The energy storage behaviors of MnO2 for aqueous Zn‐MnO2 batteries mainly depend on the Zn2+/H+ intercalation but are limited by poor ion/electron migration dynamics and stability. Herein, a strategy is proposed that promoting proton migration kinetics ameliorates H+ storage activity by introducing Ni2+ into γ‐MnO2 (Ni‐MnO2). Ni2+ can lower the diffusion barrier of H+ and selectively induce the ion intercalation, thereby alleviating the electrostatic interaction with the lattice. Moreover, Ni2+ enables the adjacent [MnO6] octahedrons to have better electron conductivity. The Ni‐MnO2 exhibits superior rate performance (nearly four times specific capacity compared with MnO2) and ultra‐long‐cycle stability (100% of capacity retention after 11 000 cycles at 3.0 A g−1). The calculation indicates that the Ni‐MnO2 allows H+ migrate rapidly along the one‐dimensional tunnel due to reduction of the activation energy caused by Ni2+ regulating, thus achieving excellent reaction kinetics. This work brings great potential for the development of high‐performance aqueous Zn‐MnO2 batteries.

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Interleukin (IL)-26 is released in response to bacterial endotoxin (LPS) in the bronchoalveolar space of humans in vivo and it may potentiate neutrophil chemotaxis by enhanced IL-26 receptor stimulation. However, the effects of extracellular IL-26 protein on the innate immune response in the lungs in vivo remain unknown. Here, we characterized these effects of IL-26 on a wide range of aspects of the innate immune response to LPS in different compartments of the lungs in vivo over time. We administrated recombinant human (rh) IL-26 protein in the bronchoalveolar space using intranasal instillation in a mouse in vivo model, with and without prior instillation of LPS. We verified gene expression of the IL-26 receptor complex in mouse lungs and observed that, after instillation of LPS, rhIL-26 increases the phosphorylation of STAT3, a signaling molecule of the IL-26 receptor complex. We also observed that rhIL-26 exerted additional stimulatory and inhibitory actions that are compartment- and time-dependent, resulting in alterations of cytokines, proteinases, tissue inflammation and the accumulation of innate effector cells. Without the prior instillation of LPS, rhIL-26 exerted time-dependent effects on total gelatinase activity but few other effects. Most important, after instillation of LPS, rhIL-26 cleared inflammatory cells from local tissue and increased the accumulation of innate effector cells in the bronchoalveolar space. Tentatively, rhIL-26 may facilitate the innate immune response towards the bronchoalveolar space in vivo and represents a potential target for therapy in lung disorders involving the innate immune response.

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