Thiaminpyrophosphatase bei der experimentellen Diphtherieintoxikation

Summary The determinations of thiamine pyrophosphatase activity were carried out in the liver homogenates of normal guinea-pigs and those poisoned with diphtheria toxin.The enzyme activity in the toxaemic liver tissue is twice that of normal guinea-pigs. It is supposed that this result may partly explain the increased level of pyruvic acid in the blood of patients with diphtheria. Further studies on this problem are under way.     

Studies on the relationships between biotin and the behaviour of B and T lymphocytes in the guinea-pig

Summary In biotin-deficient guinea-pigs the number of circulating neutrophils is increased; lymphocytes carrying B and T markers are decreased. Incubation with biotin increases significantly the number of lymphocytes carrying B and T markers, from biotin-deficient guinea-pigs; no increase was observed when the lymphocytes from normal guinea-pigs were incubated.     

Hemagglutination of neuraminidase-treated human erythrocytes by Leishmania enriettii infected guinea-pig sera.

Sera from guinea-pigs infected with the protozoan parasite Leishmania enriettii showed higher hemagglutination (HA) titres for neuraminidase treated human erythrocytes than those of normal guinea-pig sera. This HA activity was associated mostly with the 19S fraction of the immune serum and could be absorbed out with an antigenic fraction of the parasite membrane. Antigenic determinants involved in this HA reaction consisted of, at least, beta-D-galactosyl or lactosyl residues.     

From immune response to cancer: a spot on the low molecular weight protein tyrosine phosphatase

Reversible tyrosine phosphorylation is a key posttranslational regulatory modification of proteins in all eukaryotic cells in normal and pathological processes. Recently a pivotal janus-faced biological role of the low molecular weight protein tyrosine phosphatase (LMWPTP) has become clear. On the one hand this enzyme is important in facilitating appropriate immune responses towards infectious agents, on the other hand it mediates exaggerated inflammatory responses toward innocuous stimuli. The evidence that LMWPTP plays a role in oncological processes has added a promising novel angle. In this review we shall focus on the regulation of LMWPTP enzymatic activity of signaling pathways of different immunological cells, the relation between genetic polymorphism of LMWPTP and predisposition to some type of inflammatory disorders and the contribution of this enzyme to cancer cell onset, growth and migration. Therefore, the LMWPTP is an interesting target for pharmacological intervention, thus modifying both inappropriate cellular immune responses and cancer cell aggressiveness. Received 15 August 2008; received after revision 06 October 2008; accepted 14 October 2008     

Lymphocyte reactivity in Imuran-treated guinea-pigs and in vitro effect of colchicine

Summary Imuran treatment significantly diminished macrophage migration inhibition in immunized guinea-pigs and the percentage of E-rosette forming cells in all treated animals. 10^–6 M colchicine in vitro significantly increased the percentage of E-rosette forming cells in Imuran-treated animals. The results suggest possible alteration of the lymphocyte receptors after treatment with Imuran.This work was supported by the grants of the Republic Research Fund of Serbia.     

Action d'une irradiation générale sur les échanges d'eau entre le sang et la cavité gastrique pendant l'absorption du glucose

Summary A sublethal dose of X-rays, delivered to guinea-pigs 14 days before a glucose absorption test, alters the pattern of water exchange between the blood and the gastric cavity. The normal dilution, which proves to be a main factor in the regulation of the intestinal absorption of sugar, is no longer achieved.     

Effect of aldosterone and methylprednisolone on cardiac NaK-ATPase.

Aldosterone (15 microgram BID) and methylprednisolone (8 mg QD) administration to female guinea-pigs augmented both the total and the specific activity of NaK-ATPase but not the activity of adenylate cyclase in the cardiac sarcolemma. The rise in NaK-ATPase was due to increase in the number of enzyme molecules; catalytic activity and ouabain-sensitivity of individual molecules did not change.     

Superiority of human complement for assaying bacterial lipopolysaccharides by their anticomplementary activity.

In assaying bacterial lipopolysaccharides (LPS) for anticomplementary activity, human complement (C) allowed detection of approximately 200 times smaller amounts of LPS than guinea-pigs C. Pig C was slightly inferior to human.     

Hemagglutination of neuraminidase-treated human erythrocytes byLeishmania enriettii infected guinea-pig sera

Summary Sera from guinea-pigs infected with the protozoan parasiteLeishmania enriettii showed higher hemagglutination (HA) titres for neuraminidase treated human erythrocytes than those of normal guinea-pig sera. This HA activity was associated mostly with the 19S fraction of the immune serum and could be absorbed out with an antigenic fraction of the parasite membrane. Antigenic determinants involved in this HA reaction consisted of, at least, -d-galactosyl or lactosyl residues.     

Destruction of the platelet aggregating activity of ristocetin A

Hydrolysis of ristocetin A in 0.1 N HCl at 37 degrees C for 2 h resulted in the loss of its ability to induce platelet aggregation in platelet-rich plasma derived from guinea-pigs and humans. However its antibiotic activity against Staph. aureus was not lost.     

Trigeminal stimulation modulates vestibular unitary activity

Summary 139 vestibular neurons were analyzed in 38 guinea-pigs after the stimulation of trigeminal fibers: increase or decrease of discharge rate and also rhythmic modulation of vestibular unitary activity were observed.This work was supported by grants of MPI and CNR.     

Type III (Arthus) allergic reactions and endotoxin toxicity in guinea-pigs.

Lipoplysaccharide (endotoxin) from E. coli cells produced lethal effects in guinea-pigs. Endotoxin caused no visible dermal change in normal animals, but produced skin reactions characterized by specific Arthus-type (Type III immune hypersensitivity) vascular inflammation in immunized animals. It is concluded that Arthus allergic reactions were evoked by endotoxin, however, endotoxin lethal toxicity appears independent of this process.     

