Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “NEUTROPHILS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed2000

No apparent role for neutrophils and neutrophil-derived myeloperoxidase in experimental subarachnoid haemorrhage and vasospasm: a preliminary study.

OBJECTIVE: The literature contains investigations and discussion of the role of neutrophils and neutrophil-derived myeloperoxidase (MPO) in inflammatory processes, local ischaemia, and ischaemia-reperfusion injury models. Our aim was to determine whether the same roles existed for neutrophils and the system involving neutrophil-derived MPO in experimental subarachnoid haemorrhage (SAH) and associated ischaemia. MATERIAL AND METHOD: Forty-eight adult New Zealand white rabbits were divided into six groups of eight. The first SAH model was applied to 16 animals. Eight of these rabbits were sacrificed after 48 hours (Group 1) and the remaining eight were killed after 96 hours (Group 2). The second SAH model applied to another 16 rabbits, which were sacrificed in two groups at the above time periods, forming Groups 3 and 4, respectively. There were two groups of 8 control animals, one group per SAH model, and these rabbits were sacrificed after 48 hours. We carried out histopathological studies using haematoxylin and eosin (H&E) stain, elastin stain, MPO immunohistochemistry, and determination of basilar artery cross-sectional diameter. We also did biochemical analysis of cerebral hemisphere and brainstem specimens, measuring tissue lipid peroxidase and MPO activity. Results were compared between the groups and with their related controls. RESULTS: In contrast to previous experimental findings in local ischaemia and ischaemia-reperfusion models, we found no histopathological or biochemical evidence to suggest a role for neutrophils and neutrophil-derived MPO in relation to subarachnoid haemorrhage and resultant vasospasm. Although we confirmed the successful induction of significant vasospasm and observed the clinical evidences of subsequent ischaemia, there was no notable accumulation of neutrophils or activity of neutrophil-derived MPO in the tissues studied. This suggests that the biological process induced by SAH follows a different pattern from that seen in local ischaemia and ischaemia-reperfusion injury.

Animals↗
PubMedDate not supplied

Neutrophil chemotaxis in the horse is not mediated by a complex of equine neutrophil elastase and equine alpha-1-proteinase inhibitor.

Studies have demonstrated that as a result of proteolytic inactivation or complex formation (with neutrophil elastase), human alpha-1-proteinase inhibitor (API) becomes a potent chemoattractant for human neutrophils. The present study aimed to investigate the in vitro chemotactic response of equine neutrophils to an equivalent complex of equine API and neutrophil elastase. No evidence of neutrophil migration was observed towards purified complex derived from equine neutrophil elastase and the Spi 1 isoform of equine API, or to crude mixtures of porcine pancreatic elastase and unseparated equine API isoforms, although the same neutrophil preparations actively migrated towards zymosan activated plasma. It was concluded that, in the horse, complexes of API are not involved in the migration of neutrophils to sites of inflammation.

Animals↗
PubMed2001

Fc gamma RIII mediates neutrophil recruitment to immune complexes. a mechanism for neutrophil accumulation in immune-mediated inflammation.

Neutrophil accumulation is a hallmark of immune complex-mediated inflammatory disorders. Current models of neutrophil recruitment envision the capture of circulating neutrophils by activated endothelial cells. We now demonstrate that immobilized immune complexes alone support the rapid attachment of neutrophils, under physiologic flow conditions. Initial cell tethering requires the low-affinity Fc gamma receptor IIIB (Fc gamma RIIIB), and the beta(2) integrins are additionally required for the subsequent shear-resistant adhesion. The attachment function of Fc gamma RIIIB may be facilitated by its observed presentation on neutrophil microvilli. In vivo, in a model of acute antiglomerular basement membrane nephritis in which immune complexes are accessible to circulating neutrophils, Fc gamma RIII-deficient mice had a significant reduction in neutrophil recruitment. Thus, the interaction of immune complexes with Fc gamma RIII may mediate early neutrophil recruitment in immune complex-mediated inflammation.

Animals↗
PubMed1993

Viral infection of bovine bronchial epithelial cells induces increased neutrophil chemotactic activity and neutrophil adhesion.

