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Article: Peitu Shengjin Recipe Attenuates Airway Inflammation via the TLR4/NF-kB Signaling Pathway on Chronic Obstructive Pulmonary Disease.

Hu, Xuzhen / Hong, Bo / Sun, Minghuan

Evidence-based complementary and alternative medicine : eCAM

2022 Volume 2022, Page(s) 2090478

Abstract: Background: Chronic obstructive pulmonary disease (COPD) is a common respiratory disease, but there is no specific medicine for COPD. In this study, we aimed to evaluate the effects of Peitu Shengjin Recipe (PSR) and Biostime Probiotic Powder on COPD ... ...

Abstract	Background: Chronic obstructive pulmonary disease (COPD) is a common respiratory disease, but there is no specific medicine for COPD. In this study, we aimed to evaluate the effects of Peitu Shengjin Recipe (PSR) and Biostime Probiotic Powder on COPD rats. Methods: UPLC-Q/TOF-MS was used to detect the chemical constituents in PSR. The COPD rat model was established by cigarette smoke combined with tracheal injection of lipopolysaccharide. We assessed lung function by calculating FEV Results: There were 53 ESI Conclusion: Our findings suggest that PSR and Biostime Probiotic Powder have protective effects on COPD rats, which may be achieved by modulating the TLR4/NF-kB signaling pathway.
Language	English
Publishing date	2022-08-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2171158-6
ISSN	1741-4288 ; 1741-427X
ISSN (online)	1741-4288
ISSN	1741-427X
DOI	10.1155/2022/2090478
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Article ; Online: BAM15 treats mouse sepsis and kidney injury, linking mortality, mitochondrial DNA, tubule damage, and neutrophils.

Tsuji, Naoko / Tsuji, Takayuki / Yamashita, Tetsushi / Hayase, Naoki / Hu, Xuzhen / Yuen, Peter St / Star, Robert A

The Journal of clinical investigation

2023 Volume 133, Issue 7

Abstract: Sepsis pathogenesis is complex and heterogeneous; hence, a precision-medicine strategy is needed. Acute kidney injury (AKI) following sepsis portends higher mortality. Overproduction of mitochondrial ROS (mtROS) is a potential mediator of sepsis and ... ...

Abstract	Sepsis pathogenesis is complex and heterogeneous; hence, a precision-medicine strategy is needed. Acute kidney injury (AKI) following sepsis portends higher mortality. Overproduction of mitochondrial ROS (mtROS) is a potential mediator of sepsis and sepsis-induced AKI. BAM15, a chemical uncoupler, dissipates mitochondrial proton gradients without generating mtROS. We injected BAM15 into mice at 0, 6, or 12 hours after cecal ligation and puncture (CLP), and these mice were treated with fluids and antibiotics. BAM15 reduced mortality, even after 12 hours, when mice were ill, and BAM15 reduced kidney damage and splenic apoptosis. Serial plasma and urinary mitochondrial DNA (mtDNA) levels increased after CLP and decreased after BAM15 administration (at 0 or 6 hours). In vitro septic serum proportionately increased mtROS overproduction and mtDNA release from kidney tubule cells, which BAM15 prevented. BAM15 decreased neutrophil apoptosis and mtDNA release; neutrophil depletion counteracted BAM15 benefits. Further, mtDNA injection in vivo replicated inflammation and kidney injury, which was prevented by BAM15. A large dose of exogenous mtDNA reversed protection by BAM15. We conclude that BAM15 is an effective preventive and therapeutic candidate in experimental sepsis and that BAM15 and mtDNA, a potential drug-companion diagnostic/drug-efficacy pair for clinical sepsis, are mechanistically linked via mtROS.
MeSH term(s)	Mice ; Animals ; DNA, Mitochondrial/genetics ; Neutrophils/pathology ; Kidney/pathology ; Acute Kidney Injury/pathology ; Sepsis/genetics ; Mice, Inbred C57BL
Chemical Substances	DNA, Mitochondrial
Language	English
Publishing date	2023-04-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI152401
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Article: Macrophage Depletion Protects Against Cisplatin-Induced Ototoxicity and Nephrotoxicity.

