scholarly journals IL35 Attenuated LPS-Induced Acute Lung Injury by Regulating Macrophage Polarization

2022 ◽  
Author(s):  
Shengsong Chen ◽  
Jingen Xia ◽  
Yi Zhang ◽  
Qingyuan Zhan
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Macrophage Polarization ◽  
Tunel Staining ◽  
M2 Macrophage ◽  
Rt Pcr ◽  
Expression Levels ◽  
M2 Macrophage Polarization ◽  
The Relationship ◽  
Masson Staining

Abstract Background Interleukin 35 (IL35) has been reported to play a role in acute lung injury (ALI); however, the current results on the relationship between IL35 and ALI are inconsistent. Therefore, we will further determine the function of IL35 in mouse ALI and its potential mechanism in this paper. Materials and Methods HE staining and Masson staining were used to evaluate lung injury in mice. Immunohistochemical staining was used to calculate the expression of IL35 p35, TLR4 and MD2 and the ratio of Bax/Bcl2 and p-P65/P65. The expression levels of IL35 EBi3, CD68, CD206 and MPO were detected by immunofluorescence staining. RT–PCR was used to examine the expression levels of IL1β and IL6. TUNEL staining was performed to detect apoptotic cells. Results Overexpression of IL35 alleviated LPS-induced acute lung injury in mice. IL35 overexpression decreased the expression of CD68 and increased the expression of CD206 in ALI mice. Furthermore, upregulation of IL35 expression obviously reduced the expression of MPO, IL1β and IL6 in lung tissues of mice with ALI. Mechanistically, IL35 suppressed the TLR4/NFκB-P65 pathway, leading to the promotion of M1 to M2 macrophage transition and inflammation relief in ALI in mice.Conclusions IL35 relieved LPS-reduced inflammation and ALI in mice by regulating M1/M2 macrophage polarization and inhibiting the activation of the TLR4/NFκB-P65 pathway.

scholarly journals IL35 Attenuated LPS-Induced Acute Lung Injury by Regulating Macrophage Polarization

2021 ◽  
Author(s):  
Shengsong Chen ◽  
Jingen Xia ◽  
Yi Zhang ◽  
Qing Yuan Zhan
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Macrophage Polarization ◽  
Tunel Staining ◽  
M2 Macrophage ◽  
Potential Mechanism ◽  
Rt Pcr ◽  
Expression Levels ◽  
The Relationship ◽  
Masson Staining

Abstract Interleukin 35 (IL35) has been reported to play a role in acute lung injury (ALI); however, the current results on the relationship between IL35 and ALI are inconsistent. Therefore, we will further determine the function of IL35 in mouse ALI and its potential mechanism in this paper. HE staining and Masson staining were used to evaluate lung injury in mice. Immunohistochemical staining was used to calculate the expression of IL35 p35, TLR4 and MD2 and the ratio of Bax/Bcl2 and p-P65/P65. The expression levels of IL35 EBi3, CD68, CD206 and MPO were detected by immunofluorescence staining. RT–PCR was used to examine the expression levels of IL1β and IL6. TUNEL staining was performed to detect apoptotic cells. Overexpression of IL35 alleviated LPS-induced acute lung injury in mice. IL35 overexpression decreased the expression of CD68 and increased the expression of CD206 in ALI mice. Furthermore, upregulation of IL35 expression obviously reduced the expression of MPO, IL1β and IL6 in lung tissues of mice with ALI. Mechanistically, IL35 suppressed the TLR4/NFκB-P65 pathway, leading to the promotion of M1 to M2 macrophage transition and inflammation relief in ALI in mice.

scholarly journals Extracellular CIRP-Impaired Rab26 Restrains EPOR-Mediated Macrophage Polarization in Acute Lung Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Wen Zhang ◽  
Yao Wang ◽  
Chuanwei Li ◽  
Yu Xu ◽  
Xia Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Rna Binding ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Molecular Pattern ◽  
Persistent Inflammation ◽  
M1 Phenotype ◽  
M2 Macrophage Polarization ◽  
Inflammation Resolution

