scholarly journals Depletion of phagocytes in the reticuloendothelial system causes increased inflammation and mortality in rabbits withPseudomonas aeruginosapneumonia

2009 ◽  
Vol 296 (2) ◽  
pp. L198-L209 ◽  
Author(s):  
Kiyoyasu Kurahashi ◽  
Teiji Sawa ◽  
Maria Ota ◽  
Osamu Kajikawa ◽  
Keelung Hong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Proinflammatory Cytokine ◽  
Systemic Infection ◽  
Dry Weight ◽  
Reticuloendothelial System ◽  
Bacterial Clearance ◽  
Blood Samples ◽  
Tnf Α ◽  
Inflammatory Modulation

Phagocytes of the reticuloendothelial system are important in clearing systemic infection; however, the role of the reticuloendothelial system in the response to localized infection is not well-documented. The major goals of this study were to investigate the roles of phagocytes in the reticuloendothelial system in terms of bacterial clearance and inflammatory modulation in sepsis caused by Pseudomonas pneumonia. Macrophages in liver and spleen were depleted by administering liposome encapsulated dichloromethylene diphosphonate (clodronate) intravenously 36 h before the instillation of Pseudomonas aeruginosa into the lungs of anesthetized rabbits. Blood samples were analyzed for bacteria and cytokine concentrations. Lung injury was assessed by the bidirectional flux of albumin and by wet-to-dry weight ratios. Blood pressure and cardiac outputs decreased more rapidly and bacteremia occurred earlier in the clodronate-treated rabbits compared with the nondepleted rabbits. Plasma TNF-α (1.08 ± 0.54 vs. 0.08 ± 0.02 ng/ml) and IL-8 (6.8 ± 1.5 vs. 0.0 ± 0.0 ng/ml) were higher in the depleted rabbits. The concentration of IL-10 in liver of the macrophage-depleted rabbits was significantly lower than in normal rabbits at 5 h. Treatment of macrophage-depleted rabbits with intravenous IL-10 reduced plasma proinflammatory cytokine concentrations and reduced the decline in blood pressure and cardiac output. These results show that macrophages in the reticuloendothelial system have critical roles in controlling systemic bacteremia and reducing systemic inflammation, thereby limiting the systemic effects of a severe pulmonary bacterial infection.

scholarly journals The Role of TNF-α as a Proinflammatory Cytokine in Pathological Processes

2019 ◽  
Vol 13 (1) ◽  
pp. 332-338
Author(s):  
Luciano B. Silva ◽  
Alexandrino P. dos Santos Neto ◽  
Sandra M.A.S. Maia ◽  
Carolina dos Santos Guimarães ◽  
Iliana L. Quidute ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Literature Review ◽  
Adaptive Immunity ◽  
Proinflammatory Cytokine ◽  
Antigen Presenting Cells ◽  
Tnf Α ◽  
Antigen Presenting

TNF-α is a member of the vast cytokine family being considered a proinflammatory substance produced many by macrophages and other cells belonging to the innate immunity, many of them classified as indeed Antigen Presenting Cells (APCs) involved in the complex chemotactic process of activation of the adaptive immunity. The aim of this work was to accomplish a literature review concerning the main pathologies that have TNF-α as a modulating agent in other to bring light to the main interactions present in the inflammation installed.

scholarly journals Regulatory Role of Interleukin-10 in Experimental Group B Streptococcal Arthritis

2002 ◽  
Vol 70 (6) ◽  
pp. 2862-2868 ◽  
Author(s):  
Manuela Puliti ◽  
Christina von Hunolstein ◽  
Claudie Verwaerde ◽  
Francesco Bistoni ◽  
Graziella Orefici ◽  
...  
Keyword(s):  
Systemic Infection ◽  
Interleukin 10 ◽  
Dose Dependence ◽  
Necrosis Factor Alpha ◽  
Clear Cut ◽  
Type Iv ◽  
Clinical Observations ◽  
Tnf Α ◽  
Group B