1. Acute bronchitis secondary to viral infection is associated with an influx of neutrophils. We hypothesized that bronchial epithelial cells are capable of releasing neutrophil chemotactic activity in response to viral infection. 2. To test this hypothesis, primary cultures of bovine bronchial epithelial cells were inoculated with a bovine respiratory pathogen, bovine herpes virus-1. 3. Supernatants collected from inoculated cells, before signs of toxicity, demonstrated significant neutrophil chemotactic activity using a blind well chamber neutrophil chemotaxis assay. Lipoxygenase inhibitors markedly reduced the amount of neutrophil chemotactic activity released after bovine herpes virus-1 inoculation. Analysis of arachidonic acid metabolites in cell supernatants by reverse-phase h.p.l.c. confirmed that leukotriene B4, a potent neutrophil chemoattractant, was released. 4. We also confirmed that adhesion of neutrophils to bovine herpes virus-1-inoculated bronchial epithelial cells was increased and mediated in part by the neutrophil integrin, LFA-1. 5. Thus, virally infected airway epithelial cells release leucocyte chemoattractants and hence adhesive interactions, functions that are likely to be important in the inflammatory acute response to viral infection.

Animals↗
PubMed1990

Anti-neutrophil cytoplasmic autoantibodies induce neutrophils to degranulate and produce oxygen radicals in vitro.

Anti-neutrophil cytoplasmic autoantibodies (ANCA) are in the circulation of most patients with pauci-immune necrotizing vasculitis and pauci-immune crescentic glomerulonephritis. The current study demonstrates an effect of these autoantibodies on neutrophil function in vitro. ANCA cause normal human neutrophils to undergo an oxidative burst and degranulate. Both ANCA phenotypes (i.e., cytoplasmic-pattern ANCA and myeloperoxidase-specific ANCA) induce neutrophil activation. ANCA sera and purified immunoglobulins significantly increase the release of reactive oxygen species when compared with controls. ANCA, in a dose-dependent manner, induce the release of primary granule contents. These effects are markedly enhanced by priming neutrophils with tumor necrosis factor. Flow cytometry studies demonstrate the presence of myeloperoxidase on the surface of neutrophils after cytokine priming, indicating that primed neutrophils have ANCA antigens at their surfaces to interact with ANCA. These observations suggest an in vivo pathogenetic role for ANCA. We propose that, in patients with necrotizing vasculitis, ANCA-induced release of toxic oxygen radicals and noxious granule enzymes from cytokine-primed neutrophils could be mediating vascular inflammation.

Autoantibodies↗
PubMed1994

Neutrophils roll on adherent neutrophils bound to cytokine-induced endothelial cells via L-selectin on the rolling cells.

Specific arrest of neutrophils in venules is central to their rapid accumulation during local inflammatory responses. Initial neutrophil rolling on endothelium is mediated by leukocyte L-selectin and the inducible vascular adhesion proteins P- and E-selectin. This rolling is a prerequisite for endothelial-dependent neutrophil arrest. Here we describe rolling of neutrophils on the surface of previously arrested neutrophils and demonstrate that this interaction involves L-selectin exclusively on rolling cells. The adherent neutrophil support of L-selectin-dependent neutrophil rolling in vivo can promote continuous and augmented leukocyte recruitment at sites of previous neutrophil accumulation.

Antibodies, Monoclonal↗
PubMed1995

Inflammatory microcrystals differentially regulate the secretion of macrophage inflammatory protein 1 and interleukin 8 by human neutrophils: a possible mechanism of neutrophil recruitment to sites of inflammation in synovitis.

