glycogen and Peritonitis

Topics: Adaptation, Physiological; Burns; Dietary Carbohydrates; Dietary Fats; Dietary Proteins; Enteral Nutrition; Fats; Fractures, Bone; Glycogen; Humans; Metabolic Clearance Rate; Nutrition Disorders; Nutritional Physiological Phenomena; Parenteral Nutrition; Parenteral Nutrition, Total; Peritonitis; Postoperative Care; Postoperative Complications; Proteins

Calcium-binding protein S100A9 (MRP-14) induces antinociceptive effect in an experimental model of painful sensibility and participates of antinociception observed during neutrophilic peritonitis induced by glycogen or carrageenan in mice. In this study, the direct antinociceptive role of the protein S100A9 in neutrophilic cell-free exudates obtained of mice injected with glycogen was investigated. Mice were intraperitoneally injected with a glycogen solution, and after 4, 8, 24, and 48 hours, either the pattern of cell migration of the peritoneal exudate or the nociceptive response of animals was evaluated. The glycogen-induced neutrophilic peritonitis evoked antinociception 4 and 8 hours after inoculation of the irritant. Peritoneal cell-free exudates, collected in different times after the irritant injection, were transferred to naive animals which were submitted to the nociceptive test. The transference of exudates also induced antinociceptive effect, and neutralization of S100A9 activity by anti-S100A9 monoclonal antibody totally reverted this response. This effect was not observed when experiments were made 24 or 48 hours after glycogen injection. These results clearly indicate that S100A9 is secreted during glycogen-induced neutrophilic peritonitis, and that this protein is responsible by antinociception observed in the initial phase of inflammatory reaction. Thus, these data reinforce the hypothesis that the calcium-binding protein S100A9 participates of the endogenous control of inflammatory pain.

Topics: Analgesics; Animals; Antibodies, Monoclonal; Calgranulin B; Cell Movement; Cell-Free System; Glycogen; Leukocytes; Male; Mice; Neutrophils; Pain Measurement; Peritonitis; Time Factors

The effect of alpha-MSH on reactive oxygen species (ROS) production by rat peritoneal neutrophils and the effect of cyclooxygenase (COX) inhibition were investigated using the chemiluminescence (CL) technique. Cells were obtained by peritoneal lavage 4h after administration of oyster glycogen to rats and were stimulated with lipopolysaccharide (LPS) from Salmonella enderitidis and phorbol 12-myristate 13-acetate (PMA). The increasing concentrations of alpha-MSH (10(-12)-10(-6) M) were added to stimulated cells alone or along with the COX inhibitors indomethacin, ketorolac or nimesulide (10(-8)-10(-5) M). Luminol and lucigenin CL levels were significantly increased in cells stimulated with LPS and PMA compared to unstimulated ones. alpha-MSH significantly reduced lucigenin CL values and this effect was completely reversed in the presence of indomethacin (10(-8) and 10(-7) M). In conclusion, alpha-MSH inhibits the production of superoxide radicals by activated rat peritoneal neutrophils and COX contributes to this effect.

Topics: alpha-MSH; Animals; Carcinogens; Cyclooxygenase Inhibitors; Enzyme Repression; Glycogen; Lipopolysaccharides; Neutrophil Activation; Neutrophils; Ostreidae; Peritonitis; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Tetradecanoylphorbol Acetate

We previously reported that neutrophils produce sulfite in response to stimulation with lipopolysaccharide, and sulfite production is dependent on inorganic sulfate contained in culture media. Microorganisms such as yeast assimilate sulfate, during which process sulfite is generated by reduction of 3'-phosphoadenosine 5'-phosphosulfate (PAPS), an activated sulfate donor. However, little is known about how sulfite is produced in mammalian cells. In the current study, we demonstrated that chlorate, a specific inhibitor for PAPS synthesis, significantly suppressed production of sulfite by activated neutrophils obtained from rat peritoneal cavity that had been injected with glycogen to induce inflammation. Addition of excess amounts of PAPS could partially overcome the inhibitory effect of chlorate. Moreover, sulfite production from PAPS was clearly demonstrated in the cytosolic fraction of activated neutrophils. These findings strongly suggest that sulfite is generated, at least in part, from PAPS by activated neutrophils.

