF-??B reporter assays, transwell migration, and LPS stimulation. Co-immunoprecipitation can further probe S100A9/TLR4/RAGE interactions. For additional details, please contact Ascent Research.