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a condition with an imbalanced inflammatory response and delayed resolution of inflammation. Macrophage polarization plays an important role in inflammation and resolution. However, the mechanism of macrophage polarization in ALI/ARDS is not fully understood. We found that mice with lipopolysaccharide administration developed lung injury with the accumulation of extracellular cold-inducible RNA-binding protein (eCIRP) in the lungs. eCIRP, as a damage-associated molecular pattern (DAMP), inhibited M2 macrophage polarization, thereby tipping the balance toward inflammation rather than resolution. Anti-CIRP antibodies reversed such phenotypes. The levels of macrophage erythropoietin (EPO) receptor (EPOR) were reduced after eCIRP treatment. Myeloid-specific EPOR-deficient mice displayed restrained M2 macrophage polarization and impaired inflammation resolution. Mechanistically, eCIRP impaired Rab26, a member of Ras superfamilies of small G proteins, and reduced the transportation of surface EPOR, which resulted in macrophage polarization toward the M1 phenotype. Moreover, EPO treatment hardly promotes M2 polarization in Rab26 knockout (KO) macrophages through EPOR. Collectively, macrophage EPOR signaling is impaired by eCIRP through Rab26 during ALI/ARDS, leading to the restrained M2 macrophage polarization and delayed inflammation resolution. These findings identify a mechanism of persistent inflammation and a potential therapy during ALI/ARDS.

scholarly journals Protective effects of recombinant 53-kDa protein of Trichinella spiralis on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization

2021 ◽  
pp. 175342592110133
Author(s):  
Ling-yu Wei ◽  
An-qi Jiang ◽  
Ren Jiang ◽  
Si-ying Duan ◽  
Xue Xu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Trichinella Spiralis ◽  
Macrophage Polarization ◽  
Control Group ◽  
M2 Macrophage ◽  
Protective Effects ◽  
Activated Macrophages ◽  
Arginase 1 ◽  
M2 Macrophage Polarization

Trichinella spiralis represents an effective treatment for autoimmune and inflammatory diseases. The effects of recombinant T. spiralis (TS) 53-kDa protein (rTsP53) on acute lung injury (ALI) remain unclear. Here, mice were divided randomly into a control group, LPS group, and rTsP53 + LPS group. ALI was induced in BALB/c mice by LPS (10 mg/kg) injected via the tail vein. rTsP53 (200 µl; 0.4 μg/μl) was injected subcutaneously three times at an interval of 5 d before inducing ALI in the rTsP53+LPS group. Lung pathological score, the ratio and markers of classic activated macrophages (M1) and alternatively activated macrophages (M2), cytokine profiles in alveolar lavage fluid, and pyroptosis protein expression in lung tissue were investigated. RTsP53 decreased lung pathological score. Furthermore, rTsP53 suppressed inflammation by increasing IL-4, IL-10, and IL-13. There was an increase in alveolar M2 macrophage numbers, with an increase in CD206 and arginase-1-positive cells and a decrease in alveolar M1 markers such as CD197 and iNOS. In addition, the polarization of M2 macrophages induced by rTsP53 treatment could alleviate ALI by suppressing lung pyroptosis. RTsP53 was identified as a potential agent for treating LPS-induced ALI via alleviating lung pyroptosis by promoting M2 macrophage polarization.

scholarly journals Regulatory Effects of Quercetin on M1/M2 Macrophage Polarization and Oxidative/Antioxidative Balance

Nutrients ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 67
Author(s):  
Cheng-Fang Tsai ◽  
Guan-Wei Chen ◽  
Yen-Chang Chen ◽  
Ching-Kai Shen ◽  
Dah-Yuu Lu ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Glutamate Cysteine Ligase ◽  
Expression Levels ◽  
M1 Polarization ◽  
Chemokine Ligand ◽  
Endogenous Antioxidants ◽  
M2 Macrophage Polarization ◽  
Quercetin Treatment ◽  
Pro Inflammatory Cytokines