ABSTRACT Intravenous inoculation of CD-1 mice with 107 CFU of type IV group B Streptococcus (GBS) results in a high incidence of diffuse septic arthritis , associated with high levels of systemic and local production of interleukin-1β (IL-1β) and IL-6. In this study, the role of the anti-inflammatory cytokine IL-10 in the evolution of GBS systemic infection and arthritis was evaluated. IL-10 production was evident in sera and joints of GBS-infected mice. Neutralization of endogenous IL-10 by administration of anti-IL-10 antibodies (1 mg/mouse) at the time of infection resulted in worsening of articular lesions and 60% mortality associated with early sustained production of IL-6, IL-1β, and tumor necrosis factor alpha (TNF-α). The effect of IL-10 supplementation was assessed by administering IL-10 (100, 200, or 400 ng/mouse) once a day for 5 days, starting 1 h after infection. Treatment with IL-10 had a beneficial effect on GBS arthritis, and there was a clear-cut dose dependence. The decrease in pathology was associated with a significant reduction in IL-6, IL-1β, and TNF-α production. Histological findings showed limited periarticular inflammation and a few-cell influx in the articular cavity of IL-10-treated mice, confirming clinical observations. In conclusion, this study provides further information concerning the role of IL-10 in regulating the immune response and inflammation and calls attention to the potential therapeutic use of IL-10 in GBS arthritis.

scholarly journals Differential Involvement of Toll-Like Receptors 2 and 4 in the Host Response to Acute Respiratory Infections with Wild-Type and Mutant Haemophilus influenzae Strains

2005 ◽  
Vol 73 (4) ◽  
pp. 2075-2082 ◽  
Author(s):  
Eva Lorenz ◽  
Diana C. Chemotti ◽  
Alice L. Jiang ◽  
Letitia D. McDougal
Keyword(s):  
Haemophilus Influenzae ◽  
Host Response ◽  
Respiratory Infections ◽  
Acute Respiratory Infections ◽  
Bacterial Clearance ◽  
Wild Type ◽  
Tlr2 Expression ◽  
Neutrophil Influx ◽  
Tnf Α

ABSTRACT We used a mouse model of acute respiratory infections to investigate the role of Toll-like receptor 2 (TLR2) and TLR4 in the host response to Haemophilus influenzae. Acute aerosol exposures to wild-type strains of H. influenzae showed that TLR4 function was essential for TNF-α induction, neutrophil influx, and bacterial clearance. To determine how lipooligosaccharide (LOS) modifications would affect the role of TLR4 in inducing the host response, we used acute infections with an H. influenzae strain expressing a mutation in the htrB gene. This mutant strain expresses an LOS subunit with decreased acylation. In response to H. influenzae htrB infection, tumor necrosis factor alpha (TNF-α) secretion remained TLR4 dependent. But the decrease in LOS acylation made the neutrophil influx and the bacterial clearance also dependent on TLR2, as shown by the decreased host response elicited in TLR2 knockout mice compared to C57BL/6 mice. A subsequent analysis of TLR2 and TLR4 gene expression by quantitative PCR indicated that TLR4 function induces TLR2 expression and vice versa. These results indicate that some changes in the LOS subunit of H. influenzae can favor signaling through non-TLR4 receptors, such as TLR2. The results also indicate a close interaction between TLR4 and TLR2 that tightly regulates the expression of both receptors.

scholarly journals Effect of AT1 receptor antagonism on vascular and circulating inflammatory mediators in SHR: role of NF-κB/IκB system

2005 ◽  
Vol 288 (1) ◽  
pp. H111-H115 ◽  
Author(s):  
David Sanz-Rosa ◽  
M. Pilar Oubiña ◽  
Eva Cediel ◽  
Natalia de las Heras ◽  
Onofre Vegazo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Mrna Expression ◽  
Inflammatory Mediators ◽  
Plasma Levels ◽  
Inflammatory Markers ◽  
Angiotensin Ii Receptor ◽  
Tnf Α ◽  
Wistar Kyoto

