spd1672, a novel in vivo-induced gene, affects inflammatory response in a murine model of Streptococcus pneumoniae infection

spd1672, a novel Streptococcus pneumoniae (hereinafter S. pn) gene induced in vivo, has been identified to contribute to the virulence of S. pn; however, the role of spd1672 during host innate immune reaction against S. pn infection is unknown. In the present study, mice were infected with wild-type D39 and mutant D39Δspd1672 strains. Compared with the D39-infected mice, reduced bacterial load and attenuated inflammatory response were observed in the D39Δspd1672-treated mice. The levels of proinflammatory cytokines, including IFN-γ, TNF-α, and IL-1β, in the blood of D39Δspd1672-infected mice were lower than that in the D39-infected group. Additionally, attenuated activation of STAT3 and AKT was observed in the D39Δspd1672-infected mice. In conclusion, our data indicated that spd1672 expression modulates the release of proinflammatory cytokines, and AKT–STAT3 signaling appears to participate in the process. In conclusion, the present study extends our understanding of the role of an in vivo-induced gene in S. pn–host interaction.

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Endogenous Pro- and Anti-Inflammatory Cytokines Differentially Regulate an In Vivo Humoral Response to Streptococcus pneumoniae

Infection and Immunity ◽

10.1128/iai.70.2.749-761.2002 ◽

2002 ◽

Vol 70 (2) ◽

pp. 749-761 ◽

Cited By ~ 66

Author(s):

Abdul Q. Khan ◽

Yi Shen ◽

Zheng-Qi Wu ◽

Thomas A. Wynn ◽

Clifford M. Snapper

Keyword(s):

Streptococcus Pneumoniae ◽

Inflammatory Cytokines ◽

Proinflammatory Cytokines ◽

Humoral Response ◽

Lymphoid Cells ◽

Primary Immunization ◽

Tnf Α ◽

Ifn Γ ◽

Anti Inflammatory

ABSTRACT Proinflammatory cytokines play a critical role in innate host defense against extracellular bacteria. However, little is known regarding the effects of these cytokines on the adaptive humoral response. Mice injected with a neutralizing anti-tumor necrosis factor alpha (TNF-α) monoclonal antibody (MAb) at the time of primary immunization with intact Streptococcus pneumoniae (strain R36A) showed a substantial reduction in both the primary immunoglobulin G (IgG) response specific for the cell wall protein, pneumococcal surface protein A (PspA), as well as in the development of PspA-specific memory. In contrast, anti-TNF-α MAb injected only at the time of secondary immunization with R36A failed to alter the boosted anti-PspA response. TNF-α was required only within the first 48 to 72 h after primary immunization with R36A and was induced both by non-B and non-T cells and by lymphoid cells, within 2 to 6 h after immunization, with levels returning to normal by 24 h. Thus, the early innate release of TNF-α was critical for optimal stimulation of the subsequent adaptive humoral response to R36A. Additional proinflammatory (interleukin 1 [IL-1], IL-6, IL-12, and gamma interferon [IFN-γ]) as well as anti-inflammatory (IL-4 and IL-10) cytokines were also transiently induced. Mice genetically deficient in IL-6, IFN-γ, or IL-12 also showed a reduced IgG anti-PspA response of all IgG isotypes. In contrast, IL-4−/− and IL-10−/− mice immunized with R36A showed a significant elevation in the IgG anti-PspA response, except that there was decreased IgG1 in IL-4−/− mice. In this regard, a marked enhancement in the induction of proinflammatory cytokines was observed in the absence of IL-10, relative to controls. Ig isotype titers specific for the phosphorycholine determinant of C-polysaccharide were similarly regulated, but to a much more modest degree. These data suggest that proinflammatory and anti-inflammatory cytokines differentially regulate an in vivo protein- and polysaccharide-specific Ig response to an extracellular bacteria.

