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PubMed2006

[Feasibility of percutaneous exclusion of the left atrial appendage: results of 11 cases].

Atrial fibrillation is associated with a risk of cerebral embolism, the only proven effective prevention of which is anticoagulant therapy. There is no known alternative in cases with contra-indications to this treatment. Percutaneous exclusion of the left atrial appendage by the implantation of a prosthesis (PLAATO System, ev3 Inc., Plymouth, Minnesota) is a new approach to the prevention of these complications. The authors report the results observed in a series of 11 consecutive patients (7 men, mean age 72 +/- 9 years) in whom this procedure was proposed. All patients had atrial fibrillation for over 3 months, were at high risk and had contra-indications to oral anticoagulants. The implantation of the prosthesis was performed after treatment with aspirin and clopidogrel, under general anaesthesia radioscopy and transoesophageal echocardiographic guidance with success in 9 cases (1 implantation refused in the catheter laboratory and 1 failure). The only complication observed was transient ST elevation treated by emergency angioplasty. The echographic and angiographic criteria of success of left atrial appendage exclusion were fulfilled in all implanted patients. The hospital course was uncomplicated. One recurrence of stroke was observed at the second month: transoesophageal echocardiography confirmed the absence of thrombosis, of migration of the prosthesis and its impermeability in all the patients. After 7 +/- 5 months' follow-up, no other adverse event was observed. This new procedure is technically feasible. Despite encouraging results, its long-term efficacy in the prevention of thromboembolic complications of atrial fibrillation remains to be demonstrated.

Aged↗
PubMed1991

Metabolic response of isolated liver cells to in vivo phagocytic challenge.

This study elucidates the in vivo metabolic response of different liver cells after a single phagocytic challenge. In vivo glucose uptake of different tissues and isolated liver cells was determined by a sequential double labeling version of the 2-deoxyglucose technique. After latex administration, glucose uptake more than doubled in the liver, increased by about 50% in the spleen and lung and was not changed in muscle and testis. Within 10 min after intravenous injection of latex beads, neutropenia developed, with no change in the number of lymphocytes. This was accompanied by a marked influx of polymorphonuclear leukocytes into the liver. Latex was found in 52%, 35%, and 14% of the isolated Kupffer cells, polymorphonuclear leukocytes and endothelial cells, respectively. In vivo glucose uptake increased by 111%, 142%, and 43% in these cells. Glucose uptake by the latex-free hepatocytes was also elevated, presumably by way of intercellular signals between parenchymal and non-parenchymal liver cells. Indomethacin pretreatment resulted in the delay of neutrophil immigration into tissues without any change in the glucose response of different liver cells. Thus phagocytic stimulation in vivo results in marked neutropenia, migration of neutrophils into the liver, increased glucose uptake by phagocytic cells of the liver and enhanced glucose metabolism by the non-phagocytic parenchymal cells.

Animals↗
PubMed1984

Early ultrastructural changes in choroidal arterioles of spontaneously hypertensive rats.

Ultrastructural changes in the vascular smooth muscle cells of spontaneously hypertensive rats (SHR) aged 7-9 months were studied in the long posterior ciliary artery (LPCA) and they were compared with the findings in the same aged control Wistar Kyoto rats (WKY). The systolic blood pressure was higher than 200 mmHg in the SHR at the postnatal fourth month. The muscle cells in the media of the LPCA in the SHR could be divided into three types according to the electron density of their sarcoplasm, i.e., dark, intermediate or light cells. The electron density depended on the content of actin filaments; the number of the filaments per one micron 2 was determined in the specimens where cross sections of the filaments prevailed, and it averaged 48.7 in the dark cells, 34.1 in the light cells. In WKY, all the muscle cells showed the intermediate density and the number of actin filaments averaged 37.9 per micron 2. It was also observed that the muscle cells migrated into the intima and they were called the intimal cells. These cells in SHR appeared as an aggregated mass underneath the endothelium, but in WKY the individual intimal cells were scattered. These findings were thought to be early ultrastructural changes in response to a rapid elevation of the arterial pressure.