Human neutrophils at inflammatory sites may be an important source of the chemotactic cytokines macrophage inflammatory protein 1 alpha (M1P-1 alpha; a C-C chemokine) and interleukin 8 (IL-8; a C-X-C chemokine). In this study, we show that the inflammatory microcrystals monosodium urate monohydrate (MSU) and calcium pyrophosphate dihydrate (CPPD), the major mediators of gout and pseudogout, differentially regulate the production of these two chemokines by human neutrophils. Both MSU and CPPD increased the secretion of IL-8 by neutrophils in a dose- and time-dependent manner, but had no effect on that of MIP-1 alpha. Since inflammatory cytokines are likely to be present in the synovium during crystal-induced inflammation, we examined the interaction between TNF-alpha and GM-CSF and the crystals. Both TNF-alpha and GM-CSF stimulated IL-8 production; however, only TNF-alpha exerted a significant effect on MIP-1 alpha secretion in neutrophils. IL-8 production induced by TNF-alpha and GM-CSF was synergistically enhanced in the presence of MSU or CPPD, whereas MIP-1 alpha secretion induced by TNF was completely inhibited in the presence of either MSU or CPPD. Interestingly, no interaction between the crystals and the inflammatory cytokines was observed with respect to synthesis of the C-X-C chemokine MGSA in neutrophils. These results suggest that the combination of TNF-alpha and GM-CSF with MSU or CPPD will lead to the production of IL-8 by neutrophils and abolish the release of MIP-1 alpha, an event that will theoretically lead to recruitment of neutrophils but not mononuclear cells. These results are in accordance with the pathological state of gout and pseudogout, where the predominant inflammatory cell is the neutrophil.

Calcium Pyrophosphate↗
PubMed2000

The ability of Helicobacter pylori to activate neutrophils is determined by factors other than H. pylori neutrophil-activating protein.

The ability of Helicobacter pylori to activate neutrophils is associated with peptic ulcer disease (PUD). One of the H. pylori factors previously suggested to stimulate neutrophil activation is the H. pylori neutrophil-activating protein (HpNAP). The primary aims of this study were to investigate the relationships between H. pylori neutrophil activation and reported variations in HpNAP expression and the napA gene sequence. The association between neutrophil activation and vacuolating cytotoxin activity was also investigated. The ability to activate neutrophils was found here to be associated with the development of PUD and was a characteristic more frequently identified in H. pylori isolates with vacuolating cytotoxin activity. However, no relationship was found between neutrophil activation and the expression of HpNAP or differences in the napA sequence. In conclusion, the ability to activate neutrophils contributes to the ulcerative potential of individual H. pylori isolates, but this activity is not mediated by differences in HpNAP.

Bacterial Proteins↗
PubMed2006

Human fallopian tube neutrophils--a distinct phenotype from blood neutrophils.

PROBLEM: The role of neutrophils in the human Fallopian tube (FT) is unknown. In order to provide insights into their functions in the FT, we systematically compared neutrophils from normal FT and peripheral blood (PB). METHOD OF STUDY: Flow cytometric analysis of surface receptors, granule proteins, and intracellular cytokines expressed by neutrophils from enzymatically dispersed FT and PB was performed. RESULTS: Fallopian tube neutrophils expressed significantly higher levels of CD64, human class II histocompatibility antigen DR (HLA-DR), gamma-interferon, and vascular endothelial growth factor than those from PB. Fewer FT neutrophils expressed IL-8 receptors compared to PB, while more expressed the receptor for the bacterial-derived chemoattractant formyl-Met-Leu-Phe (fMLP). The number of FT neutrophils containing the granule proteins matrix metalloproteinase-9, lactoferrin, and myeloperoxidase was decreased versus PB. CONCLUSION: Fallopian tube neutrophils exhibit a phenotype distinct from PB neutrophils, suggesting functional activation of innate immune defense in the female reproductive tract as well as a potential role in maintaining normal FT physiology.

Cell Separation↗
PubMed2006

rHuG-CSF increases the platelet-neutrophil complex formation and neutrophil adhesion molecule expression in volunteer granulocyte and stem cell apheresis donors.