We investigated the role of angiotensin II in vascular and circulating inflammatory markers in spontaneously hypertensive rats (SHR). IL-1β, IL-6, and TNF-α aortic mRNA expression and plasma levels were measured in adult SHR untreated or treated with the angiotensin II receptor antagonist candesartan (2 mg·kg−1·day−1) or antihypertensive triple therapy (TT; in mg·kg−1·day−1: 20 hydralazine + 7 type 1 hydrochlorothiazide + 0.15 reserpine) for 10 wk. Likewise, aortic expression of NF-κB p50 subunit precursor p105 and its inhibitor (IκB) were measured. Age-matched Wistar-Kyoto rats (WKY) served as normotensive reference. High blood pressure levels were associated with increased ( P < 0.05) aortic mRNA expression of IL-1β, IL-6, and TNF-α. Hypertension was also accompanied by increased IL-1β and IL-6 plasma levels. No differences were observed in circulating TNF-α levels between SHR and WKY. SHR presented elevated aortic mRNA expression of the transcription factor NF-κB and reduction in its inhibitor, IκB. Candesartan decreased ( P < 0.05) blood pressure levels, aortic mRNA expression of IL-1β, IL-6, and TNF-α, and ( P < 0.05) IL-1β and IL-6 plasma concentration. However, although arterial pressure decrease was comparable for the treatments, TT only partially reduced the increments in inflammatory markers. In fact, candesartan-treated rats showed significantly lower levels of circulating and vascular inflammatory markers than TT-treated animals. The treatments increased IκB mRNA expression similarly. However, only candesartan reduced NF-κB mRNA expression. In summary, 1) SHR presented a vascular inflammatory process; 2) angiotensin II, and increased hemodynamic forces associated with hypertension, seems to be involved in stimulation of inflammatory mediators through NF-κB system activation; and 3) reduction of inflammatory mediators produced by candesartan in SHR could be partially due to both downregulation of NF-κB and upregulation of IκB.

scholarly journals MiR-26a inhibits the inflammatory response of microglia by targeting HMGA2 in intracerebral hemorrhage

2020 ◽  
Vol 48 (6) ◽  
pp. 030006052092961 ◽  
Author(s):  
Jun Jin ◽  
Feng Zhou ◽  
Jie Zhu ◽  
Weixian Zeng ◽  
Yong Liu
Keyword(s):  
Inflammatory Response ◽  
Intracerebral Hemorrhage ◽  
Test Performance ◽  
Proinflammatory Cytokine ◽  
Potential Role ◽  
Microglial Cells ◽  
Secondary Brain Injury ◽  
Rotarod Test ◽  
Tnf Α

Objective Intracerebral hemorrhage (ICH) is a common cerebrovascular disease with high mortality and poor prognosis. Therefore, the biological function and underlying molecular mechanism of miR-26a in inflammatory injury following ICH was investigated. Methods The potential role of miR-26a was investigated in lipopolysaccharide (LPS)-treated microglial cells by quantitative real-time PCR. To explore the potential role of HMGA2 in the miR-26a-regulated inflammatory response, LPS-induced microglial cells were cotransfected with an miR-26a mimic and pcDNA-HMGA2. Then, lentivirus-mediated overexpression of an miR-26a mimic in mouse microglial cells was performed, and the effects of miR-26a treatment on IL-6, IL-1β, and TNF-α expression in the mouse brain, neurological behavior, and rotarod test performance of mice after ICH were observed. Results MiR-26a was significantly downregulated in LPS-treated microglia and ICH mouse models. MiR-26a markedly reduced IL-6, IL-1β, and TNF-α expression in LPS-treated microglial cells. Furthermore, HMGA2 was verified as a direct target of miR-26a. In vivo, miR-26a overexpression in mouse microglial cells significantly suppressed proinflammatory cytokine expression in mouse brains and markedly improved the neurological behavior and rotarod test performance of mice after ICH. Conclusion MiR-26a remarkably inhibited proinflammatory cytokine release by targeting HMGA2, indicating that miR-26a could protect against secondary brain injury following ICH.

