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1.
Allergol. immunopatol ; 50(6): 187-194, 01 nov. 2022. graf, ilus
Artigo em Inglês | IBECS | ID: ibc-211520

RESUMO

Background Sepsis-induced acute kidney injury is a general critical complication having high relevance to kidney inflammation. In spite of advances in clinical and critical care, the specific and effective therapies for acute kidney injury are still insufficient. The present study aimed to investigate the protective effect of Iroquois homeobox genes (IRX) on sepsis-induced kidney dysfunction in mice. Methods In order to gain insight into sepsis-related actions in acute kidney injury, the cecal puncture-induced kidney injury animal model was established. The hematoxylin and eosin staining was used to measure the pathology of kidney tissues. The kidney function-related biomarkers, including neutrophil gelatinase-associated lipocalin, creatinine, kidney injury molecule-1, blood urea nitrogen, and inflammatory cytokines, which included tumor necrosis factor α, interleukin 1β (IL-1β), IL-6, and monocyte chemotactic protein 1, were detected by automated biochemical analyzer or their corresponding test kits. The protein expression was measured using Western blot analysis, and the apoptotic rate of kidney tissue was measured by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Results The present study revealed the protective ability of IRX1 in sepsis-induced acute kidney injury. This study also determined the potential mechanism of IRX1 on sepsis-induced inflammatory response and cell apoptosis. Finally, it highlighted that IRX1 exerted a protective influence on CLP-induced acute kidney injury by suppressing the activation of chemokine (C-X-C motif) ligand 14 (CXCL14). Conclusion To conclude, the results suggest that overexpression of IRX1 could promote survival rate and suppress the CLP-induced apoptosis, inflammatory response, and kidney dysfunction through the activation of CXCL14. IRX1 and CXCL14 are essential to elucidate the mechanism of acute kidney injury. These findings may help to identify the promising targets for clinical sepsis therapy (AU)


Assuntos
Animais , Camundongos , Quimiocinas CXC/uso terapêutico , Injúria Renal Aguda , Sepse/tratamento farmacológico , Sepse/patologia , Injúria Renal Aguda/etiologia , Injúria Renal Aguda/metabolismo , Injúria Renal Aguda/patologia , Camundongos Endogâmicos BALB C , Modelos Animais de Doenças , Quimiocinas CXC/farmacologia , Apoptose , Rim/metabolismo , Rim/patologia , Fator de Necrose Tumoral alfa
2.
Allergol. immunopatol ; 50(4): 10-16, jul. 2022. graf
Artigo em Inglês | IBECS | ID: ibc-208889

RESUMO

Background: CXCL3 (C-X-C motif chemokine ligand 3) is a member of chemokines family, which binds to the receptor to recruit neutrophils to lungs, thus participating in the pathogenesis of asthmatic lung. The role of CXCL3 in sepsis-induced acute lung injury is investigated here.Methods: Human lung epithelial cell line (BEAS-2B) and human pulmonary artery endothelial cell line (HPAEC) were treated with lipopolysaccharides (LPS). MTT and flow cytometry were performed to detect cell viability and apoptosis, respectively. Enzyme-linked immunosorbent assay (ELISA) and real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) were used to assess the levels of inflammatory factors.Results: Treatment with LPS resulted in the decrease of cell viability in BEAS-2B and HPAEC. CXCL3 was particularly upregulated in LPS-treated BEAS-2B and HPAE cells. Knockdown of CXCL3 enhanced viability and suppressed apoptosis i006E LPS-treated BEAS-2B and HPAE cells. Knockdown of CXCL3 also upregulated TNF-α, I L-1β, and IL-18 in LPS-treated BEAS-2B and HPAE cells. Moreover, knockdown of CXCL3 suppressed the activation of mitogen-activated protein kinases (MAPKs) signaling in LPS-treated BEAS-2B and HPAE cells through downregulation of p-ERK1/2, p-p38, and p-JNK. On the other hand, overexpression of CXCL3 caused completely opposite results in LPS-treated BEAS-2B and HPAE cells.Conclusion: Knockdown of CXCL3 exerted antiapoptotic and anti-inflammatory effects against LPS-treated BEAS-2B and HPAE cells, at least partially, through inactivation of MAPKs signaling, suggesting a potential strategy for the intervention of sepsis-induced acute lung injury (AU)


