Instilled air promotes lipopolysaccharide-induced acute lung injury

Zou, Yinggang; Dong, Chunling; Mingzhen, Yuan; Gao, Guangyuan; Wang, Siyi; Liu, Xiaoding; Han, Huiqiao; Li, Bo

doi:10.3892/etm.2014.1523

Cited by 9 publications

(6 citation statements)

References 26 publications

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“…Supporting our hypothesis that TXA 2 production may be responsible for edema in ALI, PGE 2 but not TXB 2 was detected in these lungs. In contrast to our observations, previous reports showed that LPS challenge induces edema in mouse lung 27 28 29 . We also previously showed that the LPS instillation caused lung hyper-permeability 16 .…”

Section: Discussioncontrasting

confidence: 99%

Thromboxane A2 exacerbates acute lung injury via promoting edema formation

Kobayashi

Horikami

Omori

et al. 2016

Sci Rep

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Thromboxane A2 (TXA2) is produced in the lungs of patients suffering from acute lung injury (ALI). We assessed its contribution in disease progression using three different ALI mouse models. The administration of hydrochloric acid (HCl) or oleic acid (OA)+ lipopolysaccharide (LPS) caused tissue edema and neutrophil infiltration with TXA2 production in the lungs of the experimental mice. The administration of LPS induced only neutrophil accumulation without TXA2 production. Pretreatment with T prostanoid receptor (TP) antagonist attenuated the tissue edema but not neutrophil infiltration in these models. Intravital imaging and immunostaining demonstrated that administration of TP agonist caused vascular hyper-permeability by disrupting the endothelial barrier formation in the mouse ear. In vitro experiments showed that TP-stimulation disrupted the endothelial adherens junction, and it was inhibited by Ca2+ channel blockade or Rho kinase inhibition. Thus endogenous TXA2 exacerbates ALI, and its blockade attenuates it by modulating the extent of lung edema. This can be explained by the endothelial hyper-permeability caused by the activation of TXA2-TP axis, via Ca2+- and Rho kinase-dependent signaling.

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Section: Discussioncontrasting

confidence: 99%

Thromboxane A2 exacerbates acute lung injury via promoting edema formation

Kobayashi

Horikami

Omori

et al. 2016

Sci Rep

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“…The influence of gut microbiota on lung immunity has been vastly explored and several studies have linked changes in the gut microbiome with lung diseases (10,11). For example, gut flora is responsible for inducing lung inflammatory reaction against bacterial challenge and enhancing neutrophils infiltration through TLR4 in mice (12,13). Antibiotic treatment can cause overgrowth of particular fungal species in the gut and promote allergic airway inflammation via fungi-induced prostaglandin E2 (14).…”

Section: Introductionmentioning

confidence: 99%

Alteration of Gut Microbiome in Lung Cancer Patients

Fang

Chen

et al. 2019

Preprint

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Lung cancer is the leading cause of cancer death. Better 24 understanding of factors and pathways involved in lung cancer is needed to improve 25 diagnose and treatment strategies. Recent studies have provided insights into the 26 possible correlation between intestinal dysbiosis and cancer development. Although 27 the immunological relationship between gut and lung had been suggested by many 28 researches, however, to date, no study had investigated the characterization of gut 29 microbiome in treatment naïve lung cancer patients, whether it is distinct from that of 30 health individuals and contribute to the onset and development of lung cancer remain 31 unclear. In this study, we investigated whether gut microbiome of lung cancer patients 32 (LC, n=28) is altered compare with that of matched healthy individuals (HC, n=19) by 33 high throughout sequencing of the V3-V4 regions of 16S rDNA in their fecal samples. 34 We also identified microbiota signatures specific for different histological types of 35 lung cancer, including SSC, ADC, and SCLC. The gut microbiome of lung cancer 36 patients is characterized by decreased relative abundance of Prevotella, and increased 37 bacteria groups such as Actinomyces, and Streptococcus, etc. We also detected a mild 38 structural shift in gut microbiome between ADC and SCLC patients. Our results 39 showed that the gut microbiome of lung cancer patients altered significantly 40 compared with healthy individuals. However, the association between microbial 41 dysbiosis and lung cancer is not clearly understood, future studies involving larger 42 cohorts and metagenomics, or metabolomics, may elucidate the correlations between 43 gut microbiota and lung cancer development. 44 IMPORTANCE This is the first report to show the alteration of gut microbiome in 45 4 lung cancer patients. Our results showed that the gut microbiome of lung cancer 46 patients altered significantly compared with healthy individuals. 47 48