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MiR-22-3p suppresses sepsis-induced acute kidney injury by targeting PTEN

Bioscience Reports ◽

10.1042/bsr20200527 ◽

2020 ◽

Vol 40 (6) ◽

Author(s):

Xudong Wang ◽

Yali Wang ◽

Mingjian Kong ◽

Jianping Yang

Keyword(s):

Acute Kidney Injury ◽

Inflammatory Response ◽

Periodic Acid ◽

Kidney Injury ◽

Luciferase Reporter ◽

Tunel Staining ◽

Tnf Α

Abstract Background: Septic acute kidney injury is considered as a severe and frequent complication that occurs during sepsis. The present study was performed to understand the role of miR-22-3p and its underlying mechanism in sepsis-induced acute kidney injury. Methods: Rats were injected with adenovirus carrying miR-22-3p or miR-NC in the caudal vein before cecal ligation. Meanwhile, HK-2 cells were transfected with the above adenovirus following LPS stimulation. We measured the markers of renal injury (blood urea nitrogen (BUN), serum creatinine (SCR)). Histological changes in kidney tissues were examined by hematoxylin and eosin (H&E), Masson staining, periodic acid Schiff staining and TUNEL staining. The levels of IL-1β, IL-6, TNF-α and NO were determined by ELISA assay. Using TargetScan prediction and luciferase reporter assay, we predicted and validated the association between PTEN and miR-22-3p. Results: Our data showed that miR-22-3p was significantly down-regulated in a rat model of sepsis-induced acute kidney injury, in vivo and LPS-induced sepsis model in HK-2 cells, in vitro. Overexpression of miR-22-3p remarkably suppressed the inflammatory response and apoptosis via down-regulating HMGB1, p-p65, TLR4 and pro-inflammatory factors (IL-1β, IL-6, TNF-α and NO), both in vivo and in vitro. Moreover, PTEN was identified as a target of miR-22-3p. Furthermore, PTEN knockdown augmented, while overexpression reversed the suppressive role of miR-22-3p in LPS-induced inflammatory response. Conclusions: Our results showed that miR-22-3p induced protective role in sepsis-induced acute kidney injury may rely on the repression of PTEN.

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In Vivo Regulation of Replicative Legionella pneumophila Lung Infection by Endogenous Interleukin-12

Infection and Immunity ◽

10.1128/iai.66.1.65-69.1998 ◽

1998 ◽

Vol 66 (1) ◽

pp. 65-69 ◽

Cited By ~ 52

Author(s):

J. K. Brieland ◽

D. G. Remick ◽

M. L. LeGendre ◽

N. C. Engleberg ◽

J. C. Fantone

Keyword(s):

Legionella Pneumophila ◽

Lung Infection ◽

Interleukin 12 ◽

Necrosis Factor Alpha ◽

Protein Levels ◽

Tnf Α ◽

Factor Alpha ◽

Ifn Γ

ABSTRACT The in vivo role of endogenous interleukin 12 (IL-12) in modulating intrapulmonary growth of Legionella pneumophila was assessed by using a murine model of replicative L. pneumophila lung infection. Intratracheal inoculation of A/J mice with virulent bacteria (106 L. pneumophilacells per mouse) resulted in induction of IL-12, which preceded clearance of the bacteria from the lung. Inhibition of endogenous IL-12 activity, via administration of IL-12 neutralizing antiserum, resulted in enhanced intrapulmonary growth of the bacteria within 5 days postinfection (compared to untreated L. pneumophila-infected mice). Because IL-12 has previously been shown to modulate the expression of cytokines, including gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), and IL-10, which regulate L. pneumophila growth, immunomodulatory effects of endogenous IL-12 on intrapulmonary levels of these cytokines during replicative L. pneumophila lung infection were subsequently assessed. Results of these experiments demonstrated that TNF-α activity was significantly lower, while protein levels of IFN-γ and IL-10 in the lung were similar, in L. pneumophila-infected mice administered IL-12 antiserum, compared to similarly infected untreated mice. Together, these results demonstrate that IL-12 is critical for resolution of replicativeL. pneumophila lung infection and suggest that regulation of intrapulmonary growth of L. pneumophila by endogenous IL-12 is mediated, at least in part, by TNF-α.

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Dietary Fiber Ameliorates Lipopolysaccharide-Induced Intestinal Barrier Function Damage in Piglets by Modulation of Intestinal Microbiome

mSystems ◽

10.1128/msystems.01374-20 ◽

2021 ◽

Vol 6 (2) ◽

Author(s):

Xiao Sun ◽

Yalei Cui ◽

Yingying Su ◽

Zimin Gao ◽

Xinying Diao ◽

...