Topics: Animals; Chlorates; Cytosol; Glycogen; Male; Neutrophil Activation; Neutrophils; Peritoneal Cavity; Peritonitis; Phosphoadenosine Phosphosulfate; Rats; Rats, Wistar; Sulfites

Patients with malnutrition are susceptible to infection. Polymorphonuclear neutrophils (PMNs) are the major effector of the nonspecific immune response in host resistance to infection. Dietary restriction may impair PMN-mediated immunity in the peritoneal cavity by reducing PMN exudation, adhesion molecule expression on PMNs, and chemokine production.. Randomized study of murine glycogen-induced peritonitis with dietary restriction.. University research laboratory.. Male C57BL/6J mice.. Mice (N = 204) were assigned to ad libitum, moderate, and severe diet-restricted groups receiving mouse chow ad libitum (132 g/kg, 66 g/kg, and 33 g/kg daily for 7 days, respectively). After dietary restriction with or without 1 day of refeeding, mice were administered glycogen intraperitoneally to induce cell exudation.. CD11b, CD18, and CD62L expressions on circulating PMNs, phagocytosis, and reactive oxygen intermediate production by exudative PMNs were measured after glycogen installation. The levels of PMN-specific chemokine, macrophage inflammatory protein 2 (MIP-2), in peritoneal lavage fluid were also measured. These parameters were measured after glycogen installation in the refeeding experiment.. Seven days of dietary restriction decreased CD11b/CD18 expression on circulating PMNs, MIP-2 levels in peritoneal lavage fluid, and subsequent PMN exudation into the peritoneal cavity early in peritonitis. Both CD11b and CD18 expression on circulating PMNs and MIP-2 levels correlated significantly with numbers of exudative PMNs. Seven days of dietary restriction also impaired phagocytosis, while up-regulating reactive oxygen intermediate production by exudative PMNs. Only 1 day of ad libitum refeeding normalized CD11b/CD18 expression with PMN exudation into the peritoneal cavity.. Short-term dietary restriction impairs PMN exudation into local inflammatory sites in murine peritonitis by reducing CD11b/CD18 expression and MIP-2 production. Even brief nutritional replenishment in diet-restricted patients may improve host defense via restoring these PMN functions and chemokine production at local inflammatory sites.

Topics: Animals; CD18 Antigens; Chemokine CXCL2; Chemokines; Glycogen; Immune Tolerance; L-Selectin; Macrophage-1 Antigen; Male; Mice; Mice, Inbred C57BL; Neutrophils; Peritoneal Lavage; Peritonitis; Phagocytosis; Starvation

We characterized the relative biological activity and expression of two murine chemokines that may serve as functional homologues for human IL-8, KC, and macrophage inflammatory protein 2 (MIP2). Recombinant chemokines were produced in bacterial expression systems and antibodies specific for KC or MIP2 were raised. In vitro assays showed that KC elicited 4-fold greater neutrophil chemotaxis compared with MIP2, while MIP2 elicited significantly greater release of elastase. Lipopolysaccharide- (LPS) stimulated macrophages (8 h) secreted more MIP2 (approximately 10 ng/mL) compared with KC (approximately 4 ng/ml) and expression of either murine chemokine was independent of TNFalpha or IL-1beta production. Thioglycollate (thio) and glycogen (gly) induced peritonitis produced more KC (thio = 7.1 and gly = 2.5 ng/mL) in the peritoneum compared with MIP2 (thio = 4.5 and gly = 0.3 ng/mL). Plasma KC levels were very high after either challenge (approximately 24 ng/mL), which was >50-fold more than the systemic increase in MIP2 (approximately 0.3 ng/mL). Our data demonstrate that while KC and MIP2 have similar in vitro production characteristics, KC appears to be a more potent and systemically distributed chemokine during acute in vivo inflammation, while MIP2 expression appears limited to localized expression.

