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"Dong, Yi"
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Macrophage autophagy in macrophage polarization, chronic inflammation and organ fibrosis
As the essential regulators of organ fibrosis, macrophages undergo marked phenotypic and functional changes after organ injury. These changes in macrophage phenotype and function can result in maladaptive repair, causing chronic inflammation and the development of pathological fibrosis. Autophagy, a highly conserved lysosomal degradation pathway, is one of the major players to maintain the homeostasis of macrophages through clearing protein aggregates, damaged organelles, and invading pathogens. Emerging evidence has shown that macrophage autophagy plays an essential role in macrophage polarization, chronic inflammation, and organ fibrosis. Because of the high heterogeneity of macrophages in different organs, different macrophage types may play different roles in organ fibrosis. Here, we review the current understanding of the function of macrophage autophagy in macrophage polarization, chronic inflammation, and organ fibrosis in different organs, highlight the potential role of macrophage autophagy in the treatment of fibrosis. Finally, the important unresolved issues in this field are briefly discussed. A better understanding of the mechanisms that macrophage autophagy in macrophage polarization, chronic inflammation, and organ fibrosis may contribute to developing novel therapies for chronic inflammatory diseases and organ fibrosis.
Journal Article
Air pollutant particulate matter 2.5 induces dry eye syndrome in mice
In this study, we explored the effects of particulate matter 2.5 (PM
2
.
5
) eye drops on the ocular surface structure and tear function in mice and established a novel animal model for dry eye research. We found that, following treatment with PM
2.5
, the tear volume and, the tear film break-up time showed statistical differences at each time point (P < 0.05). The FL score of the PM
2.5
-treated group was higher than that of others (P < 0.05). The average number of corneal epithelial layer cells in groups A and B was significantly lower than that in group C (P < 0.05). Scanning electron microscopy and transmission electron microscopy revealed that the number of corneal epithelial microvilli and corneal desmosomes was drastically reduced in group C. PM
2.5
induced apoptosis in the corneal superficial and basal epithelium and led to abnormal differentiation and proliferation of the ocular surface with higher expression levels of Ki67 and a reduced number of goblet cells in the conjunctival fornix in group C. PM
2.5
significantly increased the levels of TNF-α, NF-κB p65 (phospho S536), and NF-κB in the cornea. Thus, the topical administration of PM
2.5
in mice induces ocular surface changes that are similar to those of dry eye in humans, representing a novel model of dry eye.
Journal Article
حول (الاستعمار وكل الرجعيين نمور من ورق) /
يتناول كتاب (ماوتسي يونج) وهو صاحب سيرة طويلة عبر ما يقرب من سبعين عاما، نشأ في ريف الصين لأب فلاح فقير، استهوته الماركسية فانتمى إليها، ثم صار أحد نجومها في الحزب الشيوعي الصيني، ثم صار رئيسا للحزب، ثم استقل بعرش الصين وجلس عليه حوالي ثلاثين عاما، قاد فيها الصين برؤيته الخاصة فصنع منها دولة قوية في وقت وجيز، ولا يزال كتابه الأحمر مرجعا أساسيا للفكر الصيني والسياسة الصينية، بل إن دواوين شعره هي الأكثر مبيعا في الصين، ولا تزال سيرته مقصد كثير من المطلعين.
Book
Anti-Inflammatory and Immunomodulatory Effects of Paeonia Lactiflora Pall., a Traditional Chinese Herbal Medicine
In China, Korea, and Japan, a decoction of the dried root without bark of Paeonia lactiflora Pall. has been used in the treatment of rheumatoid arthritis, systemic lupus erythematosus, hepatitis, dysmenorrhea, muscle cramping and spasms, and fever for more than 1200 years. A water/ethanol extract of the root is now known as total glucosides of peony (TGP), which contains more than 15 components. Paeoniflorin is the most abundant ingredient and accounts for the pharmacological effects observed with TGP in both in vitro and in vivo studies. The analgesic effect of TGP was confirmed in various animal models of pain, which may be mediated partly by adenosine A1 receptor. The direct anti-inflammatory effects of TGP were observed in animal models of both acute and subacute inflammation, by inhibiting the production of prostaglandin E2, leukotriene B4, and nitric oxide, and by suppressing the increase of intracellular calcium ion concentration. TGP was also reported to have protective effects of cells against oxidative stress. In vitro, dual effects of TGP were noted on the proliferation of lymphocytes, differentiation of Th/Ts lymphocytes, and the production of proinflammatory cytokines and antibodies. In vivo, TGP inhibited the delayed-type hypersensitivity in immuno-activated mice, and enhanced the delayed-type hypersensitivity in immuno-suppressed mice. In adjuvant arthritis rats, paeoniflorin exerted immunosuppressive effects. The beneficial effects of TGP in treating rheumatoid arthritis were verified by randomized controlled trials. The adverse events of TGP were mainly gastrointestinal tract disturbances, mostly mild diarrhea.
Journal Article
Extracellular HSPs: The Potential Target for Human Disease Therapy
Heat shock proteins (HSPs) are highly conserved stress proteins known as molecular chaperones, which are considered to be cytoplasmic proteins with functions restricted to the intracellular compartment, such as the cytoplasm or cellular organelles. However, an increasing number of observations have shown that HSPs can also be released into the extracellular matrix and can play important roles in the modulation of inflammation and immune responses. Recent studies have demonstrated that extracellular HSPs (eHSPs) were involved in many human diseases, such as cancers, neurodegenerative diseases, and kidney diseases, which are all diseases that are closely linked to inflammation and immunity. In this review, we describe the types of eHSPs, discuss the mechanisms of eHSPs secretion, and then highlight their functions in the modulation of inflammation and immune responses. Finally, we take cancer as an example and discuss the possibility of targeting eHSPs for human disease therapy. A broader understanding of the function of eHSPs in development and progression of human disease is essential for developing new strategies to treat many human diseases that are critically related to inflammation and immunity.
Journal Article
HPV-positive status associated with inflamed immune microenvironment and improved response to anti-PD-1 therapy in head and neck squamous cell carcinoma
Chemotherapy and radiotherapy predominantly improve the clinical outcomes of patients with human papillomavirus (HPV)-related head and neck squamous cell carcinoma (HNSCC). Whether this superiority goes on when treated with immune checkpoint inhibitors is still unclear. This study sought to determine the predictive value and potential mechanisms of HPV status for the treatment of programmed cell death 1 (PD-1)/ligand 1(PD-L1) inhibitors. We conducted an integrated analysis of the relationships between HPV status and PD-L1, tumor mutation burden (TMB) and inflammation-related immune cells and molecules, based on the analysis of repository databases and resected HNSCC specimens. The pooled analysis of overall survival (OS) and objective response rate (ORR) suggested that HPV-positive patients benefited more from PD-1/PD-L1 inhibitors than HPV-negative patients (OS: hazard ratio (HR) = 0.71,
p
= 0.02; ORR: 21.9% vs 14.1%, odds ratio (OR) = 1.79,
p
= 0.01). Analysis of public databases and resected HNSCC specimens revealed that HPV status was independent of PD-L1 expression and TMB in HNSCC. However, HPV infection significantly increased T-cell infiltration, immune effector cell activation and the diversity of T-cell receptors. Notably, HPV-positivity correlated with increased immune cytolytic activity and a T-cell-inflamed gene expression profile. This work provides evidence that HPV status can be used to predict the effectiveness of PD-1 inhibitors in HNSCC, independently of PD-L1 expression and TMB, and probably results from an inflamed immune microenvironment induced by HPV infection.
Journal Article