Assuntos
Humanos , Lesão Pulmonar Aguda/metabolismo , Quimiocinas CXC/metabolismo , Sepse/metabolismo , Apoptose , Células Epiteliais/metabolismo , Inflamação/metabolismo , Lipopolissacarídeos/metabolismo , Proteínas Quinases Ativadas por Mitógeno/metabolismo
3.
Clin. transl. oncol. (Print) ; 23(4): 846-855, abr. 2021. graf
Artigo em Inglês | IBECS | ID: ibc-220921

RESUMO

Purpose The tumor immune microenvironment (TIME) is now considered as an important factor during gastric cancer (GC) development. This study identified a novel immune-related risk model for predicting prognosis and assessing the immune status of GC patients. Methods Transcriptomic data were obtained from the TCGA database. The differential expressed immune-related genes (IRGs) were identified through the ImmPort portal. Enrichment analysis was performed to explore the potential molecular mechanism of these IRGs. By the Cox regression analysis, we constructed the immune prognostic model. Then, the association between the model and the immune microenvironment was estimated. The model was validated in the GSE84433 dataset. Results Totally, we identified 222 differentially expressed IRGs. These IRGs were closely correlated with immune response and immune signaling pathways. Through the Cox regression analysis, we developed the immune prognostic model based on the expression of seven IRGs (CXCL3, NOX4, PROC, FAM19A4, RNASE2, IGHD2-15, CGB5). Patients were stratified into two groups according to immune-related risk scores. Survival analysis indicated that the prognosis of high-risk patients was poorer than low-risk patients. Moreover, the immune-related risk score was an independent prognostic biomarker. More importantly, we found that the infiltration level of immunosuppressive cells and the expression of inhibitory immune checkpoints were higher in high-risk patients. The immune microenvironment tended to be a suppressive status in patients with high-risk scores. Conclusion This study demonstrated that our model had predictive value for prognosis and the TIME in GC. It might be a robust tool to improve personalized patient management (AU)


Assuntos
Humanos , Microambiente Tumoral/imunologia , Neoplasias Gástricas/genética , Neoplasias Gástricas/imunologia , Quimiocinas CXC/genética , Citocinas/genética , Bases de Dados Genéticas , Progressão da Doença , Nanismo Hipofisário/genética , Neurotoxina Derivada de Eosinófilo/genética , Regulação Neoplásica da Expressão Gênica , Prognóstico , Microambiente Tumoral/genética
4.
Inmunología (1987) ; 27(1): 22-35, ene.-mar. 2008. ilus, tab
Artigo em En | IBECS | ID: ibc-67249

RESUMO

En mamíferos adultos, una población celular muy restringida que da origen al tejido hematopoyético se localiza en nichos dentro de la médula ósea en los que recibe sustento y protección. Estas célulasmadre hematopoiéticas de la sangre pueden salir de estos nichos en condiciones fisiológicas y, en el contexto del transplante de médula ósea, migrar a la médula del recipiente para regenerar su sistema hematopoyético. En esta revisión se describen las evidencias que hanpermitido caracterizar los mecanismos por los cuales estas células madre migran a los nichos medulares siguiendo un camino largo y tortuoso: Desde la circulación periférica, y mediante interacciones conla vasculatura medular, hasta nichos localizados en el espacio intramedular. También se discute cómo se han generado nuevas herramientas que nos permitirán manipular el tráfico de células madre


In adult mammals, a rare population of cells that gives rise to the hematopoietic compartment dwells in niches within the bone marrow where they are nourished and protected. These blood stem cells can, however, exit these niches under physiological conditions and, in thecontext of bone marrow transplantation, migrate to the recipient’s marrow to regenerate hematopoiesis. This review will address old and new discoveries regarding the mechanisms that allow these stem cells to find their way home through long and winding roads: From the peripheral circulation, through interactions with the vessel-lining endothelial cells in the bone marrow, and into their niches located in the intramedullary space. It will also address how these discoveries have provided us with new tools to manipulate stem cell trafficking


Assuntos
Humanos , Células-Tronco Hematopoéticas/imunologia , Medula Óssea/imunologia , Mobilização de Células-Tronco Hematopoéticas , Transplante de Células-Tronco Hematopoéticas/métodos , Quimiocinas CXC/imunologia
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