Topics: Animals; Blotting, Western; Chemokine CXCL1; Chemokine CXCL2; Chemokines; Chemokines, CXC; Chemotactic Factors; Chemotaxis, Leukocyte; Enzyme-Linked Immunosorbent Assay; Gene Expression Regulation; Glycogen; Growth Substances; Intercellular Signaling Peptides and Proteins; Interleukin-6; Leukocyte Elastase; Lipopolysaccharides; Macrophage Activation; Macrophages, Peritoneal; Mice; Mice, Inbred BALB C; Models, Animal; Neutrophils; Peritonitis; Rabbits; Recombinant Fusion Proteins; Thioglycolates; Tumor Necrosis Factor-alpha

Matrix metalloproteinase (MMP)-9 plays an important role in neutrophil extravasation and migration by its ability to degrade the major components of basement membrane. To evaluate the expression of neutrophil MMP-9 under inflammatory conditions, we examined the levels of MMP-9 and its mRNA in neutrophils of glycogen-induced peritoneal inflammation.. Male Hartley guinea pigs weighing 250-300 g were intraperitoneally injected with 0.17% glycogen solution, and 13-15 h after the injection, blood and peritoneal neutrophils were isolated. The levels of MMP-9 and its mRNA were analyzed by gelatin zymography and Northern blotting, respectively. Furthermore, MMP-9 activities in the peritoneal supernatants were measured.. MMP-9 level in peritoneal neutrophils was essentially the same as that in blood neutrophils, although peritoneal neutrophils were assumed to have extracellularly released MMP-9 from the granules during infiltration into the peritoneal cavity. Interestingly, MMP-9 mRNA was expressed more abundantly in peritoneal neutrophils than in blood neutrophils (p<0.01). Moreover, MMP-9 levels in blood and peritoneal neutrophils were reduced to 30-45% of non-treated controls by actinomycin D (500 microg/kg) or cycloheximide (10 mg/kg)-treatment (p<0.05). In contrast, MMP-9 activity increased in the peritoneal supernatants of glycogen-injected animals was not significantly affected by actinomycin D- or cycloheximide-treatment. In addition, when blood neutrophils of non-injected animals were stimulated with 10(-7) M N-formyl-Met-Leu-Phe, 10 microg/ml lipopolysaccharide, 10 ng/ml phorbol 12-myristate 13-acetate, 10(-8) M IL-8 or 100 U/ml tumor necrosis factor-a, expression of MMP-9 mRNA was markedly increased (p<0.05).. The present observations indicate that MMP-9 gene is transcribed, and MMP-9 protein is synthesized in neutrophils during glycogen-injected peritoneal inflammation. Moreover, it is likely that MMP-9 protein in the peritoneal supernatants is mostly derived from preformed MMP-9 which is stored in the neutrophil granules and extracellularly released during infiltration of neutrophils into the peritoneal cavity. Finally, the transcription of MMP-9 gene can be upregulated in neutrophils by stimulation with inflammatory mediators, even after neutrophils have been matured.

Topics: Animals; Cycloheximide; Dactinomycin; Gene Expression; Glycogen; Guinea Pigs; Lipopolysaccharides; Male; Matrix Metalloproteinase 9; N-Formylmethionine Leucyl-Phenylalanine; Neutrophils; Nucleic Acid Synthesis Inhibitors; Peritonitis; Protein Synthesis Inhibitors; RNA, Messenger; Tetradecanoylphorbol Acetate; Tumor Necrosis Factor-alpha

