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 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 Ginsenoside Rg3 promotes inflammation resolution through M2 macrophage polarization

2018 ◽  
Vol 42 (1) ◽  
pp. 68-74 ◽  
Author(s):  
Saeromi Kang ◽  
Soo-Jin Park ◽  
Ae-Yeon Lee ◽  
Jin Huang ◽  
Hae-Young Chung ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Ginsenoside Rg3 ◽  
M2 Macrophage Polarization ◽  
Inflammation Resolution

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
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