Keyword(s):

Inflammatory Response ◽

Growth Performance ◽

Proinflammatory Cytokines ◽

Barrier Function ◽

Intestinal Microflora ◽

Intestinal Barrier ◽

Intestinal Morphology ◽

Intestinal Barrier Function ◽

Tnf Α

ABSTRACT Weaning of piglets is accompanied by intestinal inflammation, impaired intestinal barrier function, and intestinal microflora disorder. Regulating intestinal microflora structure can directly or indirectly affect intestinal health and host growth and development. However, whether dietary fiber (DF) affects the inflammatory response and barrier function by affecting the intestinal microflora and its metabolites is unclear. In this study, we investigated the role of intestinal microflora in relieving immune stress and maintaining homeostasis using piglets with lipopolysaccharide (LPS)-induced intestinal injury as a model. DF improved intestinal morphology and barrier function, inhibited the expression of inflammatory signal pathways (Toll-like receptor 2 [TLR2], TLR4, and NF-κB) and proinflammatory cytokines (interleukin 1β [IL-1β], IL-6, and tumor necrosis factor alpha [TNF-α]), and upregulated the expression of barrier-related genes (encoding claudin-1, occludin, and ZO-1). The contents of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) and the activity of diamine oxidase in plasma were decreased. Meanwhile, DF had a strong effect on the composition and function of intestinal microflora at different taxonomic levels, the relative abundances of cellulolytic bacteria and anti-inflammatory bacteria were increased, and the concentrations of propionate, butyrate, and total short-chain fatty acids (SCFAs) in intestinal contents were increased. In addition, the correlation analysis also revealed the potential relationship between metabolites and certain intestinal microflora, as well as the relationship between metabolites and intestinal morphology, intestinal gene expression, and plasma cytokine levels. These results indicate that DF improves intestinal barrier function, in part, by altering intestinal microbiota composition and increasing the synthesis of SCFAs, which subsequently alleviate local and systemic inflammation. IMPORTANCE Adding DF to the diet of LPS-challenged piglets alleviated intestinal and systemic inflammation, improved intestinal barrier function, and ultimately alleviated the growth retardation of piglets. In addition, the addition of DF significantly increased the relative abundance of SCFA-producing bacteria and the production of SCFAs. We believe that the improvement of growth performance of piglets with LPS-induced injury can be attributed to the beneficial effects of DF on intestinal microflora and SCFAs, which reduced the inflammatory response in piglets, improving intestinal barrier function and enhancing body health. These research results provide a theoretical basis and guidance for the use of specific fiber sources in the diet to improve intestinal health and growth performance of piglets and thus alleviate weaning stress. Our data also provide insights for studying the role of DF in regulating gastrointestinal function in human infants.

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Role ofβ2 Integrins in the Binding of Thymocytes to Rat Thymic Macrophages

Developmental Immunology ◽

10.1155/1994/95687 ◽

1994 ◽

Vol 4 (1) ◽

pp. 65-77 ◽

Cited By ~ 1

Author(s):

Miodrag Čolić ◽

Vesna Ilić ◽

Takuya Tamatani ◽

Masayuki Miyasaka ◽

Miloš D. Pavlović

Keyword(s):