Several recent studies have suggested that nitric oxide (NO) derived from the inducible isoform of NO synthase (NOS) may act as an endogenous modulator of the inflammatory response by inhibiting adhesion of leukocytes to endothelial cells in vitro. Few studies have addressed specifically the role of iNOS in regulating leukocyte recruitment in vivo in a model of acute inflammation. Thus, the objective of this study was to assess the role of iNOS in modulating neutrophil (PMN) extravasation in an oyster glycogen-induced model of acute peritonitis in rats. Data obtained in the present study demonstrates that injection (IP) of oyster glycogen induces massive and selective PMN recruitment into the peritoneal cavity of rats at 6 hrs following OG administration. These extravasated cells were found to contain significant amounts of iNOS protein as assessed by Western blot analysis. Treatment of rats with the selective iNOS inhibitor L-iminoethyl-lysine (L-NIL) dramatically reduced NO levels in lavage fluid as measured by decreases in nitrate and nitrite concentrations without significantly affecting iNOS protein levels. Although L-NIL inhibited NO production by >70%, it did not alter oyster glycogen-induced PMN recruitment when compared to vehicle-treated rats. We conclude that PMN-associated, iNOS-derived NO does not play an important role in modulating extravasation of these leukocytes in this model of acute inflammation.

Topics: Acute Disease; Animals; Ascitic Fluid; Blotting, Western; Cell Movement; Disease Models, Animal; Enzyme Induction; Female; Glycogen; Inflammation; Lysine; Neutrophils; Nitrates; Nitric Oxide; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Nitrites; Ostreidae; Peritonitis; Rats; Rats, Inbred Lew

Requirements for cytokines and adhesion molecules for peritoneal neutrophil recruitment during glycogen-induced peritonitis in rats were systematically defined.. Male Long Evans rats (275-300 g).. Four hours after intraperitoneal injection of 25 mg oyster glycogen, neutrophilic exudates were harvested. Effects of blocking reagents (injected intravenously) to rat E-, L- and P-selectins, beta1 (VLA-4) and beta2 integrins (LFA-1 and Mac-1), ICAM-1, and the cytokines TNFalpha, IL- and IL-8 were assessed.. Administration of synthetic sialyl Lewis(x) oligosaccharide reduced neutrophil recruitment to the peritoneum by 26%. Antibody to E-selectin reduced neutrophil accumulation by 71%, while anti-L-selectin reduced neutrophil accumulation by 59%, and anti-P-selectin was without an effect. Similar patterns of inhibition were found when selectin-Ig chimeras were employed. Antibodies to LFA-1 (CD11a), Mac-1 (CD11b) or CD18 reduced neutrophil accumulation by 62 percent, 59 percent and 86%, respectively, while anti-VLA-4 was without effect. Anti-ICAM-1 reduced cell influx by 65%. IL-1 receptor antagonist and antibodies to IL-1 and human IL-8 reduced neutrophil accumulation by 43alpha, 40% and 62 percent, respectively. Unexpectedly, blockade of TNFalpha had no effect.. These studies identify requirements for selectins, beta2 integrins, IL-1 and a rat chemokine(s) similar to human IL-8 for neutrophil recruitment during glycogen-induced peritonitis. The lack of participation of VLA-4, P-selectin and TNFalpha suggests organ-specific cytokine and adhesion molecule requirements for neutrophil recruitment.

Topics: Animals; Antibodies; CD18 Antigens; Cell Adhesion Molecules; Cytokines; E-Selectin; Glycogen; Humans; Integrin beta1; Intercellular Adhesion Molecule-1; L-Selectin; Male; P-Selectin; Peritoneal Cavity; Peritonitis; Rats

