Reticuloendothelial system blockade-induced humoral factor depletion and susceptibility to hemorrhagic shock

1978 ◽  
Vol 56 (6) ◽  
pp. 1055-1057 ◽  
Author(s):  
Daniel J. Loegering ◽  
Marlowe J. Schneidkraut
Keyword(s):  
Hemorrhagic Shock ◽  
Host Defense ◽  
Lipid Emulsion ◽  
Reticuloendothelial System ◽  
Humoral Factor ◽  
Phagocytic Index ◽  
Phagocytic Function ◽  
Opsonic Activity ◽  
Circulating Levels ◽  
Increased Susceptibility

This study was carried out to determine if reticuloendothelial system (RES) Mockade-induced depletion of circulating alpha-2-glycoprotein opsonic activity resulted in increased susceptibility to hemorrhagic shock. RES blockade induced by the injection of gelatinized lipid emulsion was associated with a 45.9% decrease in phagocytic index and a 85.7% decrease in plasma alpha-2-glycoprotein opsonic activity. Animals subjected to RES blockade 30 min prior to hemorrhagic shock showed a decrease in time to decompensation and a decrease in maximum shed volume. These results are consistent with the concept that circulating levels of this opsonic protein are important in modulating RES phagocytic function and in host defense to shock.

Humoral factor depletion and reticuloendothelial depression during hemorrhagic shock

1977 ◽  
Vol 232 (3) ◽  
pp. H283-H287
Author(s):  
D. J. Loegering
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Arterial Blood Pressure ◽  
Liver Slice ◽  
Phagocytic Index ◽  
Phagocytic Function ◽  
Opsonic Activity ◽  
Shed Blood ◽  
Arterial Blood

Circulating opsonic activity and reticuloendothelial system (RES) phagocytic function were determined in anesthetized rats subjected to hemorrhagic shock. Animals were hemorrhaged to and maintained at 40 mmHg arterial blood pressure until they spontaneously took back 5% or 40% of the maximum bled volume. The phagocytic index, as determined by colloid clearance kinetics, was decreased in both groups following reinfusion of the shed blood. The reduction in phagocytic index was associated with decreased liver, unchanged spleen, and increased lung test colloid localization. Plasma opsonic activity, as determined by liver slice bioassay, was decreased 50-60% at 5% and 40% uptake of the maximum shed volume, decreased further 15 min after reinfusion in both groups, and tended to recover 1 h after reinfusion in the 5% uptake group. In vitro hepatic phagocytic activity of liver slices from shocked animals in the presence of normal rat plasma was decreased only in the 40% uptake animals after reinfusion when the arterial blood pressure had decreased to 50 mmHg. These data indicate that the depression of RES phagocytic function during hemorrhagic shock is associated with and may be mediated, in part, by decreased circulating opsonic activity.

Reticuloendothelial system function and humoral factor deficiency following acute hemorrhage

1978 ◽  
Vol 56 (2) ◽  
pp. 299-303 ◽  
Author(s):  
Freddie K. Carr ◽  
Daniel J. Loegering
Keyword(s):  
Time Course ◽  
Reticuloendothelial System ◽  
Phagocytic Index ◽  
Opsonic Activity ◽  
Acute Hemorrhage ◽  
Shed Blood ◽  
Factor Deficiency ◽  
Carbon Clearance ◽  
Close Temporal Relationship

The present study has shown that following acute hemorrhage (equivalent to 3% body weight withdrawn over 20 min) in the rat, there is a large reduction (56% of control) in circulating α-2-glycoprotein opsonic activity. The reduction in this plasma opsonic activity was near maximal by the completion of blood withdrawal and was maintained throughout a 2-h hypotension period. There was no trend toward recovery of the opsonic activity when evaluated 15 min following reinfusion of shed blood in animals that were hypotensive for 0, 30, and 120 min. Reticuloendothelial system (RES) phagocytic function, as assessed from the carbon clearance rate (phagocytic index) following reinfusion of the shed blood, was depressed in animals that were hypotensive for 0, 30, and 120 min. Thus, phagocytic index followed a time course similar to the depression of opsonic activity. The observed close temporal relationship between α-2-glycoprotein opsonic deficiency and depression of RES clearance further supports the possible role of a humoral opsonic deficiency in mediating the RES phagocytic depression during circulatory shock.