Significant Role ◽

Inhibitory Effect ◽

Adherent Cells ◽

Experimental Conditions ◽

Tnf Α ◽

Significant Difference ◽

Ifn Γ ◽

And Function

A role of β2 integrins and one of their ligands, ICAM-1, in thymic macrophage (TMF)/thymocyte interactions was studied. TMF were isolated as adherent cells from 4-day old culture of thymic-cell suspensions either from normal or hydrocortisone-treated rats. Adherent cells were 94-98% positive with ED1 (a pan-macrophage marker). The majority of them (75-95%) expressed the CD11b and CD18 molecules, and 60-70% expressed CD54 (ICAM-1). A low proportion of TMF (10-20%) expressed CDlla (LFA-1). The expression of all these antigens was upregulated by IFN-α and TNF-α. The effect of these mAbs on TMF/thymocyte binding was studied using a simple rosette assay by incubating unstimulated or IFN-γ or TNF-α stimulated TMF, grown on microscopic slides with resting or ConA +IL-2 activated thymocytes. It was found that LFA-1/CD18 and ICAM-1 play a significant role in the TMF/thymocyte adhesion. In addition, a LFA-l-dependent/ICAM- 1-independent adhesion pathway was observed, suggesting that LFA-1 might use another ligand. The inhibitory effect of anti-CD18 mAb (WT-3) was higher than the effect of anti-LFA-1 mAb (WT-1) and was a consequence of blocking the CD18 chain both on thymocytes and TMF. No significant difference in the expression and function of adhesion molecules was found between TMF obtained from normal or hydrocortisone-treated rats. The involvement of CD1 1b in these processes was of lesser importance than the role of the CD11a molecule. By using mAbs to different epitopes of the CD11b molecule, such as OX-42 (anti-CD11b/CD11c), ED7, and ED8 (anti-CD11b), it was found that they were either slightly or moderately inhibitory under certain experimental conditions or did not significantly modulate TMF/thymocyte binding. Oχ-42 was slightly stimulatory in some experiments. Cumulatively, these results show that 2 integrins play a significant role in TMF/thymocyte interactions and probably contribute to T-cell development in vivo.

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Expression and role of ABIN1 in sepsis: In vitro and in vivo studies

Open Medicine ◽

10.1515/med-2021-0008 ◽

2020 ◽

Vol 16 (1) ◽

pp. 033-040

Author(s):

Haolan Li ◽

Aichen Sun ◽

Taocheng Meng ◽

Yan Zhu

Keyword(s):

Inflammatory Response ◽

Molecular Mechanisms ◽

Organ Injury ◽

In Vivo Studies ◽

Inflammatory Factors ◽

Septic Mouse ◽

Raw264.7 Macrophages ◽

Tnf Α

AbstractIn this research, we attempted to explain the effect and the related molecular mechanisms of ABIN1 in lipopolysaccharide (LPS)-induced septic mice or RAW264.7 macrophages. LPS was adopted to treat RAW264.7 macrophages for 4 h, and the levels of inflammatory factors were assessed by ELISA. Besides, ABIN1 expression was measured by quantitative reverse transcription polymerase chain reaction. Apparently, LPS enhanced immunoreaction, suggested by increased expression of IL-1β, tumor necrosis factor (TNF)-α, and IL-6. ABIN1 levels were obviously reduced compared to the control. Furthermore, we evaluated the roles of ABIN1-plasmid in immunoreaction and nuclear factor-κB (NF-κB) pathway. We found that ABIN1-plasmid significantly reduced the expression of IL-1β, TNF-α, and IL-6 in LPS-treated cells and inhibited NF-κB pathway activation. Meanwhile, a septic mouse mode was conducted to validate the role of ABIN1 in inflammatory response and organ damage in vivo. These data suggested that ABIN1-plasmid significantly inhibited the secretion of inflammatory cytokines and Cr, BUN, AST, and ALT levels in the serum of LPS-stimulated mice compared to LPS + control-plasmid group, reflecting the relieved inflammation and organ injury. In summary, the present findings indicated that ABIN1 alleviated sepsis by repressing inflammatory response through NF-κB signaling pathway, emphasizing the potential value of ABIN1 as therapeutic strategy for sepsis.

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TNF, IFN-γ, and endotoxin increase expression of DMT1 in bronchial epithelial cells

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00428.2003 ◽

2005 ◽

Vol 289 (1) ◽

pp. L24-L33 ◽

Cited By ~ 37

Author(s):

Xinchao Wang ◽

Michael D. Garrick ◽

Funmei Yang ◽

Lisa A. Dailey ◽

Claude A. Piantadosi ◽

...

Keyword(s):