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“…34 The histopathological analysis in the present study showed alveolar structure destruction, edema of the alveolar wall, massive inflammatory cell infiltration, and increased concentration of MPO, a marker for neutrophils, in the LPS group, which is consistent with a previous study. 35,36 Thus, we believe that we successfully established ALI with an intratracheal instillation of LPS. However, our results with the SB pretreatment showed that the destruction of the lung tissue and the number of infiltrating inflammatory cells could be significantly alleviated in the LSB group compared to the LPS group, as proven in a previous study.…”

Section: ■ Discussionmentioning

confidence: 94%

Sodium Butyrate Inhibits the Inflammation of Lipopolysaccharide-Induced Acute Lung Injury in Mice by Regulating the Toll-Like Receptor 4/Nuclear Factor κB Signaling Pathway

Liu

Chang

Huang

et al. 2019

J. Agric. Food Chem.

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Bacterial pneumonia is a common disease in dairy herds worldwide, which brings great economic losses to farmers. Sodium butyrate (SB), an inhibitor of histone deacetylase, plays an important role in limiting inflammation. The purpose of this study was to investigate the protective effects of SB on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and explore the potential mechanism of SB protection. A total of 30 ICR mice were randomly divided into three groups (n = 10): a phosphate-buffered saline (PBS) intratracheal instillation group, a LPS intratracheal instillation group, and a SB gavage group (SB was given 1 h before the LPS stimulation). After 12 h, samples of the blood and lung tissue were collected from the mice for experimental analysis. The results showed that the concentration of inflammatory cytokines [interleukin 1β (IL1β) and tumor necrosis factor α (TNF-α)], myeloperoxidase (MPO) activity in the lung tissue and blood, protein abundance of toll-like receptor 4 (TLR4), nuclear factor κB (NF-κB, p65), phosphorylated p65 (p-p65), inhibitor κBα (IκBα), and phosphorylated IκBα (p-IκBα), and relative mRNA expression of genes associated with inflammation, such as TLR4, NF-κB, IL1β, interleukin 6 (IL6), and TNF-α, were significantly upregulated in the LPS group compared to the PBS group. However, the SB addition markedly downregulated the levels of these parameters in the LSB group compared to those in the LPS group. Furthermore, the structure of the lung tissue from the LPS group was severely disrupted in comparison to that of the PBS group. However, with SB administration, the severe structural disruption was relieved. In addition, an immunohistochemical analysis showed that positive immunoreactions to TLR4, p65, and TNF-α were significant in the LPS group; however, SB addition markedly attenuated this phenomenon. In conclusion, the ALI mouse model was successfully established with an intratracheal instillation of LPS. Furthermore, gavage with SB inhibited inflammation in LPS-induced ALI.

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Instilled air promotes lipopolysaccharide-induced acute lung injury

Cited by 9 publications

References 26 publications

Thromboxane A2 exacerbates acute lung injury via promoting edema formation

Thromboxane A2 exacerbates acute lung injury via promoting edema formation

Alteration of Gut Microbiome in Lung Cancer Patients

Sodium Butyrate Inhibits the Inflammation of Lipopolysaccharide-Induced Acute Lung Injury in Mice by Regulating the Toll-Like Receptor 4/Nuclear Factor κB Signaling Pathway

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