Plasma catecholamines in rats during rewarming from induced hypothermia

1984 ◽  
Vol 57 (3) ◽  
pp. 808-814 ◽  
Author(s):  
S. B. Jones ◽  
F. Depocas ◽  
C. C. Chan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Carotid Artery ◽  
Plasma Catecholamines ◽  
Male Rats ◽  
Induced Hypothermia ◽  
Blood Samples ◽  
Arterial Blood ◽  
Colonic Temperature

The present study sought to quantitate the levels of plasma catecholamines [norepinephrine (NE), epinephrine (E), and dopamine (DA)] during induction and rewarming from hypothermia. Male rats (317 +/- 8 g) were made hypothermic by exposure to 0.9% halothane at -10 to -15 degrees C while blood pressure (carotid artery), heart rate, and colonic temperature (Tc) were monitored. Anesthesia was discontinued when Tc reached 28 degrees C. Tc continued to fall but was held at 20–20.5 degrees C for 30 min. Rewarming was then initiated by raising ambient temperature to 22 degrees C. Arterial blood samples were taken 1) before cooling, 2) just before rewarming, 3) when Tc reached 22 degrees C during rewarming, and 4) when Tc reached 27 degrees C during rewarming. Plasma was assayed radioenzymatically for catecholamines using both phenylethanolamine-N-methyltransferase and catechol-O-methyltransferase procedures, and hypothermic induction resulted in significant increases in NE, E, and DA above control levels (P less than 0.01). With rewarming to Tc = 22 degrees C, all catecholamines increased above the level observed during hypothermia (P less than 0.01), and NE and DA increased still further (P less than 0.01) when Tc reached 27 degrees C. The levels of plasma catecholamines observed during hypothermia and during the rewarming phase indicate a role of the sympathoadrenal medullary system in the metabolic adjustments associated with hypothermia and recovery. During rewarming, the levels of E and NE attained exceed those at which both substances may be expected to act as circulating hormones.

scholarly journals MONOCYTE CHEMOATTRACTANT PROTEIN-1 (MCP-1) CONCENTRATIONS IN CARRAGEENAN-INDUCED GASTROENTEROCOLITIS

2017 ◽  
pp. 64-67
Author(s):  
A. S. Tkachenko ◽  
O. A. Nakonechnaya ◽  
T. V. Gorbach ◽  
A. I. Onischenko ◽  
T. N. Chubukova
Keyword(s):  
Oxidative Stress ◽  
Blood Serum ◽  
Proinflammatory Cytokine ◽  
Food Additive ◽  
Control Group ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Tnf Α

Aim: to study MCP-1 concentrations in chronic carrageenan-induced gastroenterocolitis and the role of this protein in the development and progression of the disease. Material and methods . Thirty female WAG rats were divided into three groups (each group consisted of ten individuals): 1) introduction of 1% carrageenan solution for 14 days; 2) introduction of 1 % carrageenan solution for 28 days; 3) the control group. The animals of the first two groups were developing gastroenterocolitis. The MCP-1 and TNF-α concentrations were measured in the blood serum by ELISA. Results. Development of carrageenan-induced gastroenterocolitis was accompanied by increased levels of both MCP-1 and TNF-α in the blood serum. The level of the increase of both the parameters was more evident after four-week oral taking of the food additive carrageenan. Conclusion. The increased MCP-1 production in carrageenan-induced gastroenterocolitis may be directly due to the toxic effect of carrageenan on the macrophages of the gastrointestinal tract, development of oxidative stress, as well as due to the stimulating effect of the proinflammatory cytokine TNF-α.

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