Epithelial Cells ◽

Proinflammatory Cytokines ◽

Airway Epithelial Cells ◽

Divalent Metal Transporter 1 ◽

Divalent Metal Transporter ◽

Metal Transporter ◽

Tnf Α ◽

Ifn Γ

Regulation of the metal transport protein divalent metal transporter-1 (DMT1) may contribute to the uptake and detoxification of iron by cells resident in the respiratory tract. Inflammation has been associated with an increased availability of this metal resulting in an oxidative stress. Because proinflammatory cytokines and LPS have been demonstrated to affect an elevated expression of DMT1 in a macrophage cell line, we tested the hypothesis that tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and LPS increase DMT1 expression in airway epithelial cells. We used RT-PCR to detect mRNA for both −IRE DMT1 and +IRE DMT1 in BEAS-2B cells. Treatment with TNF-α, IFN-γ, or LPS increased both forms. Western blot analysis also demonstrated an increase in the expression of both isoforms of DMT1 after these treatments. Twenty-four hours after exposure of an animal model to TNF-α, IFN-γ, or LPS, a significant increase in pulmonary expression of −IRE DMT1 was seen by immunohistochemistry; the level of +IRE DMT1 was too low in the lung to be visualized using this methodology. Finally, iron transport into BEAS-2B cells was increased after inclusion of TNF-α, IFN-γ, or LPS in the media. We conclude that proinflammatory cytokines and LPS increase mRNA and protein expression of DMT1 in airway cells in vitro and in vivo. Furthermore, both −IRE and +IRE isoforms are elevated after exposures. Increased expression of this protein appears to be included in a coordinated response of the cell and tissue where the function might be to diminish availability of metal.

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Bacterium-Dependent Induction of Cytokines in Mononuclear Cells and Their Pathologic Consequences In Vivo

Infection and Immunity ◽

10.1128/iai.67.5.2125-2130.1999 ◽

1999 ◽

Vol 67 (5) ◽

pp. 2125-2130 ◽

Cited By ~ 32

Author(s):

Yanling Jiang ◽

Luciano Magli ◽

Michael Russo

Keyword(s):

Inflammatory Response ◽

Mononuclear Cells ◽

Oral Bacteria ◽

Interleukin 12 ◽

Potent Inducer ◽

Tnf Α ◽

Oral Pathogens ◽

Ifn Γ

ABSTRACT Viridans streptococci are a heterogeneous group of gram-positive bacteria that are normal inhabitants of the mouth. These organisms are thought to contribute significantly to the etiology of infective endocarditis, although recently they have been implicated in serious infections in other settings. Another group of oral bacteria, gram-negative anaerobes, is associated with chronic dental infections, such as periodontal diseases or endodontic lesion formation. We evaluated the ability of the oral pathogens Streptococcus mutans and Porphyromonas endodontalis to induce a pathogenic response in vivo, with the goal of quantifying the inflammatory response in soft tissue by measuring leukocyte recruitment and hard tissues by measuring osteoclastogenesis. S. mutansinduced a strong inflammatory response and was a potent inducer of osteoclast formation, while P. endodontalis was not. To further study the mechanisms by which P. endodontalis andS. mutans elicit significantly different levels of inflammatory responses in vivo, we tested the capacity of each to induce production of cytokines by mononuclear cells in vitro. S. mutans stimulated high levels of interleukin-12 (IL-12), gamma interferon (IFN-γ), and tumor necrosis factor alpha (TNF-α), all of which are associated with inflammation, enhanced monocyte function, and generation of a Th1 response. In contrast, P. endodontalisstimulated production of IL-10 but not of TNF-α, IL-12, or IFN-γ. These results demonstrate that oral pathogens differ dramatically in their abilities to induce inflammatory and immunoregulatory cytokines. Moreover, there is a high degree of correlation between the cytokine profile induced by these bacteria in vitro and their pathogenic capacity in vivo.

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Giardia duodenalis extracellular vesicles regulate the proinflammatory immune response in mouse macrophages in vitro via the MAPK, AKT and NF-κB pathways

Parasites & Vectors ◽

10.1186/s13071-021-04865-5 ◽

2021 ◽

Vol 14 (1) ◽

Author(s):

Panpan Zhao ◽

Lili Cao ◽

Xiaocen Wang ◽

Jianhua Li ◽

Jingquan Dong ◽

...