Sung, Cathy Yea Won / Hayase, Naoki / Yuen, Peter S T / Lee, John / Fernandez, Katharine / Hu, Xuzhen / Cheng, Hui / Star, Robert A / Warchol, Mark E / Cunningham, Lisa L

bioRxiv : the preprint server for biology

2023

Abstract: Cisplatin is a widely used and highly effective anti-cancer drug with significant side effects including ototoxicity and nephrotoxicity. Macrophages, the major resident immune cells in the cochlea and kidney, are important drivers of both inflammatory ... ...

Abstract	Cisplatin is a widely used and highly effective anti-cancer drug with significant side effects including ototoxicity and nephrotoxicity. Macrophages, the major resident immune cells in the cochlea and kidney, are important drivers of both inflammatory and tissue repair responses. To investigate the roles of macrophages in cisplatin-induced ototoxicity and nephrotoxicity, we used PLX3397, an FDA-approved inhibitor of the colony-stimulating factor 1 receptor (CSF1R), to eliminate tissue-resident macrophages during the course of cisplatin administration. Mice treated with cisplatin alone (cisplatin/vehicle) had significant hearing loss (ototoxicity) as well as kidney injury (nephrotoxicity). Macrophage ablation using PLX3397 resulted in significantly reduced hearing loss measured by auditory brainstem responses (ABR) and distortion-product otoacoustic emissions (DPOAE). Sensory hair cells in the cochlea were protected against cisplatin-induced death in mice treated with PLX3397. Macrophage ablation also protected against cisplatin-induced nephrotoxicity, as evidenced by markedly reduced tubular injury and fibrosis as well as reduced plasma blood urea nitrogen (BUN) and neutrophil gelatinase-associated lipocalin (NGAL) levels. Mechanistically, our data suggest that the protective effect of macrophage ablation against cisplatin-induced ototoxicity and nephrotoxicity is mediated by reduced platinum accumulation in both the inner ear and the kidney. Together our data indicate that ablation of tissue-resident macrophages represents a novel strategy for mitigating cisplatin-induced ototoxicity and nephrotoxicity.
Language	English
Publishing date	2023-11-17
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.11.16.567274
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Article ; Online: Erratum for Baranova et al., "Class B Scavenger Receptors BI and BII Protect against LPS-Induced Acute Lung Injury in Mice by Mediating LPS Clearance".

Baranova, Irina N / Bocharov, Alexander V / Vishnyakova, Tatyana G / Chen, Zhigang / Birukova, Anna A / Ke, Yunbo / Hu, Xuzhen / Yuen, Peter S T / Star, Robert A / Birukov, Konstantin G / Patterson, Amy P / Eggerman, Thomas L

Infection and immunity

2022 Volume 90, Issue 10, Page(s) e0040422

Language	English
Publishing date	2022-09-27
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/iai.00404-22
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Article ; Online: Class B Scavenger Receptors BI and BII Protect against LPS-Induced Acute Lung Injury in Mice by Mediating LPS.

Infection and immunity

2021 Volume 89, Issue 10, Page(s) e0030121

Abstract: Recent studies suggest an anti-inflammatory protective role for class B scavenger receptor BI (SR-BI) in endotoxin-induced inflammation and sepsis. Other data, including ours, provide evidence for an alternative role of SR-BI, facilitating bacterial and ... ...

