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Lipopolysaccharide (LPS) fragments from gram-negative bacteria are on the order of nanometers in size, far smaller than the 220-nanometer pore of a 0.22-micron filter

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This mechanism involves: Sequestration of monomeric actin (G-actin) to prevent premature polymerization Promotion of actin polymerization into functional microfilaments (F-actin) when needed Enhanced cellular migration through cytoskeletal reorganization Facilitation of cell shape changes necessary for wound healing Research indicates TB-500 may work with the Arp2/3 protein complex to orchestrate actin polymerization, though this mechanism requires further clarification[4]