Animals↗
PubMed1999

Elevated plasma level of plasminogen activator inhibitor-1 (PAI-1) in patients with relapsing-remitting multiple sclerosis.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system and one of the earliest changes in inflammatory focus involves the activation of vascular endothelial cells. We determined the plasma level of plasminogen activator inhibitor-1 (PAI-1), a key regulator of fibrinolysis and cell migration, in patients with MS. The level of plasma PAI-1 was significantly higher in active MS cases when compared to stable MS and controls. Plasma concentrations of tissue plasminogen activator, transforming growth factor beta-1, and lipoprotein-a remained normal in spite of disease activity. These results suggested that PAI-1 plasma levels are associated with MS disease activity and is a good marker for MS relapse.

Adult↗
PubMed2002

Histochemical analysis of macrophage migration inhibitory factor in psoriasis vulgaris.

Psoriasis is a persistent cutaneous disease characterized by skin inflammation and infiltration of immunocytes such as lymphocytes and monocytes/macrophages, concomitant with abnormal epidermal hyperproliferation. We previously showed that the serum level of macrophage migration inhibitory factor (MIF) and its production by peripheral blood mononuclear cells of patients with psoriasis were closely correlated with the severity of clinical symptoms; however, the precise role of MIF in psoriatic epidermis remains to be clarified. The current study was carried out to elucidate the possible involvement of MIF in psoriasis, using immunohistochemistry and in situ hybridization. In contrast to elevated serum MIF in psoriasis, MIF-positive staining in the lesional psoriatic epidermis was significantly decreased, as demonstrated by immunohistochemical analysis using an anti-MIF antibody. Consistent with this finding, we found, by in situ hybridization, that MIF mRNA concomitantly decreased in the psoriatic lesions. Although the reason for the different MIF levels in the psoriatic epidermis and in the circulation remains unknown, it is hypothesized that MIF, a potential growth factor, might be decreased in psoriatic lesions to counterregulate the abnormal epidermal proliferation caused by dysregulation of cytokines and growth factors.

Adult↗
PubMed1997

Challenge of human Jurkat T-cells with the adenylate cyclase activator forskolin elicits major changes in cAMP phosphodiesterase (PDE) expression by up-regulating PDE3 and inducing PDE4D1 and PDE4D2 splice variants as well as down-regulating a novel PDE4A splice variant.

The cAMP phosphodiesterase (PDE) 3 and PDE4 isoforms provide the major cAMP-hydrolysing PDE activities in Jurkat T-cells, with additional contributions from the PDE1 and PDE2 isoforms. Challenge of cells with the adenylate cyclase activator forskolin led to a rapid, albeit transient, increase in PDE3 activity occurring over the first 45 min, followed by a sustained increase in PDE3 activity which began after approximately 3 h and continued for at least 24 h. Only this second phase of increase in PDE3 activity was blocked by the transcriptional inhibitor actinomycin D. After approximately 3 h of exposure to forskolin, PDE4 activity had increased, via a process that could be inhibited by actinomycin D, and it remained elevated for at least a 24 h period. Such actions of forskolin were mimicked by cholera toxin and 8-bromo-cAMP. Forskolin increased intracellular cAMP concentrations in a time-dependent fashion and its action was enhanced when PDE induction was blocked with actinomycin D. Reverse transcription (RT)-PCR analysis, using generic primers designed to detect transcripts representing enzymically active products of the four PDE4 genes, identified transcripts for PDE4A and PDE4D but not for PDE4B or PDE4C in untreated Jurkat T-cells. Forskolin treatment did not induce transcripts for either PDE4B or PDE4C; however, it reduced the RT-PCR signal for PDE4A transcripts and markedly enhanced that for PDE4D transcripts. Using RT-PCR primers for PDE4 splice variants, a weak signal for PDE4D1 was evident in control cells whereas, in forskolin-treated cells, clear signals for both PDE4D1 and PDE4D2 were detected. RT-PCR analysis of the PDE4A species indicated that it was not the PDE4A isoform PDE-46 (PDE4A4B). Immunoblotting of control cells for PDE4 forms identified a single PDE4A species of approximately 118 kDa, which migrated distinctly from the PDE4A4B isoform PDE-46, with immunoprecipitation analyses showing that it provided all of the PDE4 activity in control cells. Forskolin treatment led to a marked decrease of this novel PDE4A species and allowed the detection of a strong signal for an approximately 67 kDa PDE4D species, suggested to be PDE4D1, but did not induce PDE4B and PDE4C isoforms. Elevation of intracellular cAMP concentrations in Jurkat T-cells thus exerts a highly selective effect on the transcriptional activity of the genes encoding the various PDE4 isoforms. This leads to the down-regulation of a novel PDE4A splice variant and the induction of PDE4D1 and PDE4D2 splice variants, leading to a net increase in the total PDE4 activity of Jurkat T-cells.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1992

Healing of the medial collateral ligament following a triad injury: a biomechanical and histological study of the knee in rabbits.

