The spleen as a bidirectional signal transducer in acute kidney injury

Kinsey, Gilbert R.

doi:10.1016/j.kint.2017.01.004

Cited by 6 publications

(6 citation statements)

References 9 publications

(7 reference statements)

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“…It is noteworthy that the IL-6 produced in response to liver and kidney injury is a signal in the event of tissue damages [ 33–35 ]. The IL-6 produced in response to kidney damage directly causes inflammation and injury to lung tissue [ 35 ], which is consistent with the results shown in the present study. However, IL-6 activates splenocytes to produce IL-10 via α-7nAchR that is required to temper tissue injury, as reported in the study of Kinsey [ 35 ].…”

Section: Discussionsupporting

confidence: 92%

“…The IL-6 produced in response to kidney damage directly causes inflammation and injury to lung tissue [ 35 ], which is consistent with the results shown in the present study. However, IL-6 activates splenocytes to produce IL-10 via α-7nAchR that is required to temper tissue injury, as reported in the study of Kinsey [ 35 ]. The γ-irradiation microenvironment could direct the persistent activation of the IL-6 in tissues and systemic pro-inflammatory mediators (TNF-α and IL-1β) to be detrimental rather than beneficial, as manifested by the down-regulation of splenic α-7nAchR and IL-10 levels as observed in the present study.…”

Section: Discussionsupporting

confidence: 92%

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Fucoxanthin alters the apelin-13/APJ pathway in certain organs of γ-irradiated mice

Bakary

Thabet

Fatih

et al. 2021

Journal of Radiation Research

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Apelin-13 and APJ are implicated in different key physiological processes. This work aims at exploring the radioprotective effect of fucoxanthin (FX) on γ-radiation (RAD)-induced changes in the apelin-13/APJ pathway, which causes damage in the liver, kidney, lung and spleen of mice. Mice were administered FX (10 mg kg–1 day–1, i.p) and exposed to γ-radiation (2.5 Gy week–1) for four consecutive weeks. The treatment of irradiated mice by FX resulted in a significant amendment in protein expression of the apelin-13/APJ/NF-κB signalling pathway concurrently with reduced hypoxia (hypoxia-inducible factor-1α), suppressed oxidative stress marker (malondialdehyde), enhanced antioxidant defence mechanisms (reduced glutathione and glutathione peroxidase), a modulated inflammatory response [interleukin-6 (IL-6), monocyte chemoattractant protein-1, IL-10 and α-7-nicotinic acetylcholine receptor) and ameliorated angiogenic regulators [matrix metalloproteinase (MMP-2), MMP-9 and tissue inhibitor of metalloproteinase-1), as well as the tissue damage indicator (lactate dehydrogenase) in organ tissues. In addition, there were significant improvement in serum inflammatory markers tumour necrosis factor-α, IL-10, IL-1β and C-reactive protein compared with irradiated mice. The histopathological investigation of the FX + RAD organ tissues support the biochemical findings where the improvements in the tissues’ architecture were obvious when compared with those of RAD. FX was thus shown to have a noticeable radioprotective action mediated through its regulatory effect on the apelin-13/APJ/NF-κB signalling pathway attributed to its antioxidant and anti-inflammatory activity that was reflected in different physiological processes. It could be recommended to use FX in cases of radiation exposure to protect normal tissues.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 92%

Fucoxanthin alters the apelin-13/APJ pathway in certain organs of γ-irradiated mice

Bakary

Thabet

Fatih

et al. 2021

Journal of Radiation Research

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“…35 Furthermore, the spleen coordinates interleukin (IL)-6-dependent IL-10 production, which reduces lung injury during experimental acute kidney injury (AKI). 36 Splenic factors also exacerbate severe acute pancreatitis (SAP)associated lung injury. 30 In animal experiments, the splenectomy model can be used as an auxiliary method to distinguish high and low inflammatory subtypes.…”

Section: Discussionmentioning

confidence: 99%

“…The spleen is necessary for the recruitment of classical monocytes and neutrophil extravasation into the injured lungs, 34 and it can play an important role in intestinal ischemia–reperfusion (IIR)‐induced ALI 35 . Furthermore, the spleen coordinates interleukin (IL)‐6‐dependent IL‐10 production, which reduces lung injury during experimental acute kidney injury (AKI) 36 . Splenic factors also exacerbate severe acute pancreatitis (SAP)‐associated lung injury 30 …”

Section: Discussionmentioning

confidence: 99%

Exploring the metabolic phenotypes associated with different host inflammation of acute respiratory distress syndrome (ARDS) from lung metabolomics in mice