Macrophages secrete a variety of chemical mediators that play a central role in the pathophysiology of inflammatory pain. Therefore, the activation or deactivation of these cells in an inflammatory focus could modulate the intensity of the algogenic response. Based on these premises and on our previous demonstration that the calcium-binding protein MRP-14, highly expressed in neutrophils, deactivates activated macrophages in vitro, we decided to investigate the role of MRP-14 and of neutrophils in the control of inflammatory pain in mice. Our results show that this protein is endowed with antinociceptive activity. When tested in the writhing model it was able to inhibit pain response but did not change the behavior of the animals in the hot plate test. This observation indicates that MRP-14 down-regulates inflammatory but not central pain. Using a model of acute neutrophilic peritonitis induced by glycogen, a close correlation between neutrophil migration and antinociception was detected. Surgical adrenalectomy demonstrated that the antinociceptive response induced by glycogen was not due to endogenous liberation of glucocorticoids. The treatment of animals either with a monoclonal antibody anti-MRP-14 or a monoclonal antibody that depletes the animals of neutrophils reverts the antinociceptive response observed in the glycogen-induced peritonitis. These data define the calcium-binding protein MRP-14 as a novel mediator for the control of inflammatory pain and consequently discloses an anti-inflammatory role for the neutrophil.

Topics: Abdomen; Adrenalectomy; Animals; Antibodies, Monoclonal; Antigens, Differentiation; Behavior, Animal; Calcium-Binding Proteins; Calgranulin A; Calgranulin B; Cell Movement; Glycogen; Hot Temperature; Irritants; Macrophages; Male; Mice; Neutrophils; Nociceptors; Pain; Peritonitis

In order to study the regulation of cellular 5-lipoxygenase activity under inflammatory conditions, the effects of inflammatory exudates on rat leukocyte 5 lipoxygenase activity were investigated.. Peritoneal leukocytes and inflammatory exudates were collected from glycogen treated rats.. Glycogen (1 g/kg body weight, in a final volume of 3 ml PBS) was injected intraperitoneally into male Wistar rats. After 4 h, the inflammatory exudate was collected.. Rat peritoneal leukocytes were isolated and the cellular 5-lipoxygenase activity was determined by HPLC after cell stimulation with calcium ionophore A23187.. Inflammatory exudates from glycogen treated animals strongly inhibited cellular 5-lipoxygenase activity of ionophore challenged leukocytes. Albumin was identified as the inhibitor in exudates. Inhibition of cellular 5-lipoxygenase activity by albumin was pH-dependent and was strongly increased by the alkaline pH (7.9-8.0) of the exudate. The albumin effect increased in the range of pH 7.4-8.2 where albumin undergoes a conformational change called neutral to base (N-B) transition. S-Carboxymethyl-albumin had a similar activity to that of albumin, which indicated that the free SH-group at Cys-34 of albumin is not necessary for the effect. The albumin dimer showed a significantly higher inhibition than albumin and it suppressed cellular 5-lipoxygenase activity by 98%. Peptic and tryptic fragments of albumin which comprise domains I, II and II, III, respectively, were less active or inactive. Thus, an intact albumin molecule or the dimer are required for efficient inhibition of cellular 5-lipoxygenase activity.. Our data suggest that during inflammation, albumin extravasation and changes in pH-value are involved in the regulation of the inflammatory reaction by suppression of leukotriene release.

Topics: Animals; Arachidonate 5-Lipoxygenase; Ascitic Fluid; Cattle; Enzyme Inhibitors; Glycogen; Humans; Hydrogen-Ion Concentration; Leukocytes; Lipoxygenase Inhibitors; Male; Peptide Fragments; Peritoneal Lavage; Peritonitis; Rats; Rats, Wistar; Serum Albumin; Serum Albumin, Bovine

Glucocorticoids are potent anti-inflammatory and immunosuppressive therapeutic agents. The protective effect of dexamethasone (DEX) on hepatic phosphoenolpyruvate carboxykinase (PEPCK) transcript level, hepatic NF-kB (nuclear factor-kB) activation, and serum tumor necrosis factor alpha (TNF) formation was investigated in peritoneal sepsis induced by cecal incision in rats. For the control the rats were sham-operated with laparotomies only. Each group (N = 6) was pretreated with either normal saline (NS) or DEX before surgery (NS/Sham, NS/Sepsis, DEX/Sham, and DEX/Sepsis). At 3 hr post cecal incision, DEX treatment inhibited sepsis-induced hepatic NF-kB activation by 23%, suppressed circulating TNF by 50%, reduced serum glucose by 36%, reduced hepatic glycogen depletion by 76%, and attenuated PEPCK mRNA level. These findings suggested that DEX treatment was beneficial in attenuating glucose dyshomeostasis and significantly inhibited two sepsis-induced inflammatory mediators, NF-kB and TNF, in the early phase of peritoneal sepsis. However, in the late (6 hr) septic phase, DEX treatment inhibited serum TNF by 69%, but had no effect on NF-kB activation, glycogen depletion, and PEPCK mRNA level suggesting liver function failure injury.

