Human placental extract regulates polarization of macrophages via IRGM/NLRP3 in allergic rhinitis

Wo, Beibei; Du, Chunyang; Yang, Yan; qi, huimin; Liang, Zihui; He, Conghui; yao, fang; Li, Xiaoming

doi:10.1016/j.biopha.2023.114363

Cited by 5 publications

(1 citation statement)

References 38 publications

(25 reference statements)

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“…Recent evidence suggests that M1 and M2 macrophages can coexist, with changes in cellular metabolism to regulate their polarization ( Tang et al, 2023 ). An OVA-induced macrophage injury model showed the coexistence of M1 and M2 macrophages ( Wo et al, 2023 ), indicating that macrophage polarization may promote OVA-induced lung damage. We also found that knockdown of S100A8 or S100A9 inhibited lactate acid and LDHA levels.…”

Section: Discussionmentioning

confidence: 99%

S100A8/9 modulates perturbation and glycolysis of macrophages in allergic asthma mice

Ji,

Nie,

Yao

et al. 2024

PeerJ

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Background Allergic asthma is the most prevalent asthma phenotype and is associated with the disorders of immune cells and glycolysis. Macrophages are the most common type of immune cells in the lungs. Calprotectin (S100A8 and S100A9) are two pro-inflammatory molecules that target the Toll-like receptor 4 (TLR4) and are substantially increased in the serum of patients with severe asthma. This study aimed to determine the effects of S100A8/A9 on macrophage polarization and glycolysis associated with allergic asthma. Methods To better understand the roles of S100A8 and S100A9 in the pathogenesis of allergic asthma, we used ovalbumin (OVA)-induced MH-S cells, and OVA-sensitized and challenged mouse models (wild-type male BALB/c mice). Enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction, flow cytometry, hematoxylin-eosin staining, and western blotting were performed. The glycolysis inhibitor 3-bromopyruvate (3-BP) was used to observe changes in glycolysis in mice. Results We found knockdown of S100A8 or S100A9 in OVA-induced MH-S cells inhibited inflammatory cytokines, macrophage polarization biomarker expression, and pyroptosis cell proportion, but increased anti-inflammatory cytokine interleukin (IL)-10 mRNA; also, glycolysis was inhibited, as evidenced by decreased lactate and key enzyme expression; especially, knockdown of S100A8 or S100A9 inhibited the activity of TLR4/myeloid differentiation primary response gene 88 (MyD88)/Nuclear factor kappa-B (NF-κB) signaling pathway. Intervention with lipopolysaccharides (LPS) abolished the beneficial effects of S100A8 and S100A9 knockdown. The observation of OVA-sensitized and challenged mice showed that S100A8 or S100A9 knockdown promoted respiratory function, improved lung injury, and inhibited inflammation; knockdown of S100A8 or S100A9 also suppressed macrophage polarization, glycolysis levels, and activation of the TLR4/MyD88/NF-κB signaling pathway in the lung. Conversely, S100A9 overexpression exacerbated lung injury and inflammation, promoting macrophage polarization and glycolysis, which were antagonized by the glycolysis inhibitor 3-BP. Conclusion S100A8 and S100A9 play critical roles in allergic asthma pathogenesis by promoting macrophage perturbation and glycolysis through the TLR4/MyD88/NF-κB signaling pathway. Inhibition of S100A8 and S100A9 may be a potential therapeutic strategy for allergic asthma.

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Section: Discussionmentioning

confidence: 99%

S100A8/9 modulates perturbation and glycolysis of macrophages in allergic asthma mice

Ji,

Nie,

Yao

et al. 2024

PeerJ

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The role of NLRP3 inflammasome in type 2 inflammation related diseases

Xu,

Wang,

Tan

et al. 2024

Autoimmunity

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Pathogenesis and Key Cells in Allergic Rhinitis

He,

Chen,

et al. 2024

Int Arch Allergy Immunol

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Background: Allergic rhinitis (AR) is one of the most common chronic diseases worldwide, with prevalence rates as high as 50% in high-income countries. Patients with AR often have symptoms such as runny nose, itchy nose, nasal congestion, sneezing, and signs of edema and pallor of the nasal mucosa, and these pathologies have a major impact on the patient’s learning, sleep, and quality of life, often resulting in significant pain and a huge economic burden for the patient. Summary: Among the current treatments for AR, immunotherapy is able to achieve satisfactory clinical outcomes. This shows the importance of immune cells in AR. However, current therapies do not provide a complete cure for AR. The reason for this is that current research on AR focuses on the mechanism of Th1 and Th2 immune cells in AR, ignoring the role of other key cells in AR. Key Messages: Group 2 innate lymphoid cells, B cells, T cells, and macrophages can play a role in the pathogenesis of AR by producing appropriate cytokines and mediating the inflammatory response. M2 macrophages can promote Th2 cells and eosinophils in AR to enhance the type 2 inflammatory response and further promote AR.

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Human placental extract regulates polarization of macrophages via IRGM/NLRP3 in allergic rhinitis

Cited by 5 publications

References 38 publications

S100A8/9 modulates perturbation and glycolysis of macrophages in allergic asthma mice

S100A8/9 modulates perturbation and glycolysis of macrophages in allergic asthma mice

The role of NLRP3 inflammasome in type 2 inflammation related diseases

Pathogenesis and Key Cells in Allergic Rhinitis

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