Macrophage polarization plays essential and diverse roles in most diseases, such as atherosclerosis, adipose tissue inflammation, and insulin resistance. Homeostasis dysfunction in M1/M2 macrophage polarization causes pathological conditions and inflammation. Neuroinflammation is characterized by microglial activation and the concomitant production of pro-inflammatory cytokines, leading to numerous neurodegenerative diseases and psychiatric disorders. Decreased neuroinflammation can be obtained by using natural compounds, including flavonoids, which are known to ameliorate inflammatory responses. Among flavonoids, quercetin possesses multiple pharmacological applications and regulates several biological activities. In the present study, we found that quercetin effectively inhibited the expression of lipocalin-2 in both macrophages and microglial cells stimulated by lipopolysaccharides (LPS). The production of nitric oxide (NO) and expression levels of the pro-inflammatory cytokines, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, were also attenuated by quercetin treatment. Our results also showed that quercetin significantly reduced the expression levels of the M1 markers, such as interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β, in the macrophages and microglia. The M1 polarization-associated chemokines, C–C motif chemokine ligand (CCL)-2 and C-X-C motif chemokine ligand (CXCL)-10, were also effectively reduced by the quercetin treatment. In addition, quercetin markedly reduced the production of various reactive oxygen species (ROS) in the microglia. The microglial phagocytic ability induced by the LPS was also effectively reduced by the quercetin treatment. Importantly, the quercetin increased the expression levels of the M2 marker, IL-10, and the endogenous antioxidants, heme oxygenase (HO)-1, glutamate-cysteine ligase catalytic subunit (GCLC), glutamate-cysteine ligase modifier subunit (GCLM), and NAD(P)H quinone oxidoreductase-1 (NQO1). The enhancement of the M2 markers and endogenous antioxidants by quercetin was activated by the AMP-activated protein kinase (AMPK) and Akt signaling pathways. Together, our study reported that the quercetin inhibited the effects of M1 polarization, including neuroinflammatory responses, ROS production, and phagocytosis. Moreover, the quercetin enhanced the M2 macrophage polarization and endogenous antioxidant expression in both macrophages and microglia. Our findings provide valuable information that quercetin may act as a potential drug for the treatment of diseases related to inflammatory disorders in the central nervous system.

scholarly journals M2 macrophage polarization in chronic spontaneous urticaria refractory to antihistamine treatment

2021 ◽  
Author(s):  
Roberta F.J. Criado ◽  
Paulo Ricardo Criado ◽  
Carla Pagliari ◽  
Mirian N. Sotto ◽  
Carlos D'Apparecida Machado Filho ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
Chronic Spontaneous Urticaria ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization

Nucleolin Improves Heart Function During Recovery From Myocardial Infarction by Modulating Macrophage Polarization

2021 ◽  
pp. 107424842198957
Author(s):  
Yuting Tang ◽  
Xiaofang Lin ◽  
Cheng Chen ◽  
Zhongyi Tong ◽  
Hui Sun ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Early Phase ◽  
Heart Function ◽  
Macrophage Polarization ◽  
Late Phase ◽  
Macrophage Infiltration ◽  
Enzyme Linked Immunosorbent Assay ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization ◽  
Nucleolin Expression

Background: Nucleolin has multiple functions within cell survival and proliferation pathways. Our previous studies have revealed that nucleolin can significantly reduce myocardial ischemia-reperfusion injury by promoting myocardial angiogenesis and reducing myocardial apoptosis. In this study, we attempted to determine the role of nucleolin in myocardial infarction (MI) injury recovery and the underlying mechanism. Methods: Male BALB/c mice aged 6–8 weeks were used to set up MI models by ligating the left anterior descending coronary artery. Nucleolin expression in the heart was downregulated by intramyocardial injection of a lentiviral vector expressing nucleolin-specific small interfering RNA. Macrophage infiltration and polarization were measured by real-time polymerase chain reaction, flow cytometry, and immunofluorescence. Cytokines were detected by enzyme-linked immunosorbent assay. Results: Nucleolin expression in myocardium after MI induction decreased a lot at early phase and elevated at late phase. Nucleolin knockdown impaired heart systolic and diastolic functions and decreased the survival rate after MI. Macrophage infiltration increased in the myocardium after MI. Most macrophages belonged to the M1 phenotype at early phase (2 days) and the M2 phenotype increased greatly at late phase after MI. Nucleolin knockdown in the myocardium led to a decrease in M2 macrophage polarization with no effect on macrophage infiltration after MI. Furthermore, Notch3 and STAT6, key regulators of M2 macrophage polarization, were upregulated by nucleolin in RAW 264.7 macrophages. Conclusions: Lack of nucleolin impaired heart function during recovery after MI by reducing M2 macrophage polarization. This finding probably points to a new therapeutic option for ischemic heart disease.

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