Clearance rate in relation to agglutinins for gelatin-stabilized colloid in the rat

1963 ◽  
Vol 204 (4) ◽  
pp. 655-659 ◽  
Author(s):  
I. MacKay Murray
Keyword(s):  
Iron Oxide ◽  
Clearance Rate ◽  
Reticuloendothelial System ◽  
Transient Increase ◽  
Clearance Rates ◽  
Time Intervals ◽  
Thorium Dioxide ◽  
Plasma Response ◽  
Circulating Levels

Intravascular clearance rates of gelatin-stabilized gold were compared with circulating titers of gelatin agglutinins in rats at increasing time intervals after blockading injections of gelatin-stabilized gold and S. marcescens endotoxin. The degree and duration of reticuloendothelial system (RES) blockade against the homologous colloid were directly related to the circulating levels of gelatin agglutinins. In contrast, plasma agglutinins were not decreased in endotoxin-induced blockade against the gelatin-stabilized colloid. In a further experiment, the plasma response to blockading injections of colloidal thorium dioxide, iron oxide, and zymosan was characterized by a transient increase in gelatin agglutinins suggesting the nonspecific release of opsonins from an extravascular source. The findings indicated that clearance rates of gelatin-stabilized colloids were dependent on the total available opsonin in the rat rather than the total circulating opsonin. It is suggested that RES blockade is effected by the prior nonspecific depletion of opsonins from an extravascular reserve which is the major component of the total available opsonin.

Electroimmunoassay of alpha-2-opsonic protein during reticuloendothelial blockade

1977 ◽  
Vol 232 (3) ◽  
pp. R80-R87 ◽  
Author(s):  
F. Blumenstock ◽  
P. Weber ◽  
T. M. Saba ◽  
R. Laffin
Keyword(s):  
Serum Concentration ◽  
Phagocytic Activity ◽  
Lipid Emulsion ◽  
Protein Concentration ◽  
Normal Values ◽  
Serum Levels ◽  
Physiological Control ◽  
Opsonic Activity ◽  
Physiological Regulation ◽  
Monospecific Antiserum

Physiological regulation of reticuloendothelial (RE) phagocytic activity by a plasma opsonic factor has been documented. In the recent study, serum levels of this alpha-2-opsonic protein in rats during colloid-induced RE blockade were measured utilizing an electroimmunoassay (Rocket immunoelectrophoresis) with monospecific antiserum to the purified alpha-2-glycoprotein. RE blockade was produced by the intravenous injection of the gelatinized "RE-test-lipid emulsion" at a dose of 50 mg/100 g body wt. The opsonic activity of serum at various intervals during colloid-induced RE blockade as measured by tissue slice bioassay manifested a high correlation (r = 0.98) with the serum opsonic protein concentration as measured by the electroimmunoassay. During RE blockade (30 min), there was a rapid depletion of the opsonic alpha-2-glycoprotein to 20% of the initial preinjection levels. Serum concentration of this glycoprotein remained low for at least 2-3 h after which time its concentration progressively increased with approximation of normal values by 6 h postblockade. Opsonic protein concentration at 24 h postinjection were significantly (P less than 0.05) elevated above controls. Thus, colloid-induced RE blockade is associated with the removal of this glycoprotein from the serum and recovery from RE blockade is accompanied by a restoration of opsonin levels. The electroimmunoassay can provide a sensitive technique to monitor this humoral factor known to exert a physiological control on the RE system.

scholarly journals 2262

2017 ◽  
Vol 1 (S1) ◽  
pp. 4-5
Author(s):  
Derrick Richard Samuelson ◽  
Vincent Maffei ◽  
Eugene Blanchard ◽  
Meng Luo ◽  
Christopher Taylor ◽  
...  
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Microbial Communities ◽  
Intestinal Permeability ◽  
Intestinal Microbiota ◽  
Host Defense ◽  
Intestinal Tract ◽  
Liver Inflammation ◽  
Host Defenses ◽  
Increased Susceptibility