Abstract	Recent studies suggest an anti-inflammatory protective role for class B scavenger receptor BI (SR-BI) in endotoxin-induced inflammation and sepsis. Other data, including ours, provide evidence for an alternative role of SR-BI, facilitating bacterial and endotoxin uptake and contributing to inflammation and bacterial infection. Enhanced endotoxin susceptibility of SR-BI-deficient mice due to their anti-inflammatory glucocorticoid deficiency complicates the understanding of SR-BI's role in endotoxemia/sepsis, calling for the use of alternative models. In this study, using human SR-BI (hSR-BI) and hSR-BII transgenic mice, we found that SR-BI and, to a lesser extent, its splicing variant SR-BII protect against LPS-induced lung damage. At 20 h after intratracheal LPS instillation, the extent of pulmonary inflammation and vascular leakage was significantly lower in hSR-BI and hSR-BII transgenic mice than in wild-type mice. Higher bronchoalveolar lavage fluid (BALF) inflammatory cell count and protein content and lung tissue neutrophil infiltration found in wild-type mice were associated with markedly (2 to 3 times) increased proinflammatory cytokine production compared to these parameters in transgenic mice following LPS administration. The markedly lower endotoxin levels detected in BALF of transgenic versus wild-type mice and the significantly increased BODIPY-LPS uptake observed in lungs of hSR-BI and hSR-BII mice 20 h after the i.t. LPS injection suggest that hSR-BI- and hSR-BII-mediated enhanced LPS clearance in the airways could represent the mechanism of their protective role against LPS-induced acute lung injury.
MeSH term(s)	A549 Cells ; Acute Lung Injury/chemically induced ; Acute Lung Injury/metabolism ; Animals ; Bronchoalveolar Lavage Fluid ; Cell Line, Tumor ; Cytokines/metabolism ; Disease Models, Animal ; Endotoxemia/metabolism ; Humans ; Inflammation/immunology ; Lipopolysaccharides/pharmacology ; Lysosomal Membrane Proteins/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neutrophils/metabolism ; Receptors, Scavenger/metabolism ; Scavenger Receptors, Class B/metabolism ; Sepsis/metabolism
Chemical Substances	Cytokines ; Lipopolysaccharides ; Lysosomal Membrane Proteins ; Receptors, Scavenger ; SCARB1 protein, human ; SCARB2 protein, human ; Scarb1 protein, mouse ; Scavenger Receptors, Class B
Language	English
Publishing date	2021-06-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.00301-21
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Article ; Online: The role of adenosine 1a receptor signaling on GFR early after the induction of sepsis.

Street, Jonathan M / Koritzinsky, Erik H / Bellomo, Tiffany R / Hu, Xuzhen / Yuen, Peter S T / Star, Robert A

American journal of physiology. Renal physiology

2017 Volume 314, Issue 5, Page(s) F788–F797

Abstract: Sepsis and acute kidney injury (AKI) synergistically increase morbidity and mortality in the ICU. How sepsis reduces glomerular filtration rate (GFR) and causes AKI is poorly understood; one proposed mechanism includes tubuloglomerular feedback (TGF). ... ...

Abstract	Sepsis and acute kidney injury (AKI) synergistically increase morbidity and mortality in the ICU. How sepsis reduces glomerular filtration rate (GFR) and causes AKI is poorly understood; one proposed mechanism includes tubuloglomerular feedback (TGF). When sodium reabsorption by the proximal tubules is reduced in normal animals, the macula densa senses increased luminal sodium chloride, and then adenosine-1a receptor (A1aR) signaling triggers tubuloglomerular feedback, reducing GFR through afferent arteriole vasoconstriction. We measured GFR and systemic hemodynamics early during cecal ligation and puncture-induced sepsis in wild-type and A1aR-knockout mice. A miniaturized fluorometer was attached to the back of each mouse and recorded the clearance of FITC-sinistrin via transcutaneous fluorescence to monitor GFR. Clinical organ injury markers and cytokines were measured and hemodynamics monitored using implantable transducer telemetry devices. In wild-type mice, GFR was stable within 1 h after surgery, declined by 43% in the next hour, and then fell to less than 10% of baseline after 2 h and 45 min. In contrast, in A1aR-knockout mice GFR was 37% below baseline immediately after surgery and then gradually declined over 4 h. A1aR-knockout mice had similar organ injury and inflammatory responses, albeit with lower heart rate. We conclude that transcutaneous fluorescence can accurately monitor GFR and detect changes rapidly during sepsis. Tubuloglomerular feedback plays a complex role in sepsis; initially, TGF helps maintain GFR in the 1st hour, and over the subsequent 3 h, TGF causes GFR to plummet. By 18 h, TGF has no cumulative effect on renal or extrarenal organ damage.
MeSH term(s)	Acute Kidney Injury/etiology ; Acute Kidney Injury/genetics ; Acute Kidney Injury/metabolism ; Acute Kidney Injury/physiopathology ; Animals ; Disease Models, Animal ; Feedback, Physiological ; Fluoresceins/administration & dosage ; Fluorescent Dyes/administration & dosage ; Fluorescent Dyes/metabolism ; Fluorometry/methods ; Glomerular Filtration Rate ; Hemodynamics ; Injections, Intravenous ; Kidney/metabolism ; Kidney/physiopathology ; Mice, Inbred C57BL ; Mice, Knockout ; Oligosaccharides/administration & dosage ; Oligosaccharides/blood ; Receptor, Adenosine A1/deficiency ; Receptor, Adenosine A1/genetics ; Receptor, Adenosine A1/metabolism ; Sepsis/complications ; Sepsis/genetics ; Sepsis/metabolism ; Sepsis/physiopathology ; Signal Transduction ; Time Factors
Chemical Substances	Fluoresceins ; Fluorescent Dyes ; Oligosaccharides ; Receptor, Adenosine A1 ; fluorescein-isothiocyanate sinistrin
Language	English
Publishing date	2017-11-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00051.2017
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Article: Automated quantification of renal fibrosis with Sirius Red and polarization contrast microscopy.