The effect of a partial medial meniscectomy and anterior cruciate ligament (ACL) transection on medial collateral ligament (MCL) healing was studied in skeletally mature rabbits. Two groups of animals, group I (isolated MCL rupture) and group II (MCL rupture with ACL transection and partial medial meniscectomy), were examined. At 6 and 12 weeks postoperatively, histological examination of the healing MCL and biomechanical evaluation of the varus-valgus (V-V) knee rotation and tensile properties of the femur-MCL-tibia complex (FMTC) were performed. Group II animals experienced substantial joint degeneration by 6 weeks. Progressive osteophyte formation was observed adjacent to the MCL insertions along with proximal migration of the MCL tibial insertion between 6 and 12 weeks. Histologic examination of the healing MCL substance from both groups showed disorganized collagen, inflammation, and fibroblast proliferation that decreased over time. For group II knees, the V-V knee rotation was found to be significantly elevated (4.7 to 5.2 times the contralateral control), and did not decrease with time. In contrast, the V-V knee rotations of the group I specimens were 1.8 times greater than control immediately following injury, and approached control values by 12 weeks. Tensile testing of the FMTCs revealed that the ultimate load increased with time for both groups, but group I had significantly higher values than group II. The linear stiffness in group I was not different than that group II and did not increase with time. For the mechanical (material) properties of the healed MCL substance, the modulus of the healing tissue for group II was only 40% that of group I. The structural properties of the FMTC and the mechanical properties of the MCL substance from both groups at 6 and 12 weeks were significantly different from the contralateral controls. We further demonstrated that immediately after ACL reconstruction, the V-V rotation of group II knees could be restored to group I levels. Recent clinical studies of MCL healing following isolated complete ligament tears have suggested that nonoperative management without immobilization leads to excellent treatment outcome. However, in more severe injuries involving additional tissues, poor quality of the healed ligament tissue and articular degeneration are observed. Our results demonstrate the deleterious effects of an untreated triad injury on the healing of the MCL substance and its insertions. Examination of the MCL substance suggests that a much larger healing mass is formed following a triad injury, which partially compensates for inferior ligament mechanical properties.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1999

Hepatocyte growth factor in renal disease: cause or cure?

Hepatocyte growth factor (HGF) is an injury-released growth factor with diverse effects on epithelial and endothelial cells. These effects include proliferation, migration, extracellular matrix production and tubulogenesis. These activities allow HGF to function as an organizer of repair processes that bring about restoration of tubular function following renal injury. However, while HGF has been demonstrated to accelerate recovery of renal function after an acute insult, prolonged exposure to elevated levels of HGF can reduce renal function and may contribute to progressive renal disease. This review will describe the cellular activities of HGF, how they pertain to renal repair and the therapeutic application of regulating HGF activity in acute versus chronic renal disease.

Acute Disease↗
PubMed1998

Immunolocalization of transforming growth factor beta during wound repair in rat retina after laser photocoagulation.

BACKGROUND: Scatter photocoagulation induces regression of retinal neovascularization, but the mechanism of its therapeutic effect is incompletely understood. To elucidate the mechanism of therapeutic effect of photocoagulation is the main focus of our research. We have already demonstrated basic fibroblast growth factor (bFGF) immunolocalization during retinal wound repair following laser photocoagulation. Transforming growth factor beta (TGF beta) reportedly inhibits endothelial cell growth and bFGF-induced cell proliferation in vitro. In the present study, we evaluated the immunohistochemical localization of TGF-beta 1 and -beta 2 during wound repair in the rat retina following laser photocoagulation. METHODS: Krypton laser photocoagulation was performed on the eyes of pigmented rats. The eyes were then enucleated on day 1, 3, 7, 14, 28 or 56 following the photocoagulation and enrolled into the analysis of immunohistochemical localization of TGF-beta 1 and -beta 2. RESULTS: Immunoreactivity for TGF-beta 1 and -beta 2 was present in the ganglion cell layer and photoreceptor outer segments of the normal adult rat retina. The cytoplasm of RPE cells at the photocoagulated lesion showed intense TGF-beta 1 and -beta 2 immunoreactivity on day 3 after laser photocoagulation. Macrophages that migrated into the lesion lacked positive staining for TGF-beta 1 and -beta 2. TGF-beta immunoreactivity in RPE cells continued to be upregulated for more than 1 month compared with that in normal RPE cells. Controls did not exhibit any positive staining. CONCLUSION: An elevated expression of TGF-beta immunoreactivity for a longer period of time than bFGF was observed in RPE cells at the photocoagulated lesion in vivo. In the late phase of retinal wound repair, TGF-beta may inhibit cell proliferation induced by mitogens, introduce an end stage of cellular events, and induce extracellular matrix induction.