Several reports have shown that granulocyte colony-stimulating factor (G-CSF) administration induces a transient, mild hypercoagulable state, which might predispose certain donors to thrombotic complications. In the present study, changes in the expression of neutrophil adhesion molecules (CD11b/CD18, CD62L) and platelet-neutrophil complex formation following rHuG-CSF administration were investigated in normal granulocyte and stem cell donors. For granulocyte apheresis (N = 10), rHuG-CSF (5 microg/kg) was given subcutaneously every 12 h three times and apheresis was carried out two hours after the last dose. For stem cell apheresis (N = 8), rHuG-CSF (10 microg/kg/day) was given subcutaneously for 5 days and apheresis was carried out when peripheral CD34+ cell counts exceeded 20 cell/microL. Expression of neutrophil adhesion molecules (CD11b/CD18, CD62L) and platelet-neutrophil complex formation following rHuG-CSF administration were investigated in donors by a flow cytometric method. A significant increase in neutrophil counts (P < 0.001), and decreases in platelet counts (P < 0.01) and hemoglobin levels (P < 0.01) occurred following G-CSF administration. The expression of CD11b/CD18 significantly increased (P < 0.001) over pretreatment values with G-CSF administration and returned to baseline 1 week after stopping the drug. In contrast, CD62L expression was decreased (P < 0.01) with G-CSF and returned to normal after cessation of the drug. rHuG-CSF caused more than a two-fold increase (from 0.3 to 7.0 x 10(9)/L) in circulating platelet-neutrophil complexes (P < 0.01), which returned to normal after 1 week. Although clinical significance of these laboratory changes is not clear, the occurrence of neutrophil activation and increased platelet-neutrophil complex formation might predispose certain donors or patients to thrombotic complications following G-CSF administration.

Adult↗
PubMed1990

Neutrophil-mediated increased permeability of microcarrier-cultured endothelial monolayers: a model for the in vitro study of neutrophil-dependent mediators of vasopermeability.

Changes in the permeability of human endothelial monolayers in response to activated human neutrophils were examined in a novel, in vitro model of vasopermeability changes. Microcarrier-cultured human umbilical vein endothelial monolayers were used in a system that responds to histamine. Human neutrophils did not increase Evans Blue staining of the endothelium-covered microcarriers if added alone or if added with the neutrophil-dependent mediator of vasopermeability, formyl-methionyl-leucyl-phenylalanine (FMLP, 0.1 microM). In contrast, neutrophils, added to the endothelial cells in a ratio as low as 2.5:1 caused time-dependent increases in microcarrier staining if pretreated with cytochalasin B (5 micrograms/mL) before addition with FMLP. Neutrophil cell-free releasate and purified human sputum elastase also caused concentration-related increases in Evans Blue staining of the endothelial-covered microcarriers and these effects were inhibited by the elastase inhibitor methoxysuccinyl-alanyl-alanyl-prolyl-valyl chloromethyl ketone. This compound also inhibited neutrophil-mediated endothelial permeability increases. The microcarrier-cultured human endothelial monolayer system rapidly detects permeability alterations of endothelial monolayers in response to activated human neutrophils. This model is a potentially useful screening assay for the development of therapeutic agents, directed at neutrophil degranulation or degranulation products, for the control of inflammatory vasopermeability abnormalities.

Capillary Permeability↗
PubMed1994

Correlation between myeloperoxidase-quantified neutrophil accumulation and ischemic brain injury in the rat. Effects of neutrophil depletion.

BACKGROUND AND PURPOSE: Neutrophils have been implicated in the pathogenesis of ischemia-reperfusion injury. The aim of the present study was to evaluate the correlation between neutrophil infiltration into ischemic tissues and brain injury after transient focal ischemia. METHODS: We evaluated the effects of depletion of circulating neutrophils by administration of an antineutrophil monoclonal antibody (RP3) on brain edema formation, infarct size, and neutrophil infiltration (myeloperoxidase [MPO]-quantified) in rats with 1 hour of middle cerebral artery (MCA) occlusion. RESULTS: In the cerebral cortex perfused by the anterior cerebral artery (ACA area), there was a significant increase in MPO activity only 24 hours (P < .05) after reperfusion. In the cerebral cortex perfused by the middle cerebral artery (MCA area) and caudate putamen, MPO activity was significantly increased at 12 (MCA area, P < .01; caudate putamen, P < .05), 24 (MCA area, P < .05; caudate putamen, P < .01), and 72 hours (MCA area, P < .01; caudate putamen, P < .05) and returned to near-normal level by 168 hours after reperfusion. Brain MPO activity after transient MCA occlusion correlated well with the appearance of neutrophils. Depletion of neutrophils by RP3 treatment completely inhibited the increase in MPO activity in the ischemic brain after 24 hours of reperfusion. In addition, treatment with RP3 significantly attenuated the postischemic increase in brain water content at 24 hours after reperfusion. RP3 also significantly reduced the size of infarct area. CONCLUSIONS: These results indicate that the increase in brain MPO activity after transient focal ischemia virtually reflects the neutrophil infiltration and that neutrophil infiltration into the ischemic brain is implicated in postischemic brain injury.

