M2 macrophages participate in ILC2 activation induced by
            <i>Helicobacter pylori</i>
            infection

Peng, Ruyi; Xu, Canxia; Zhang, Linfang; Liu, Xiaoming; Peng, Dongzi; Chen, Xingcen; Liu, Deliang; Li, Rong

doi:10.1080/19490976.2024.2347025

Cited by 3 publications

References 44 publications

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Broad‐spectrum antiviral effect of MoringaA‐loaded exosomes against IAV by mediating the GCN5‐TFEB‐autolysosome pathway

Lv,

Li,

Yang

et al. 2024

Journal of Medical Virology

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Influenza virus‐induced viral pneumonia is a major threat to human health, and specific therapeutic agents for viral pneumonia are still lacking. MoringaA (MA) is an anti‐influenza virus active compound isolated from Moringa seeds, which can inhibit influenza virus by activating the TFEB‐autophagic lysosomal pathway in host cells. In this study, we obtained exosomes from M2‐type macrophages and encapsulated and delivered MA (MA‐Exos), and we investigated the efficacy of MA‐Exos in antiviral and viral pneumonia in vivo and in vitro, respectively. In addition, we provided insights into the mechanism by which MA‐Exos regulates TFEB‐lysosomal autophagy by RNA sequencing. The MA‐Exos showed broad‐spectrum inhibition of IAV, and significant promotion of the autophagic lysosomal pathway. Meanwhile, we found that GCN5 gene and protein were significantly down‐regulated in IAV‐infected cells after MA‐Exos intervention, indicating its blocking the acetylation of TFEB by GCN5. In addition, MA‐Exos also significantly promoted autophagy in lung tissue cells of mice with viral pneumonia. MA‐Exos can inhibit and clear influenza virus by mediating the TFEB‐autophagy lysosomal pathway by a mechanism related to the down‐regulation of histone acetyltransferase GCN5. Our study provides a strategy for targeting MA‐Exos for the treatment of viral pneumonia from both antiviral and virus‐induced inflammation inhibition pathways.

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Broad‐spectrum antiviral effect of MoringaA‐loaded exosomes against IAV by mediating the GCN5‐TFEB‐autolysosome pathway

Lv,

Li,

Yang

et al. 2024

Journal of Medical Virology

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Extracellular vesicles derived from lung M2 macrophages enhance group 2 innate lymphoid cells function in allergic airway inflammation

Pei,

Lv,

Zhang

et al. 2024

Preprint

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Group 2 innate lymphoid cells (ILC2s) promote the recruitment of eosinophils by secreting large amounts of type 2 cytokines (IL-5 and IL-13), thus triggering the main feature of asthma, pathological inflammation. Recent insights from mouse and human studies indicated a potential relationship between ILC2s and macrophages. However, the mechanism by which lung M2 macrophage-derived extracellular vesicles (M2 EVs) regulate ILC2s remains unclear. Here, the size, morphology, and specific markers of M2 EVs were successfully characterized in the lungs. Furthermore, we discovered that M2 EVs strongly promoted type 2 lung immunopathology induced by papain. Mechanistically, M2 EVs were internalized by ILC2s, triggering ILC2 activation and inducing pro-inflammatory cytokine (IL-5 and IL-13) production. M2 EVs also indirectly enhanced the function of ILC2s through macrophages and CD4+ T cells. Using RNA sequencing, we found that long non-coding RNA (lncRNA) 4930474H06Rik participated in mediating these effects of M2 EVs. Inhibition of 4930474H06Rik altered intracellular metabolism of activated ILC2s and enhanced NF-κB pathway signaling. Taken together, we demonstrated that M2 EVs promoted allergic airway inflammation at least partially through 4930474H06Rik, implying that 4930474H06Rik can be considered as a therapeutic target for ILC2s activation in allergic airway inflammation.

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Molecular Mechanism for Malignant Progression of Gastric Cancer Within the Tumor Microenvironment

Matsuoka,

Yashiro

2024

IJMS

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Gastric cancer (GC) is one of the most common cancers worldwide. Most patients are diagnosed at the progressive stage of GC, and progress in the development of effective anti-GC drugs has been insufficient. The tumor microenvironment (TME) regulates various functions of tumor cells, and interactions between the cellular and molecular components of the TME—e.g., inflammatory cells, fibroblasts, vasculature cells, and innate and adaptive immune cells—promote the aggressiveness of cancer cells and dissemination to distant organs. This review summarizes the roles of various TME cells and molecules in regulating the malignant progression and metastasis of GC. We also address the important roles of signaling pathways in mediating the interaction between cancer cells and the different components of the GC TME. Finally, we discuss the implications of these molecular mechanisms for developing novel and effective therapies targeting molecular and cellular components of the GC TME to control the malignant progression of GC.

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M2 macrophages participate in ILC2 activation induced by Helicobacter pylori infection

Cited by 3 publications

References 44 publications

Broad‐spectrum antiviral effect of MoringaA‐loaded exosomes against IAV by mediating the GCN5‐TFEB‐autolysosome pathway

Broad‐spectrum antiviral effect of MoringaA‐loaded exosomes against IAV by mediating the GCN5‐TFEB‐autolysosome pathway

Extracellular vesicles derived from lung M2 macrophages enhance group 2 innate lymphoid cells function in allergic airway inflammation

Molecular Mechanism for Malignant Progression of Gastric Cancer Within the Tumor Microenvironment

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