Topics: Animals; Base Sequence; Blood Glucose; Blotting, Northern; Dexamethasone; Disease Models, Animal; Gene Expression Regulation; Glucocorticoids; Glucose; Glycogen; Homeostasis; Liver; Male; NF-kappa B; Nuclear Proteins; Oligonucleotide Probes; Peritonitis; Phosphoenolpyruvate Carboxykinase (ATP); Rats; Rats, Sprague-Dawley; RNA, Messenger; Time Factors; Tumor Necrosis Factor-alpha

Smoke inhalation causes injuries to lung airways, and, at times, alveolar inflammation also develops over approximately 24 h. The pathophysiology of parenchymal lung injuries is unknown, and it is often fatal. We hypothesized that an inflammatory stress remote from the smoke-related lung insult was required for development of alveolar injuries. Spontaneously breathing rats were exposed, head only, to smoke generated by nonflaming pyrolysis (smoldering) of Douglas fir wood (DF), polyvinylchloride (PVC), or the combination of DF+PVC. Intraperitoneal injection of sterile oyster shell glycogen 4 h before smoke inhalation was used as an extra inflammatory stimulus. Histologic examinations revealed extensive airway inflammation in all smoke-exposed groups. Glycogen peritonitis alone caused no lung injuries, and in the absence of glycogen, smoke inhalation caused neither parenchymal lung injuries, assessed by [125I]bovine serum albumin (BSA) leakage, nor neutrophil infiltration, quantified by myeloperoxidase (MPO) activity. However, in rats pretreated with glycogen and studied 24 h after exposure to smoke from burning DF+PVC, [125I]BSA permeability was increased by 232 +/- 41% (SE; n = 13), MPO activity was increased 5-fold, from 2.6 +/- 0.4 (n = 7) to 13.9 +/- 1.4 (n = 19) A460/min/g lung, and histopathologic findings included extensive pulmonary inflammation. We conclude that inhalation of certain types of smoke will trigger pulmonary injury when an inflammatory process remote from the lungs is present.

Topics: Analysis of Variance; Animals; Blood Gas Analysis; Bronchoalveolar Lavage Fluid; Capillary Permeability; Fires; Glycogen; Inflammation; Male; Neutrophils; Peritonitis; Peroxidase; Polyvinyl Chloride; Pulmonary Alveoli; Rats; Rats, Inbred F344; Serum Albumin, Bovine; Smoke Inhalation Injury; Stress, Physiological; Wood

Soluble phospholipase A2 (PLA2) activity was assessed in rat peritoneal lavage fluid after an intraperitoneal injection of 6% glycogen. Enzyme activity immediately increased 5-fold above basal by 4 h. Activity decreased by only 30% at 18 h and remained at this elevated level through 72 h. The initial rise in PLA2 activity was coincident with protein extravasation but not with polymorphonuclear leukocyte infiltration, suggesting that the early PLA2 activity could be, in part, blood-derived. Mononuclear cell influx occurred later (4 h), peaked by 6-8 h but remained elevated through 72 h possibly contributing to the persistence of PLA2 activity through 20-72 h. The exudate PLA2 measured at 4-6 h (early) and 20-24 h (late), after glycogen administration, were biochemically compared. They were found to be neutral pH active, Ca(2+)-dependent and were similarly inhibited by the inhibitors, p-bromophenacylbromide, ellagic acid, gossypol and luffariellolide. Oral administration of dexamethasone to rats inhibited the appearance of PLA2 activity in the peritoneal lavage fluid as well as cellular influx and protein extravasation. Indomethacin had no effect on these parameters. These studies demonstrate that PLA2 is an integral component of glycogen-induced peritonitis and can be pharmacologically manipulated.