Street, Jonathan M / Souza, Ana Carolina P / Alvarez-Prats, Alejandro / Horino, Taro / Hu, Xuzhen / Yuen, Peter S T / Star, Robert A

Physiological reports

2014 Volume 2, Issue 7

Abstract: Interstitial fibrosis is commonly measured by histology. The Masson trichrome stain is widely used, with semiquantitative scores subjectively assigned by trained operators. We have developed an objective technique combining Sirius Red staining, ... ...

Abstract	Interstitial fibrosis is commonly measured by histology. The Masson trichrome stain is widely used, with semiquantitative scores subjectively assigned by trained operators. We have developed an objective technique combining Sirius Red staining, polarization contrast microscopy, and automated analysis. Repeated analysis of the same sections by the same operator (r = 0.99) or by different operators (r = 0.98) was highly consistent for Sirius Red, while Masson trichrome performed less consistently (r = 0.61 and 0.72, respectively). These techniques performed equally well when comparing sections from the left and right kidneys of mice. Poor correlation between Sirius Red and Masson trichrome may reflect different specificities, as enhanced birefringence with Sirius Red staining is specific for collagen type I and III fibrils. Combining whole-section imaging and automated image analysis with Sirius Red/polarization contrast is a rapid, reproducible, and precise technique that is complementary to Masson trichrome. It also prevents biased selection of fields as fibrosis is measured on the entire kidney section. This new tool shall enhance our search for novel therapeutics and noninvasive biomarkers for fibrosis.
Language	English
Publishing date	2014-07-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2724325-4
ISSN	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.12088
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Article: alpha-Melanocyte-simulating hormone and interleukin-10 do not protect the kidney against mercuric chloride-induced injury.

Miyaji, Takehiko / Hu, Xuzhen / Star, Robert A

American journal of physiology. Renal physiology

2002 Volume 282, Issue 5, Page(s) F795–801

Abstract: The anti-inflammatory cytokines alpha-melanocyte-stimulating hormone (MSH) and interleukin (IL)-10 inhibit acute renal failure (ARF) after ischemia or cisplatin administration; however, these agents have not been tested in a pure nephrotoxic model of ARF. ...