Destruction of the platelet aggregating activity of ristocetin A

Summary Hydrolysis of ristocetin A in 0.1 N HCl at 37°C for 2 h resulted in the loss of its ability to induce platelet aggregation in platelet-rich plasma derived from guinea-pigs and humans. However its antibiotic activity againstStaph. aureus was not lost.This work was supported, in part, by a contract from the National Heart, Lung, and Blood Institute (USPHS).     

The absence of an inhibitory effect of metyrapone (2-methyl-1,2-di (3-pyridyl) propan-1-one) on hepatic microsomal hydroxylation in scurvy.

Microsomes from livers of scorbutic guinea-pigs showed a reduced rate of acetanilide hydroxylation. The response of "scorbutic" liver microsomes to the inhibitor Metyrapone (2-methyl-1,2 di (3-pyridyl) propan-1-one) was different from that of liver microsomes from non-scorbutic guinea-pigs.     

Type III (Arthus) allergic reactions and endotoxin toxicity in guinea-pigs

Summary Lipopolysaccharide (endotoxin) fromE. coli cells produced lethal effects in guinea-pigs. Endotoxin caused no visible dermal change in normal animals, but produced skin reactions characterized by specific Arthus-type (Type III immune hypersensitivity) vascular inflammation in immunized animals. It is concluded that Arthus allergic reactions were evoked by endotoxin, however, endotoxin lethal toxicity appears independent of this process.Acknowledgment. Supported by a grant from the National Health and Medical Research Council of Australia.     

Leukocyte recruitment in atherosclerosis: Potential targets for therapeutic approaches?

Atherosclerosis is a complex inflammatory disease involving cellular migration and interaction. Vascular injury in response to different cardiovascular risk factors enhances endothelial dysfunction, which in turn promotes the expression of inflammatory markers and transendothelial leukocyte migration. Recruitment of leukocytes from the blood stream into the vessel intima is a crucial step for the development of the disease. Recent findings have highlighted the role of chemokines, chemokine receptors, adhesion molecules, and gap junctions in this process by acting as chemoattractant, adhesive, or intercellular communication molecules. In this short review, we summarize new data concerning the different steps from leukocyte arrest to transendothelial migration and discuss potential new therapeutic approaches concerning these processes. Received 15 March 2006; received after revision 19 May 2006; accepted 13 June 2006     

Reverse transendothelial cell migration in inflammation: to help or to hinder?

The endothelium provides a strong barrier separating circulating blood from tissue. It also provides a significant challenge for immune cells in the bloodstream to access potential sites of infection. To mount an effective immune response, leukocytes traverse the endothelial layer in a process known as transendothelial migration. Decades of work have allowed dissection of the mechanisms through which immune cells gain access into peripheral tissues, and subsequently to inflammatory foci. However, an often under-appreciated or potentially ignored question is whether transmigrated leukocytes can leave these inflammatory sites, and perhaps even return across the endothelium and re-enter circulation. Although evidence has existed to support “reverse” transendothelial migration for a number of years, it is only recently that mechanisms associated with this process have been described. Here we review the evidence that supports both reverse transendothelial migration and reverse interstitial migration within tissues, with particular emphasis on some of the more recent studies that finally hint at potential mechanisms. Additionally, we postulate the biological significance of retrograde migration, and whether it serves as an additional mechanism to limit pathology, or provides a basis for the dissemination of systemic inflammation.     

Effect of host age on the expression of acquired resistance to ticks

Summary Young guinea-pigs (350 g) expressed significantly greater levels of acquired resistance to challenge by larvalAmblyomma americanum ticks than older guinea-pigs (520–800 g). This finding suggests that younger guinea-pigs are immunologically more responsive to tick infestation than older mature individuals. Therefore, host age is an important variable in evaluating acquired resistance to ticks.Supported in part by grants from the United States Public Health Service, National Institutes of Health No. AI 17555, AI 19657, RR 05443 and from the Rockefeller Foundation.     

Purification of pig kidney diamine oxidase (histaminase) and in vivo effects on passive cutaneous anaphylaxis and histamine induced bronchoconstriction of guinea-pigs

Summary Histaminase (diamine oxidase) was purified from pig kidney using cadaverine-Sepharose affinity chromatography. Pretreatment of guinea-pigs with histaminase caused marked inhibition of the passive cutaneous anaphylaxis. The effect of histaminase on histamine induced bronchoconstriction in vivo was studied. Histaminase significantly reduced the response in guinea-pigs. Histaminase is effective as a potent antihistaminic agent in vivo.     

Regulation of phagocyte migration and recruitment by Src-family kinases

Src-family kinases (SFKs) regulate different granulocyte and monocyte/macrophage responses. Accumulating evidence suggests that members of this family are implicated in signal transduction pathways regulating phagocytic cell migration and recruitment into inflammatory sites. Macrophages with a genetic deficiency of SFKs display marked alterations in cytoskeleton dynamics, polarization and migration. This same phenotype is found in cells with either a lack of SFK substrates and/or interacting proteins such as Pyk2/FAK, c-Cbl and p190RhoGAP. Notably, SFKs and their downstream targets also regulate monocyte recruitment into inflammatory sites. Depending on the type of assay used, neutrophil migration in vitro may be either dependent on or independent of SFKs. Also neutrophil recruitment in in vivo models of inflammation may be regulated differently by SFKs depending on the tissue involved. In this review we will discuss possible mechanisms by which SFKs may regulate phagocytic cell migratory abilities.