Topics: Animals; Cell Movement; Dexamethasone; Female; Glycogen; Indomethacin; Injections, Intraperitoneal; Peritonitis; Phospholipases A; Phospholipases A2; Rats; Rats, Wistar

To determine whether extrapulmonary infection alters antibacterial defenses of the lung, we challenged mice with peritonitis due to Escherichia coli by aerosol inhalation with either Staphylococus aureus or Pseudomonas aeruginosa. In animals without peritonitis, 14% +/- 5% and 11% +/- 1% of the initially deposited viable S. aureus and P. aeruginosa, respectively, remained in the lungs at 4 hr. In contrast, in mice with peritonitis, at 4 hr 45% +/- 9% of the staphylococci were recoved, and the P. aeruginosa had increased to 948% +/- 354% of the initial inoculum. Proliferation of P. aeruginosa in mice with peritonitis was associated with impaired recruitment of polymorphonuclear neutrophils (PMNs) into the lungs. In contrast, a noninfectious stimulus induced more PMNs into the peritoneal cavity than did intraabdominal sepsis but only minimally impaired PMN recruitment into the lungs after aerosol challenge with P. aeruginosa. Sterile intraperitoneal stimulation did not significantly impair intrapulmonary killing of P. aeruginosa. Levels of antigenic C3 and functionally active C5 were significantly depleted in mice with peritonitis due to E. coli. We conclude that the systemic effects of sepsis, including complement depletion, contribute to the decreased pulmonary PMN recruitment and to impaired intrapulmonary bacterial killing of animals with peritonitis due to E. coli.

Topics: Animals; Caseins; Complement C3; Complement C5; Escherichia coli Infections; Female; Glycogen; Lung; Lung Diseases; Macrophages, Peritoneal; Mice; Neutrophils; Peritoneal Cavity; Peritonitis; Pseudomonas Infections; Staphylococcal Infections

A chemotactic factor for tumor cells was found in inflammatory exudate fluids induced by giving intraperitoneal injections of glycogen to Sprague-Dawley rats. The quantity of chemotactic activity and the period of time during which it could be detected correlated with the inflammatory reaction, measured by the cellular composition of the exudates and their content of protein and lysosomal enzymes. In gel filtration the chemotactic factor behaved mainly as a molecule having a molecular weight of approximately 6000 daltons. Its biologic activity was blocked by antiserums directed against C5 but not by antiserums against C3 or C4. In these two respects, the factor generated in vivo has the same properties as a previously described chemotactic factor that can be generated in vitro by proteolysis of purified C5 or C5a. Chemotactic activity was not detected in the glycogen-induced peritoneal exudates of rats depleted of serum complement by cobra venom factor. Intravenously injected Walker tumor cells arrested and formed metastases in the mesenteries of rats with peritonitis in greater numbers than in normal controls, animals depleted of complement during the experimental period, or animals given intraperitoneal injections of the vasopermeability agent, histamine. The growth of tumor cells in vitro was not promoted by peritoneal exudate fluids, nor was the number of metastases on vivo greater than in negative controls, in animals in which peritonitis was induced 24 hours after the intravenous injection of tumor cells. It is argued that chemotactic mechanisms can contribute to the formation of metastases at sites of tissue injury.

Topics: Animals; Antibodies; Carcinoma 256, Walker; Cell Movement; Cells, Cultured; Chemotactic Factors; Chromatography, Gel; Complement C5; Exudates and Transudates; Female; Glycogen; Neoplasm Metastasis; Neoplasm Transplantation; Neoplastic Cells, Circulating; Peritonitis; Rats; Rats, Inbred Strains; Time Factors

The functional and metabolic properties of neutrophils in white mice were studied in the course of streptococcal peritonitis and after treatment by the intraperitoneal injection of normal rabbit serum, antitryptic and antikallikrein immune sera and inhitryl. Protease inhibitors were shown to activate the bactericidal and phagocytic activity of neutrophils, to normalize oxidation processes and to enhance the metabolism of glycogen.