Abstract	The anti-inflammatory cytokines alpha-melanocyte-stimulating hormone (MSH) and interleukin (IL)-10 inhibit acute renal failure (ARF) after ischemia or cisplatin administration; however, these agents have not been tested in a pure nephrotoxic model of ARF. Therefore, we examined the effects of alpha-MSH and IL-10 in HgCl(2)-induced ARF. Mice were injected subcutaneously with HgCl(2) and then given vehicle, alpha-MSH, or IL-10 by intravenous injection. Animals were killed to study serum creatinine, histology, and myeloperoxidase activity. Treatment with either alpha-MSH or IL-10 did not alter the increase in serum creatinine, tubular damage, or leukocyte accumulation at 48 h after HgCl(2) injection. Because alpha-MSH and IL-10 are active in other injury models that involve leukocytes, we studied the time course of tubular damage and leukocyte accumulation to investigate whether leukocytes caused the tubular damage or accumulated in response to the tubular damage. Tubular damage was present in the outer stripe 12 h after HgCl(2) injection. In contrast, the number of leukocytes and renal myleoperoxidase activity were normal at 12 h but were significantly increased at 24 and 48 h after injection. We conclude that neither alpha-MSH nor IL-10 altered the course of HgCl(2)-induced renal injury. Because the tubular damage preceded leukocyte infiltration, the delayed leukocyte accumulation may play a role in the removal of necrotic tissue and/or tissue repair in HgCl(2)-induced ARF.
MeSH term(s)	Acute Kidney Injury/chemically induced ; Acute Kidney Injury/pathology ; Acute Kidney Injury/prevention & control ; Animals ; Creatinine/blood ; Esterases/analysis ; Injections, Intravenous ; Interleukin-10/administration & dosage ; Interleukin-10/therapeutic use ; Kidney Diseases/chemically induced ; Kidney Diseases/prevention & control ; Kidney Tubules/pathology ; Kinetics ; Leukocytes/pathology ; Male ; Mercuric Chloride/toxicity ; Mice ; Mice, Inbred BALB C ; Necrosis ; Peroxidase/metabolism ; alpha-MSH/administration & dosage ; alpha-MSH/therapeutic use
Chemical Substances	Interleukin-10 (130068-27-8) ; Mercuric Chloride (53GH7MZT1R) ; alpha-MSH (581-05-5) ; Creatinine (AYI8EX34EU) ; Peroxidase (EC 1.11.1.7) ; Esterases (EC 3.1.-)
Language	English
Publishing date	2002-05
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	603837-2
ISSN	1522-1466 ; 1931-857X ; 0363-6127
ISSN (online)	1522-1466
ISSN	1931-857X ; 0363-6127
DOI	10.1152/ajprenal.00203.2001
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Article ; Online: Human SR-BII mediates SAA uptake and contributes to SAA pro-inflammatory signaling in vitro and in vivo.

Baranova, Irina N / Souza, Ana C P / Bocharov, Alexander V / Vishnyakova, Tatyana G / Hu, Xuzhen / Vaisman, Boris L / Amar, Marcelo J / Chen, Zhigang / Remaley, Alan T / Patterson, Amy P / Yuen, Peter S T / Star, Robert A / Eggerman, Thomas L

PloS one

2017 Volume 12, Issue 4, Page(s) e0175824

Abstract: Serum amyloid A (SAA) is an acute phase protein with cytokine-like and chemotactic properties, that is markedly up-regulated during various inflammatory conditions. Several receptors, including FPRL-1, TLR2, TLR4, RAGE, class B scavenger receptors, SR-BI ...

