Konjac glucomannan, macrophage polarisation, and atopic dermatitis: Preclinical evidence and translational perspectives – A review

Atopic dermatitis (AD) is a chronic inflammatory skin disease arising from the interplay of epidermal barrier dysfunction, immune imbalance, and genetic susceptibility. Macrophages accumulate in both acute and chronic lesions and may contribute to disease persistence through dysregulated polarisation between pro-inflammatory (M1-like) and regulatory/repair (M2-like) states, impaired microbial defence, and altered cytokine production. Although topical and systemic therapies have improved disease control, long-term management remains limited by inadequate skin penetration, safety concerns, and poor treatment adherence. Konjac glucomannan (KGM) is a plant-derived polysaccharide obtained from Amorphophallus konjac with favourable biocompatibility, low immunogenicity, and intrinsic gel- and film-forming properties that support its use as a functional biomaterial and delivery matrix. Preclinical studies indicate that native, pulverised, or modified KGM can modulate immune responses, including macrophage polarisation, IgE regulation, and cytokine signalling, while supporting tissue repair. This review highlights macrophage-driven immune mechanisms in AD and relates them to the structural and physicochemical characteristics of KGM relevant to oral and topical delivery. Recent advances in KGM-based platforms and their potential to regulate macrophage-centred inflammation are discussed, along with current limitations and key translational considerations for developing KGM-based adjunctive strategies in AD.