scholarly journals Diet-induced obese mice exhibit altered immune responses to acute lung injury induced byEscherichia coli

Obesity ◽  
2016 ◽  
Vol 24 (10) ◽  
pp. 2101-2110 ◽  
Author(s):  
Taomei Wan ◽  
Guiqiang Yuan ◽  
Yi Ren ◽  
Zhicai Zuo ◽  
Zhengyi Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Immune Responses ◽  
Obese Mice ◽  
Byescherichia Coli

scholarly journals The Modulatory Activity of Tryptophan Displaying Nanodevices on Macrophage Activation for Preventing Acute Lung Injury

2021 ◽  
Vol 12 ◽  
Author(s):  
Liya Sun ◽  
Rui Wang ◽  
Chenchen Wu ◽  
Jiameng Gong ◽  
Huiqiang Ma ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Immune Responses ◽  
Therapeutic Strategy ◽  
Inflammatory Responses ◽  
Negative Regulator ◽  
Tlr Signaling ◽  
Immunomodulatory Agents ◽  
Inflammatory Conditions ◽  
Endosomal Acidification

Macrophages play an important role in the initiation, progression and resolution of inflammation in many human diseases. Effective regulation of their activation and immune responses could be a promising therapeutic strategy to manage various inflammatory conditions. Nanodevices that naturally target macrophages are ideal agents to regulate immune responses of macrophages. Here we described a special tryptophan (Trp)-containing hexapeptide-coated gold nanoparticle hybrid, PW, which had unique immunomodulatory activities on macrophages. The Trp residues enabled PW higher affinity to cell membranes, and contributed to inducing mild pro-inflammatory responses of NF-κB/AP-1 activation. However, in the presence of TLR stimuli, PW exhibited potent anti-inflammatory activities through inhibiting multiple TLR signaling pathways. Mechanistically, PW was internalized primarily through micropinocytosis pathway into macrophages and attenuated the endosomal acidification process, and hence preferentially affected the endosomal TLR signaling. Interestingly, PW could induce the expression of the TLR negative regulator IRAK-M, which may also contribute to the observed TLR inhibitory activities. In two acute lung injury (ALI) mouse models, PW could effectively ameliorate lung inflammation and protect lung from injuries. This work demonstrated that nanodevices with thoughtful design could serve as novel immunomodulatory agents to manage the dysregulated inflammatory responses for treating many chronic and acute inflammatory conditions, such as ALI.

PI3K-γ Inhibition Ameliorates Acute Lung Injury Through Regulation of IκBα/NF-κB Pathway and Innate Immune Responses

2011 ◽  
Vol 32 (2) ◽  
pp. 340-351 ◽  
Author(s):  
Dong Im Kim ◽  
So Ri Kim ◽  
Hee Jung Kim ◽  
Su Jeong Lee ◽  
Heung Bum Lee ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Immune Responses ◽  
Innate Immune ◽  
Innate Immune Responses

scholarly journals RAGE-induced ILC2 expansion in acute lung injury due to haemorrhagic shock

Thorax ◽  
2020 ◽  
Vol 75 (3) ◽  
pp. 209-219 ◽  
Author(s):  
Kai Zhang ◽  
Yue Jin ◽  
Dengming Lai ◽  
Jieyan Wang ◽  
Yang Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Immune Responses ◽  
Immune Dysfunction ◽  
Underlying Mechanism ◽  
Haemorrhagic Shock ◽  
Lymphoid Cells ◽  
Eosinophil Infiltration

BackgroundType 2 immune dysfunction contributes to acute lung injury and lethality following haemorrhagic shock (HS) and trauma. Group 2 innate lymphoid cells (ILC2s) play a significant role in the regulation of type 2 immune responses. However, the role of ILC2 in post-HS acute lung injury and the underlying mechanism has not yet been elucidated.ObjectiveTo investigate the regulatory role of ILC2s in HS-induced acute lung injury and the underlying mechanism in patients and animal model.MethodsCirculating markers of type 2 immune responses in patients with HS and healthy controls were characterised. Using a murine model of HS, the role of high-mobility group box 1 (HMGB1)-receptor for advanced glycation end products (RAGE) signalling in regulation of ILC2 proliferation, survival and function was determined. And the role of ILC2 in inducing type 2 immune dysfunction was assessed as well.ResultsThe number of ILC2s was significantly increased in the circulation of patients with HS that was correlated with the increase in the markers of type 2 immune responses in the patients. Animal studies showed that HMGB1 acted via RAGE to induce ILC2 accumulation in the lungs by promoting ILC2 proliferation and decreasing ILC2 death. The expansion of ILC2s resulted in type 2 cytokines secretion and eosinophil infiltration in the lungs, both of which contributed to lung injury after HS.ConclusionsThese results indicate that HMGB1-RAGE signalling plays a critical role in regulating ILC2 biological function that aggravates type 2 lung inflammation following HS.

scholarly journals PTEN–Foxo1 signaling triggers HMGB1-mediated innate immune responses in acute lung injury

2015 ◽  
Vol 62 (1) ◽  
pp. 95-105 ◽  
Author(s):  
Min Zhou ◽  
Yadi Zhang ◽  
Xulin Chen ◽  
Jianjun Zhu ◽  
Min Du ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Immune Responses ◽  
Innate Immune ◽  
Innate Immune Responses
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