Abstract	Serum amyloid A (SAA) is an acute phase protein with cytokine-like and chemotactic properties, that is markedly up-regulated during various inflammatory conditions. Several receptors, including FPRL-1, TLR2, TLR4, RAGE, class B scavenger receptors, SR-BI and CD36, have been identified as SAA receptors. This study provides new evidence that SR-BII, splice variant of SR-BI, could function as an SAA receptor mediating its uptake and pro-inflammatory signaling. The uptake of Alexa Fluor488 SAA was markedly (~3 fold) increased in hSR-BII-expressing HeLa cells when compared with mock-transfected cells. The levels of SAA-induced interleukin-8 secretion by hSR-BII-expressing HEK293 cells were also significantly (~3-3.5 fold) higher than those detected in control cells. Moderately enhanced levels of phosphorylation of all three mitogen-activated protein kinases, ERK1/2, and p38 and JNK, were observed in hSR-BII-expressing cells following SAA stimulation when compared with control wild type cells. Transgenic mice with pLiv-11-directed liver/kidney overexpression of hSR-BI or hSR-BII were used to assess the in vivo role of each receptor in SAA-induced pro-inflammatory response in these organs. Six hours after intraperitoneal SAA injection both groups of transgenic mice demonstrated markedly higher (~2-5-fold) expression levels of inflammatory mediators in the liver and kidney compared to wild type mice. Histological examinations of hepatic and renal tissue from SAA-treated mice revealed moderate level of damage in the liver of both transgenic but not in the wild type mice. Activities of plasma transaminases, biomarkers of liver injury, were also moderately higher in hSR-B transgenic mice when compared to wild type mice. Our findings identify hSR-BII as a functional SAA receptor that mediates SAA uptake and contributes to its pro-inflammatory signaling via the MAPKs-mediated signaling pathways.
MeSH term(s)	Animals ; Biological Transport ; Fluorescent Dyes/metabolism ; Fluorobenzenes/metabolism ; Gene Expression Regulation ; HEK293 Cells ; HeLa Cells ; Humans ; Inflammation/chemically induced ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/pathology ; Kidney/drug effects ; Kidney/metabolism ; Kidney/pathology ; Liver/drug effects ; Liver/metabolism ; Liver/pathology ; Lysosomal Membrane Proteins/genetics ; Lysosomal Membrane Proteins/metabolism ; MAP Kinase Kinase 4/genetics ; MAP Kinase Kinase 4/metabolism ; Mice ; Mitogen-Activated Protein Kinase 1/genetics ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/genetics ; Mitogen-Activated Protein Kinase 3/metabolism ; Receptors, Scavenger/genetics ; Receptors, Scavenger/metabolism ; Serum Amyloid A Protein/genetics ; Serum Amyloid A Protein/metabolism ; Serum Amyloid A Protein/pharmacology ; Signal Transduction ; Transfection ; Transgenes ; p38 Mitogen-Activated Protein Kinases/genetics ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Fluorescent Dyes ; Fluorobenzenes ; Lysosomal Membrane Proteins ; Receptors, Scavenger ; SCARB2 protein, human ; Serum Amyloid A Protein ; Mapk1 protein, mouse (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 4 (EC 2.7.12.2)
Language	English
Publishing date	2017-04-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0175824
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Article: TLR4 mutant mice are protected from renal fibrosis and chronic kidney disease progression.

Souza, Ana C P / Tsuji, Takayuki / Baranova, Irina N / Bocharov, Alexander V / Wilkins, Kenneth J / Street, Jonathan M / Alvarez-Prats, Alejandro / Hu, Xuzhen / Eggerman, Thomas / Yuen, Peter S T / Star, Robert A

Physiological reports

2015 Volume 3, Issue 9

Abstract: Chronic kidney disease (CKD) is associated with persistent low-grade inflammation and immunosuppression. In this study we tested the role of Toll-like receptor 4, the main receptor for endotoxin (LPS), in a mouse model of renal fibrosis and in a model of ...

Abstract	Chronic kidney disease (CKD) is associated with persistent low-grade inflammation and immunosuppression. In this study we tested the role of Toll-like receptor 4, the main receptor for endotoxin (LPS), in a mouse model of renal fibrosis and in a model of progressive CKD that better resembles the human disease. C3HeJ (TLR4 mutant) mice have a missense point mutation in the TLR4 gene, rendering the receptor nonfunctional. In a model of renal fibrosis after folic acid injection, TLR4 mutant mice developed less interstititial fibrosis in comparison to wild-type (WT) mice. Furthermore, 4 weeks after 5/6 nephrectomy with continuous low-dose angiotensin II infusion, C3HeOuJ (TLR4 WT) mice developed progressive CKD with albuminuria, increased serum levels of BUN and creatinine, glomerulosclerosis, and interstitial fibrosis, whereas TLR4 mutant mice were significantly protected from CKD progression. TLR4 WT mice also developed low-grade systemic inflammation, splenocyte apoptosis and increased expression of the immune inhibitory receptor PD-1 in the spleen, which were not observed in TLR4 mutant mice. In vitro, endotoxin (LPS) directly upregulated NLRP3 inflammasome expression in renal epithelial cells via TLR4. In summary, TLR4 contributes to renal fibrosis and CKD progression, at least in part, via inflammasome activation in renal epithelial cells, and may also participate in the dysregulated immune response that is associated with CKD.
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2724325-4
ISSN	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.12558
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