Topics: Animals; Cytoplasm; Drug Evaluation, Preclinical; Glycogen; Leukocytes; Mice; Neutrophils; Oxidoreductases; Peritonitis; Phagocytosis; Protease Inhibitors; Streptococcal Infections

To establish whether local inhibition of emigration or a centrally acting mechanism is responsible for the diminished response to a second inflammatory stimulus, three groups of young adult male Sprague-Dawley rats received in intrapleural injections of glycogen followed 4 h later by intra-peritoneal Beef Heart Infusion/protease Peptone. Two, 4 and 8 h after the second injection cell counts were made on both the pleural and peritoneal effusions. Circulating PMNs were also monitored using tail vein blood. The prior injection of glycogen intrapleurally significantly suppressed the subsequent accumulation of peritoneal PMNs in response to the second stimulus. The mechanism of this suppression is discussed.

Topics: Animals; Caseins; Cell Movement; Glycogen; Injections; Injections, Intraperitoneal; Leukocyte Count; Male; Neutrophils; Peptide Fragments; Peritonitis; Pleura; Rats

In exsudate cells separated from serous body cavities of 29 tumour patients and 30 patients with inflammatory and congestive effusion in cardiac failure or liver cirrhosis respectively the activities of acid and alkaline phosphatase were determined. In addition to sudanophilia the cell content of glycogen and that of ribonucleinic acid were evaluated. By means of cytochemical findings it could be found that an increase of unspecific esterase, acid phosphatase and ribonucleic acid in atypical cells points to a malignous ethiology of the exudate.

Topics: Acid Phosphatase; Alkaline Phosphatase; Ascitic Fluid; Esterases; Exudates and Transudates; Glycogen; Heart Failure; Histocytochemistry; Hodgkin Disease; Humans; Leukemia; Liver Cirrhosis; Lymphoma, Large B-Cell, Diffuse; Neoplasms; Peritonitis; Pleural Effusion; Pleurisy; RNA

Polymorphonuclear neutrophilic leukocytes of the dog, cat, and goat release leukocytic pyrogen under the same conditions as the heterophile polymorphonuclear leukocytes of the rabbit. The characteristics of the febrile response to an intravenous injection of homologous leukocytic pyrogen in all four species are very similar: a brisk monophasic fever reaching a peak between 30 and 50 min with smooth defervescence to the baseline by 3 hr. Shivering, which is not obvious in the rabbit, is noted in the dog, cat, and goat during the first 30 min. Quantitative differences in response reveal the cat to be the most sensitive of of these species to homologous leukocytic pyrogen, followed by the rabbit, dog, and goat. The response to heterologous pyrogen is in most cases markedly diminished compared to that after equal doses of homologous protein, suggesting the operation of species specificity, although canine and feline pyrogen behaved very similarly in all tests. Species specificity of leukocytic pyrogen is probably related to amino acid substitutions in different species of a common mammalian protein effector molecule.

Topics: Animals; Cats; Dogs; Fever; Glycogen; Goats; Leukocytes; Neutrophils; Peritonitis; Pyrogens; Rabbits; Species Specificity

Topics: Acid Phosphatase; Animals; Autoradiography; Cell Differentiation; DNA; Female; Glycogen; Leukocytes; Macrophages; Male; Mice; Peritonitis; Thymidine; Tritium

Topics: Animals; Dogs; Glycogen; Histocytochemistry; Intestinal Obstruction; Liver; Paralysis; Peritonitis; Phosphoric Monoester Hydrolases

Topics: Animals; Dextrans; Glucose; Glycogen; Guinea Pigs; Lactates; Leukocytes; Peritonitis