Animals↗
PubMed1987

Expression of abnormal von Willebrand factor by endothelial cells from a patient with type IIA von Willebrand disease.

Studies were conducted to characterize the biosynthesis of von Willebrand factor (vWf) by cultured endothelial cells (EC) derived from the umbilical vein of a patient with type IIA von Willebrand disease. The patient's EC, compared with those from normal individuals, produced vWf that had decreased amounts of large multimers and an increase in rapidly migrating satellite species, features characteristic of plasma vWf from patients with type IIA von Willebrand disease. The type IIA EC did produce a full spectrum of vWf multimers in both cell lysates and postculture medium, although the relative amounts of the largest species were decreased. The large multimers were degraded in conjunction with the appearance of rapidly migrating satellites that contained approximately equal to 170-kDa proteolytic fragments, suggesting that this patient's functional defect is due to abnormal proteolysis and not to a primary failure of vWf subunit oligomerization. Moreover, the observed degradation appears to result from an abnormal vWf molecule and not elevated protease levels. These results suggest that this patient's von Willebrand disease phenotype is caused by increased proteolytic sensitivity of his vWf protein.

Cell Division↗
PubMed1983

Clinical pathology of experimental stephanuriasis in pigs.

Haematology and serum aspartate aminotransferase and alanine aminotransferase activities were studied during the migration phase of Stephanurus dentatus in the livers of experimentally infected pigs. There was no evidence of anaemia but total leucocyte counts were raised and peripheral eosinophilia began 2 to 3 weeks after infection. Peak eosinophilia occurred 6 to 7 weeks after infection and levels were still elevated at 20 weeks. Lymphocyte and neutrophil numbers remained constant. Reinfection did not stimulate a secondary eosinophil response. Only aspartate aminotransferase was temporarily elevated. The gross pathology resulting from the infections is described. Several clinicopathological differences in the response of pigs to invasion of the liver by S. dentatus were noted compared to those produced by Ascaris suum but none are pathognomonic.

Alanine Transaminase↗
PubMed2004

Sphingosine-1-phosphate inhibits C-type natriuretic peptide activation of guanylyl cyclase B (GC-B/NPR-B).

C-type natriuretic peptide (CNP) binds and activates the transmembrane guanylyl cyclase B receptor (NPR-B), which decreases vascular tone and inhibits cell proliferation and migration. In contrast, the bioactive lipid sphingosine-1-phosphate (S1P) elicits the opposite physiological effects. Here, we demonstrate a potent acute inhibitory effect of S1P on NPR-B activity in NIH3T3 fibroblasts and A10 vascular smooth muscle cells. In fibroblasts, S1P reduced CNP-dependent cGMP elevations to the same levels as 10% fetal bovine serum, the most potent NPR-B desensitizing agent known. The reduction was dose-dependent (IC50=0.08 micromol/L) and due to decreased NPR-B activity because CNP-dependent guanylyl cyclase activities were markedly diminished in membranes prepared from S1P-treated cells. Similarly, in A10 cells, S1P inhibition was rapid (t1/2=2 to 5 minutes), dose-dependent (IC50=0.3 micromol/L S1P), and mediated by a cell surface receptor. The mechanism of the S1P-dependent desensitization in A10 cells did not require NPR-B degradation or protein kinase C activation, but did require elevated calcium concentrations because a nonspecific calcium ionophore also inhibited NPR-B and an intracellular calcium chelator blocked a significant portion of the S1P response. These are the first data demonstrating cross-talk between the natriuretic peptide and S1P signaling systems. They suggest that the effects of S1P on vascular disease and wound healing may be mediated in part through inhibition of NPR-B.