Animals↗
PubMed1990

Neutrophil elastase activity and superoxide production are diminished in neutrophils of alcoholics.

Several lines of evidence indicate that neutrophil elastase and oxidants secreted by phagocytic inflammatory cells play key roles in the development of centrilobular emphysema. A recent report suggests that ethanol consumption may have a protective role against this disease in smokers. The aim of this study was to examine the effect of ethanol consumption on neutrophil elastase activity and superoxide production of peripheral blood neutrophils. These activities were measured in neutrophils from 52 male intoxicated patients and compared to activities in neutrophils from 20 male volunteers. Neutrophils from intoxicated patients contained 31% less elastase activity than that found in controls, 0.99 +/- 0.27 versus 1.44 +/- 0.23 micrograms/10(6) neutrophils (p less than 0.0001) and produced 25 to 27% less superoxide than controls in response to phorbol 12-myristate-13-acetate, 0.90 +/- 0.17 versus 1.2 +/- 0.21 nmol/min/10(6) PMN (p less than 0.0001) or N-formylmethionylleucylphenylalanine, 0.64 +/- 0.19 versus 0.88 +/- 0.24 (p less than 0.001). In follow-up studies of 10 patients admitted for acute alcoholism, elastase activity and superoxide production remained low for 2 to 4 days. After 6 to 10 days, elastase activity and superoxide production were significantly greater than they were at Day 0 and approached normal levels. Neutrophils isolated from blood samples of healthy abstaining donors, which had been exposed to ethanol or to plasma from inebriated patients for 16 to 20 h, showed no loss of elastase activity or superoxide production.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Platelet-activating factor causes neutrophil accumulation and neutrophil-mediated increased vascular permeability in canine trachea.

Platelet-activating factor (PAF) has potent effects on the respiratory airways that may be mediated through its ability to act as an inflammatory stimulant. To study its inflammatory properties in the airways, we infused PAF into the vasculature of the canine trachea and examined (1) the kinetics of neutrophil transit through the tracheal microcirculation, (2) accompanying changes in vascular permeability, and (3) the dependence of vascular permeability changes on neutrophil accumulation. Neutrophil kinetics were assessed by measuring the transit times of fluorescein isothiocyanate-labeled canine neutrophils by in vivo microscopy. Changes in vascular permeability were measured by the extravascular leakage of radiolabeled albumin and comparison of wet-to-dry weight ratios. The importance of neutrophils in increasing vascular permeability was assessed by perfusing the trachea with either autologous blood depleted of its leukocytes, or leukocyte-depleted blood replenished with neutrophils. Our data indicate that PAF causes rapid and prolonged neutrophil accumulation in the canine trachea and an increase in vascular permeability that is partially mediated by neutrophils.

Animals↗
PubMed2004

Neutrophil extravasation in rat mesenteric venules induced by the chemotactic peptide N-formyl-methionyl-luecylphenylalanine (fMLP), with special attention to a barrier function of the vascular basal lamina for neutrophil migration.

The present study was performed to investigate morphologically the process of neutrophil extravasation induced by the synthetic bacterial peptide N-formylmethionyl-leucyl-phenylalanine (fMLP) in venules of the rat mesentery by the combined use of intravital microscopy and transmission electron microscopy (TEM). Special attention was given to the interaction of the neutrophils with the endothelial cells and endothelial basal lamina. By intravital microscopy, the rolling and adhesion of leukocytes were observed within 3 min in preparations activated by fMLP. Neutrophils remained in the vascular wall for more than 30 min even after penetration of the endothelium. In this period, neutrophils migrating between endothelial cells and their basal lamina were often observed by TEM. After 40 min application of fMLP, some of the migrating neutrophils parted from the vessel wall into the surrounding connective tissues. There were neutrophils which passed through the small pore of the basal lamina with a cytoplasmic constriction. These findings indicate that the endothelial basal lamina acts as a physical barrier against neutrophil extravasation, thus resulting in the transient retainment of neutrophils beneath the endothelial cells of the venular wall.

Animals↗
PubMed2003

Blood serum and neutrophil L-arginine concentrations and nitric oxide release by neutrophils in chronic uremic patients and healthy persons.