Keyword(s):

Immune Response ◽

Inflammatory Response ◽

Signaling Pathways ◽

Innate Immune Response ◽

Proinflammatory Cytokines ◽

Giardia Duodenalis ◽

Innate Immune ◽

Tnf Α ◽

Mouse Macrophages

Abstract Background Giardia duodenalis is an extracellular protozoan parasite that causes giardiasis in mammals. The presentation of giardiasis ranges from asymptomatic to severe diarrhea, and the World Health Organization lists it in the Neglected Diseases Initiative. Extracellular vesicles (EVs) are a key mediator of intracellular communication. Although previous studies have shown that G. intestinalis can regulate a host’s innate immune response, the role of G. intestinalis EVs (GEVs) in triggering a G. intestinalis-induced innate immune response remains to be further explored. Methods In this study, GEVs, G. intestinalis and GEVs + G. intestinalis were inoculated into macrophages, respectively. The transcription and secretion levels of proinflammatory cytokines, including interleukin (IL)-1β, IL-6 and tumor necrosis factor alpha (TNF-α), were measured using real-time quantitative PCR (qPCR) and enzyme-linked immunosorbent assays (ELISAs). The phosphorylation levels of the MAPK, AKT and NF-κB signaling pathways in GEV-stimulated mouse macrophages were examined using western blotting and immunofluorescence methods. The roles of activated pathways in the GEV-triggered inflammatory response were determined using inhibition assays, western blotting and ELISAs. Results The results showed that pretreatment with GEVs enhanced with G. intestinalis (GEVs + G. intestinalis) induced IL-1β, IL-6 and TNF-α transcription and secretion from mouse macrophages compared to stimulation with either GEVs or G. intestinalis alone. Inoculation of mouse macrophages with GEVs upregulated the phosphorylation levels of the p38 MAPK, p44/42 MAPK (Erk1/2), AKT and NF-κB signaling pathways and led to the nuclear translocation of NF-κB p65. Blocking the activated p38, Erk and NF-κB signaling pathways significantly downregulated the secretion of proinflammatory cytokines, and blocking the activated AKT signaling pathway demonstrated reverse effects. Conclusions The results of this study reveal that GEVs can enhance G. intestinalis-induced inflammatory response levels in mouse macrophages through activation of the p38, ERK and NF-κB signaling pathways. The role of GEVs in regulating host cell immune responses may provide insights into exploring the underlying mechanisms in G. intestinalis–host interactions. Graphical abstract

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Regulation of renal glucose transporters during severe inflammation

AJP Renal Physiology ◽

10.1152/ajprenal.00258.2006 ◽

2007 ◽

Vol 292 (2) ◽

pp. F804-F811 ◽

Cited By ~ 45

Author(s):

Christoph Schmidt ◽

Klaus Höcherl ◽

Michael Bucher

Keyword(s):

Renal Dysfunction ◽

Proinflammatory Cytokines ◽

Knockout Mice ◽

Glucose Transporters ◽

Renal Perfusion ◽

Tnf Α ◽

Ifn Γ ◽

Renal Tubular ◽

Glucose Excretion

Severe sepsis is accompanied by acute renal failure (ARF) with renal tubular dysfunction and glucosuria. In this study, we aimed to determine the regulation of renal tubular glucose transporters during severe experimental inflammation. Male C57BL/6J mice were injected with LPS or proinflammatory cytokines, and renal perfusion, glomerular filtration rate (GFR), fractional glucose excretion, and expression of tubular glucose transporters were determined. We found a decreased plasma glucose concentration with impaired renal tissue perfusion and GFR and increased fractional glucose excretion associated with decreased expression of SGLT2, SGLT3, and GLUT2 after LPS injection. Similar alterations were observed after application of TNF-α, IL-1β, IL-6, or IFN-γ. To clarify the role of proinflammatory cytokines, we performed LPS injections in knockout mice with deficiencies for TNF-α, IL-1 receptor type 1, IFN-γ, or IL-6 as well as LPS injections in glucocorticoid-treated wild-type mice. LPS-induced alterations of glucose transporters also were present in single-cytokine knockout mice. In contrast, glucocorticoid treatment clearly attenuated LPS-induced changes in renal glucose transporter expression and improved GFR and fractional glucose excretion. LPS-induced decrease of renal perfusion was not improved by glucocorticoids, indicating a minor role of ischemia in the development of septic renal dysfunction. Our results demonstrate modifications of tubular glucose transporters during severe inflammation that are probably mediated by proinflammatory cytokines and account for the development of ARF with increased fractional glucose excretion. In addition, our findings provide an explanation why single anti-cytokine strategies fail in the therapy of septic patients and contribute to an understanding of the beneficial effects of glucocorticoids on septic renal dysfunction.

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