Animals↗
PubMed2006

Tissue factor in cardiovascular diseases: molecular mechanisms and clinical implications.

Tissue factor (TF), formerly known as thromboplastin, is the key initiator of the coagulation cascade; it binds factor VIIa resulting in activation of factor IX and factor X, ultimately leading to fibrin formation. TF expression and activity can be induced in endothelial cells, vascular smooth muscle cells, and monocytes by various stimuli such as cytokines, growth factors, and biogenic amines. These mediators act through diverse signal transduction mechanisms including MAP kinases, PI3-kinase, and protein kinase C. Cellular TF is present in three pools as surface, encrypted, and intracellular protein. TF can also be detected in the bloodstream, referred to as circulating or blood-borne TF. Elevated levels of TF are observed in patients with cardiovascular risk factors such as hypertension, diabetes, dyslipidemia, and smoking as well as in those with acute coronary syndromes. TF may indeed be involved in the pathogenesis of atherosclerosis by promoting thrombus formation; in addition, it can induce migration and proliferation of vascular smooth muscle cells. As a consequence, therapeutic strategies have been developed to specifically interfere with the action of TF such as antibodies against TF, site-inactivated factor VIIa, or recombinant TF pathway inhibitor. Inhibition of TF action appears to be an attractive target for the treatment of cardiovascular diseases.

Animals↗
PubMed2000

Expression of endothelin-1 after endothelial denudation of thoracic aortas in experimental hypercholesterolemic rats.

Although endothelin-1 (ET-1) is involved in balloon-induced neointima formation, the role of ET-1 in balloon-induced neointima formation in hypercholesterolemia is unclear. In addition, it remains to be determined whether ET-1 is produced by endothelial cells or vascular smooth muscle cells, or both. We investigated tissue immunoreactive ET-1 levels by immunoblot analysis, localization of ET-1 immunoreactivity by immunohistochemistry, and expression of preproET-1 mRNA by in situ hybridization in balloon-induced neointima formation in experimental hypercholesterolemic rats. Serum total cholesterol levels were significantly higher (p< 0.01) in the 5%cholesterol-diet group (194 +/- 17 mg/dl, n=20) than in the normal-diet group (64 +/- 2 mg/dl, n=20). Before and after endothelial denudation, plasma ET-1 levels and tissue immunoreactive ET-1 levels were significantly higher in cholesterol-diet rats. The expression of preproET-1 mRNA by in situ hybridization was observed in the nuclei of endothelial cells, but not medial smooth muscle cells in normal- or cholesterol diet rats. After endothelial denudation, plasma ET-1 levels and serum total cholesterol levels did not change in either the normal- or the cholesterol-diet rats. Tissue level of ET-1 tended to increase at 3 days after denudation in normal-diet rats (1.0 +/- 0.1 vs 2.6 +/- 0. 2 density ratio, p< 0.05), although endothelial cells had not yet regenerated. The expression of preproET-1 mRNA by in situ hybridization was not observed at 3 days after endothelial denudation in either endothelial or medial smooth muscle cells in normal-diet rats. Four weeks after denudation, regeneration of endothelial cells was almost complete, and an intimal hyperplasia was observed. Tissue ET-1 levels were significantly elevated 4 weeks after endothelial denudation in normal-diet rats (1.0 +/- 0.1 vs 7.6 +/- 0.2 density ratio, p< 0.05). The expression of preproET-1 mRNA by in situ hybridization was observed in the nuclei of regenerated endothelial cells after endothelial denudation, and in smooth muscle cells migrating into the intima, but was not observed in medial smooth muscle cells in normal-diet rats. A similar pattern was observed in cholesterol-diet rats. We concluded that ET-1 was involved in neointima formation and that ET-1 was produced by both endothelial and neointimal smooth muscle cells, but not medial smooth muscle cells after endothelial denudation in experimental hypercholesterolemic rats.

Angioplasty, Balloon, Coronary↗
PubMedDate not supplied

High-resolution genomic and expression profiling reveals 105 putative amplification target genes in pancreatic cancer.