Zhu

Lei

et al. 2020

Rapid Comm Mass Spectrometry

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Rationale The aim of this study was to analyze the metabolomics of lung with different host inflammation of acute respiratory distress syndrome (ARDS) for the identification of biomarkers for predicting severity under different inflammatory conditions. Methods Cecal ligation and puncture (CLP) and lipopolysaccharide (LPS)‐intratracheal injection induced acute lung injury (ALI) were used. A mouse model was used to explore lung metabolomic biomarkers in ALI/ARDS. The splenectomy model was used as an auxiliary method to distinguish between hyper‐ and hypo‐inflammatory subtypes. Plasma, lung tissue and bronchoalveolar lavage fluid (BALF) samples were collected from mice after CLP/LPS. The severity of lung injury was evaluated. Expression of tumor necrosis factor‐α (TNF‐α) in mice serum and lung was tested by enzyme‐linked immunosorbent assay (ELISA) and polymer chain reaction (PCR). Polymorphonuclear cells in BALF were counted. The lung metabolites were detected by gas chromatography/mass spectrometry (GC/MS), and the metabolic pathways predicted using the KEGG database. Results The LPS/CLP‐Splen group had more severe lung injury than the corresponding ALI group; that in the CLP‐Splen group was more serious than in the LPS‐Splen group. TNF‐α expression was significantly elevated in the serum and lung tissue after LPS or CLP, and higher in the LPS/CLP‐Splen group than in the corresponding ALI group. The level of TNF‐α in the CLP‐Splen group was elevated significantly over that in the LPS‐Splen group. Both these groups also showed significant neutrophil exudation within the lungs. During differential inflammation, more differential metabolites were detected in the lungs of the CLP group ALI mice than in the LPS group. A total of 41 compounds were detected in the lungs of the CLP and CLP‐Splen groups. Contrastingly, eight compounds were detected in the lungs of the LPS and LPS‐Splen groups. The LPS‐Splen and CLP‐Splen groups had significant neutrophil exudation in the lung. Random forest analysis of lung‐targeted metabolomics data indicated 4‐hydroxyphenylacetic acid, 1‐aminocyclopentanecarboxylic acid (ACPC), cis‐aconitic acid, and hydroxybenzoic acid as strong predictors of the hyper‐inflammatory subgroup in the CLP group. Furthermore, with splenectomy, 13 differential metabolic pathways between the CLP and LPS groups were revealed. Conclusions Hyper‐inflammatory subgroups of ARDS have a greater inflammatory response and a more active lung metabolism. Combined with the host inflammation background, biomarkers from metabolomics could help evaluate the response severity of ARDS.

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“…Spleen is involved in many diseases, including thrombosis, diabetes, lipid metabolism, malaria, acute kidney injury, sepsis, ischemic cardiomyopathy, and neuron immune disease. [4][5][6][7][8][9] The role of spleen in tumor progression is complex and uncertain. Tuftsin is a spleen-derived peptide, exhibiting obvious antitumor effect.…”

Section: Introductionmentioning

confidence: 99%

Spleen-Derived CCL9 Recruits MDSC to Facilitate Tumor Growth in Orthotopic Hepatoma Mice

Li,

Liang

et al. 2023

Glob Med Genet

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Objectives Spleen is involved in multiple diseases, the role of the spleen and spleen-derived factors in hepatocellular carcinoma (HCC) is still not clarified. Methods In the current study, a murine H22 orthotopic hepatoma model was established. Three groups were divided: normal mice, tumor-bearing mice with spleen-preserving, and tumor-bearing mice with splenectomy. Spleen and tumor weights were recorded by weeks 1 and 2. The proportion of myeloid-derived suppressor cell (MDSC) in peripheral blood and tumor tissue was detected using flow cytometry. Protein chip assay was used to compare the differential cytokines between normal liver supernatant and tumor supernatant. The common upregulated cytokines both in spleen and tumor were focused and analyzed using gene expression profiling interactive analysis (GEPIA) database. Enzyme-linked immunosorbent assay was performed to verify the chip result, and to examine CCL9 expression before and after splenectomy. Spleen MDSC was sorted using flow cytometry, and chemotaxis assay was performed to demonstrate whether CCL9 attracted spleen MDSC. Results The spleen enlarged during tumor progression, and compared with splenectomy group, there were faster tumor growth, shorter survival time, and higher proportions of MDSC in spleen-preserving group. Protein chip assay and GEPIA database revealed CCL9 was the most promising chemokine involved in HCC upregulated both in spleen and tumor tissue. CCL9 attracted MDSC in vitro, the level of CCL9 in tumor tissue was downregulated, and the percentage of MDSC was decreased after splenectomy. Conclusion The results demonstrate that CCL9 may be derived from spleen; it facilitated HCC growth via the chemotaxis of MDSC, targeting CCL9 may be a promising strategy in HCC treatment.

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The spleen as a bidirectional signal transducer in acute kidney injury

Cited by 6 publications

References 9 publications

Fucoxanthin alters the apelin-13/APJ pathway in certain organs of γ-irradiated mice

Fucoxanthin alters the apelin-13/APJ pathway in certain organs of γ-irradiated mice

Exploring the metabolic phenotypes associated with different host inflammation of acute respiratory distress syndrome (ARDS) from lung metabolomics in mice

Spleen-Derived CCL9 Recruits MDSC to Facilitate Tumor Growth in Orthotopic Hepatoma Mice

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