BACKGROUND: Plasma levels of L-arginine have previously been evaluated in several studies to reveal either down- or up-regulation of the L-arginine/NO pathway in chronic uremia. MATERIAL/METHODS: We studied L-arginine plasma levels along with intracellular neutrophil concentration and NO release by peripheral blood neutrophils in patients with chronic uremia. RESULTS: The L-arginine plasma concentration was found to be significantly higher (64.4 +/- 12.0 micromol/L) in chronic uremic patients (n=25) than in healthy controls (33.0? +/- 10.0 micromol/L; n=25). Neutrophil homogenate L-arginine levels were substantially increased in uremic patients (7.95? +/- 1.10 nmol/10(8) cells) as compared with controls (5.22 +/- 0.46 nmol/10(8) cells). The in vitro release of NO by unstimulated neutrophils was lower in uremic patients (0.14? +/- 0.05? micromol s(-1)) than in healthy persons (0.48 +/- 0.20 micromol s-1). The NO release after uremic neutrophil stimulation with 10(-6) M fMLP was 21.42 +/- 2.13 micromol s(-1), while after PMA it was 31.01 +/- 1.99 micromol s(-1). NO release after normal neutrophil stimulation with 10(-7) M fMLP was 19.52 +/- 2.32 micromol s(-1), and after PMA was 28.63 +/- 3.06 micromol s(-1). CONCLUSIONS: In chronic uremic patients plasma and neutrophil concentrations of L-arginine were significantly higher. However, there were no significant differences in NO release between normal and uremic neutrophils after stimulation. Our findings may have implications for the impact of the L-arginine-nitric oxide signaling pathway on the pathophysiological changes in the L-arginine: NO pathway seen in chronic uremia.

Adult↗
PubMed1992

Neutrophil activation associated with increased neutrophil acyloxyacyl hydrolase activity during inflammation in cattle.

Acyloxyacyl hydrolase (AOAH) is a lysosomal enzyme found in neutrophils and macrophages that acts to partially deacylate the lipid-A component of the endotoxin of gram-negative bacteria rendering it less toxic, yet maintaining much of its immunostimulatory potential. We have found that the activity of neutrophil AOAH per cell increased during localized inflammation. The purpose of this study was to determine the mechanism(s) responsible for these increases in neutrophil AOAH activity. Because changes in neutrophil maturity commonly are associated with inflammation, intravascular infusion of purified gram-negative bacterial lipopolysaccharide and SC injection of bovine recombinant granulocyte colony-stimulating factor was used to induce large numbers of circulating immature neutrophils. Immature neutrophils were found to have AOAH activity equal to that of mature cells; however, when neutrophils were stimulated in vitro with known activators, AOAH activity of activated cells was more than that of unstimulated cells. The increase in AOAH activity was inversely related to prestimulation activity. Increases in AOAH activity after neutrophil activation were not a result of de novo synthesis of the enzyme, because cycloheximide did not prevent activation-induced increases in activity.

Animals↗
PubMed1990

Recombinant gamma interferon causes neutrophil migration mediated by the release of a macrophage neutrophil chemotactic factor.

A dose-dependent neutrophil migration was observed following the injection of purified (Hu IFN-gamma) or recombinant (rIFN-gamma) human gamma interferon into rat peritoneal cavities. This finding contrasts with their inability to cause chemotaxis in vitro in the Boyden chamber. Neutrophil migration into peritoneal cavities and subcutaneous air pouches induced by both preparations of interferon was abolished by pretreatment of the animals with dexamethasone. IFN-gamma-induced neutrophil migration was enhanced when the macrophage population of the peritoneal cavities was increased by previous injection of thioglycollate and reduced by peritoneal lavage. Macrophage monolayers pretreated either with rIFN-gamma or with lipopolysaccharide from E. coli release into the supernatant a factor that stimulates neutrophil recruitment in animals treated with dexamethasone. Dexamethasone blocked this release but did not affect the neutrophil recruitment induced by this factor. These results suggest that IFN-gamma-induced neutrophil migration in vivo may be mediated by the release from resident macrophages of a neutrophil chemotactic factor and that dexamethasone blockade of neutrophil recruitment by IFN-gamma is due to inhibition of the release of this factor.

Animals↗