Comparative genomic hybridization (CGH) studies have provided a wealth of information on common copy number aberrations in pancreatic cancer, but the genes affected by these aberrations are largely unknown. To identify putative amplification target genes in pancreatic cancer, we performed a parallel copy number and expression survey in 13 pancreatic cancer cell lines using a 12,232-clone cDNA microarray, providing an average resolution of 300 kb throughout the human genome. CGH on cDNA microarray allowed highly accurate mapping of copy number increases and resulted in identification of 24 independent amplicons, ranging in size from 130 kb to 11 Mb. Statistical evaluation of gene copy number and expression data across all 13 cell lines revealed a set of 105 genes whose elevated expression levels were directly attributable to increased copy number. These included genes previously reported to be amplified in cancer as well as several novel targets for copy number alterations, such as p21-activated kinase 4 (PAK4), which was previously shown to be involved in cell migration, cell adhesion, and anchorage-independent growth. In conclusion, our results implicate a set of 105 genes that is likely to be actively involved in the development and progression of pancreatic cancer.

Cell Line, Tumor↗
PubMed2006

Fas ligand is responsible for CXCR3 chemokine induction in CD4+ T cell-dependent liver damage.

Immune-mediated hepatic damage has been demonstrated in the pathogenesis of hepatitis C virus (HCV) and other hepatotrophic infections. Fas/Fas ligand (FasL) interaction plays a critical role in immune-mediated hepatic damage. To understand the molecular mechanism(s) of FasL-mediated liver inflammation, we examined the effect of CD4(+) T cells expressing high levels of FasL on the initiation of hepatic damage through analysis of chemokine and chemokine receptor expression in HCV core x TCR (DO11.10) double-transgenic mice. In vivo antigenic stimulation triggers a marked influx of core-expressing Ag-specific CD4(+) T cells into the liver of the immunized core(+) TCR mice but not their core(-) TCR littermates. Strikingly, the inflammatory process in the liver of core(+) TCR mice was accompanied by a dramatic increase in IFN-inducible protein 10 and monokine induced by IFN-gamma production. The intrahepatic lymphocytes were primarily CXCR3-positive and anti-CXCR3 Ab treatment abrogates migration of CXCR3(+) lymphocytes into the liver and hepatic damage. Importantly, the blockade of Fas/FasL interaction reduces the expression of IFN-inducible protein 10 and monokine induced by IFN-gamma and cellular infiltration into the liver. These findings suggest that activated CD4(+) T cells with elevated FasL expression are involved in promoting liver inflammation and hepatic damage through the induction of chemokines.

Animals↗
PubMedDate not supplied

The trapidil derivative AR 12456 protects against serum hyperlipidemia in guinea pigs.

The administration of the trapidil derivative AR 12465 (5 mg/kg body weight) intraperitoneally to hypercholesterolemic guinea pigs caused a stronger reduction in serum total cholesterol (TC) than trapidil (20 mg/kg, i.p.) or a vehicle injection (saline with 5% ethanol i.p.). The stronger reduction of TC is caused by a lower level in the sum of all beta-migrating lipoproteins and an enhanced level of high-density lipoprotein. The levels of free and esterified cholesterol were not changed in kidney and left cardiac ventricle, but significantly enhanced (P less than 0.05) in the liver of all groups fed a cholesterol-rich diet. The elevation in liver cholesterol was higher in the group treated with AR 12456 than in the group treated with trapidil or with vehicle. The treatment with AR 12456 diminished the ratio TXB2/6-keto-PGF1 alpha for the capacity of aorta to form these prostanoids. In conclusion, our data show that AR 12456 has a strong antilipidemic action in guinea pigs fed a cholesterol-rich diet.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1983

[The role of eosinophils in inflammatory reactions].

Recent findings have contributed substantially to a better understanding of the ontogeny and function of eosinophil leukocytes. Together with other granulocytes, the cells originate in the bone marrow from a common stem cell. Their development is regulated by genetic factors and by products of T-lymphocytes. Chemotactic factors of the complement cascade (C5a), lymphokines and eosinophil chemotactic leukotrienes (ECL) stimulate their migration to tissue sites. Generation and biological effectiveness of eosinophil chemotactic factors can be modulated in numerous ways, thus changing the outcome of the inflammatory event. The probably most important effector function of eosinophils is their cytotoxicity which plays a role in the killing of parasites. Markedly elevated numbers of eosinophils can, however, cause auto-aggression against the body's own cells, such as the Purkinje cells of the brain, cardiac muscle cells or epithelial cells of the skin and the bronchial tree. Eosinophils are therefore cells capable of both serving and damaging the human host.

Anaphylaxis↗