OBJECTIVES/SPECIFIC AIMS: Alcohol consumption perturbs the normal intestinal microbial communities (alcohol dysbiosis). To begin to investigate the relationship between alcohol-mediated dysbiosis and host defense we developed an alcohol dysbiosis fecal adoptive transfer model, which allows us to isolate the host immune response to a pathogenic challenge at a distal organ (ie, the lung). This model system allowed us to determine whether the host immune responses to Klebsiella pneumoniae are altered by ethanol-associated dysbiosis, independent of alcohol use. We hypothesized that alcohol-induced changes in intestinal microbial communities would impair pulmonary host defenses against K. pneumoniae. METHODS/STUDY POPULATION: Mice were treated with a cocktail of antibiotics daily for 2 weeks. Microbiota-depleted mice were then recolonized by gavage for 3-days with intestinal microbiota from ethanol-fed or pair-fed animals. Following recolonization groups of mice were sacrificed prior to and 48 hours post respiratory infection with K. pneumoniae. We then assessed susceptibility to Klebsiella infection by determining colony counts for pathogen burden in the lungs. We also determined lung and intestinal immunology, intestinal permeability, as well as, liver damage and inflammation. RESULTS/ANTICIPATED RESULTS: We found that increased susceptibility to K. pneumoniae is, in part, mediated by the intestinal microbiota, as animals recolonized with an alcohol-induced dysbiotic intestinal microbial community have significantly higher lung burdens of K. pneumoniae (5×104 CFU vs. 1×103 CFU) independent of EtOH. We also found that increased susceptibility in alcohol-dysbiosis recolonized animals was associated with a decrease in the recruitment and/or proliferation of CD4+ and CD8+ T-cells (1.5×109 cells vs. 2.5×109 cells) in the lung following Klebsiella infection. However, there were increased numbers of T-cells in the intestinal tract following Klebsiella infection, which may suggest that T cells are being sequestered in the intestinal tract to the detriment of host defense in the lung. Interestingly, mice recolonized with an alcohol-dysbiotic microbiota had increased intestinal permeability as measured by increased levels of serum intestinal fatty acid binding protein (55 vs. 30 ng/mL). Alcohol-dysbiotic microbiota also increased liver steatosis (Oil Red-O staining) and liver inflammation (>2-fold expression of IL-17 and IL-23). DISCUSSION/SIGNIFICANCE OF IMPACT: Our findings suggest that the commensal intestinal microbiota support mucosal host defenses against infectious agents by facilitating normal immune responses to pulmonary pathogens. Our data also suggest that increased intestinal permeability coupled with increased liver inflammation may impair the recruitment/proliferation of immune cells in the respiratory tract following infection. The role of the microbiota during host defense will be important areas of future research directed at understanding the effects of microbial dysbiosis in patients with AUDs.

RES hyperphagocytosis by rats with streptozotocin-induced diabetes mellitus

1981 ◽  
Vol 240 (3) ◽  
pp. G225-G231
Author(s):  
R. P. Cornell
Keyword(s):  
Body Weight ◽  
Insulin Dose ◽  
Reticuloendothelial System ◽  
Diabetic Rats ◽  
Phagocytic Index ◽  
Control Value ◽  
Colloidal Carbon ◽  
Significant Difference

In contrast to previous studies of neutrophils from diabetic animals and humans in vitro and of macrophages from diabetic humans in vivo, which reported phagocytic depression, reticuloendothelial system (RES) hyperphagocytosis of colloidal carbon was observed in rats at 14 and 28 days after diabetes induction with streptozotocin (STZ). Carbon clearance half times were significantly enhanced to 6.3 +/- 0.79 and 8.1 +/- 1.04 min at 14 and 28 days post-STZ, respectively, compared with the nondiabetic value (12.7 +/- 0.98 min). The severity of uncontrolled STZ-induced diabetes in rats was confirmed by significant hypoinsulinemia, hyperglucagonemia, hyperglycemia, and hyperlipidemia. Although body weights of STZ-diabetic animals declined progressively, liver weights as a percent of body weight increased above the control value at 14 and 28 days post-STZ. In fact, expression of carbon phagocytosis as the corrected phagocytic index, which accounts for changes in liver and spleen weights relative to body weight, eliminated the significant difference between STZ-diabetic and nondiabetic animals. Antibiotic treatment of diabetic rats failed to alter the hyperphagocytosis, implying that a chronic bacterial infection was not the cause of phagocytic stimulation. Daily insulin replacements, but not a single large insulin dose to 14-day post-STZ rats, reversed the enhanced phagocytosis of colloidal carbon.

The three different phases of reticuloendothelial system phagocytic function in rats with liver injury

1988 ◽  
Vol 45 (3) ◽  
pp. 314-319 ◽  
Author(s):  
Shigeki Arii ◽  
Kazunobu Monden ◽  
Shigeyuki Itai ◽  
Tetsu Sasaoki ◽  
Masafumi Shibagaki ◽  
...  
Keyword(s):  
Liver Injury ◽  
Reticuloendothelial System ◽  
Phagocytic Function
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