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  • 1.
    Nyhlen, Kristina
    et al.
    Department of Nephrology, University Hospital, Lund, and Department of Preclinical Research, Gambro Lundia AB, Lund, Sweden.
    Hultkvist-Bengtsson, U.
    Department of Preclinical Research, Gambro Lundia AB, Lund, Sweden.
    Nilsson, M.
    Department of Preclinical Research, Gambro Lundia AB, Lund, Sweden.
    Rippe, B.
    Department of Nephrology, University Hospital, Lund.
    Leukocyte sequestration in isolated guinea pig lungs during extracorporeal circulation: effects on microvascular function2000In: Blood Purification, ISSN 0253-5068, E-ISSN 1421-9735, Vol. 18, no 2, p. 121-127Article in journal (Refereed)
    Abstract [en]

    Neutrophils accumulate in patient lungs during clinical hemodialysis and in isolated blood-perfused guinea pig lungs due to the contact between blood and extracorporeal system. However, it is unclear how these sequestered and partly activated neutrophils affect the lung microvasculature. We, therefore, studied pulmonary vascular resistance, vascular permeability, gas exchange, and oxygen free radical production in isolated guinea pig lungs during perfusion with whole blood containing partly ‘activated’ neutrophils in comparison with perfusions using leukopenic blood. We also connected a Cuprophan hemodialysis membrane to the whole-blood perfusion system in order to investigate whether a dialyzer, which may further activate leukocytes, affects lung microvascular permeability, vascular resistances, and reactive oxygen species production. The sequestered neutrophils did not seem to markedly affect the lung microvascular function, since neither the leukocyte-free perfusion nor the hemodialysis membrane altered any of the measured variables as compared with whole-blood perfusion in a system without a dialyzer. We conclude that neutrophils, whether activated by a perfusion system or by a dialysis membrane, can accumulate in isolated lungs without adversely affecting the microvascular function.

  • 2.
    Nyhlen, Kritsina
    et al.
    Department of Preclinical Research, Gambro Lundia AB, Lund, Sweden and Department of Nephrology, University Hospital, Lund, Sweden.
    Rippe, B.
    Department of Nephrology, University Hospital, Lund, Sweden.
    Hultkvist-Bengtsson, U.
    Department of Preclinical Research, Gambro Lundia AB, Lund, Sweden.
    An isolated blood-perfused guinea-pig lung model for simultaneous registration of haemodynamic, microvascular and respiratory variables1997In: Acta Physiologica Scandinavica, ISSN 0001-6772, E-ISSN 1365-201X, Vol. 159, no 4, p. 293-302Article in journal (Refereed)
    Abstract [en]

    We have developed an optimized isolated lung perfusion system, which possesses several advantages. Firstly, studies of microvascular, respiratory, haematological and biochemical variables are combined in one model. Secondly, blood perfusion resulted in less oedema formation than buffer-perfused lungs, and high Po2 through ventilation with room air. Finally, data for the variables can be displayed, controlled and recorded in real time using a computerized system permitting subsequent processing (e.g. filtering without destroying original data). In this paper we discuss the basic behaviour of the model in terms of vascular resistance, vascular permeability, respiration and neutrophil sequestration. In addition, the effects of oleic acid, histamine and histamine receptor blockers were tested, and two methods of calculating vascular permeability are discussed. The way in which different anaesthetics affect the neutrophil content of lung tissue and blood was also investigated. In the model, oleic acid increased pulmonary vascular resistance and permeability, whereas histamine did not affect either permeability or the pre/postcapillary vascular resistance ratio. However, histamine receptor blockers increased this ratio, indicating that there was endogenous histamine release. The neutrophil content of the isolated lungs was increased, but this did not affect the variables measured. There was also accumulation of neutrophils in the lungs of blood donor animals, due to CO2 sedation. However, CO2 sedation proved to be superior to pentobarbital or ketamine anaesthesia in maintaining the levels of neutrophils circulating in the blood. In conclusion, this model seems to be sensitive and to yield reproducible results regarding the physiology or pathophysiology of the lung.

  • 3.
    Nyhlén, Kristina
    Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
    Leukocyte sequestration associated with inflammation: mechanisms and modulations2003Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    The inflammatory response is the first line of defence against injurious agents. It is a multi-faceted response involving several mechanisms orchestrated by inflammatory mediators such as cytokines, chemokines and adhesion molecules. The inflammatory response is characterised by leukocytes migrating through the endothelium towards the site of inflammation as well as increased capillary permeability resulting in oedema. ln some diseases such as autoimmune diseases and chronic inflammation the inflammatory response is inappropriately triggered and may be harmful to the tissue. In addition, some clinical procedures e.g. haemodialysis cause leukocytes to sequester in the lung, which may affect the pulmonary microvasculature. In this thesis, the effects and mechanisms of leukocyte sequestration were studied ex vivo and, on a molecular level, in vitro in order to get a broader understanding of the inflarmnatory response. The results indicated that leukocytes were able to sequester in the lung microvasculature without affecting the capillary permeability, microvascular resistance or release of oxygen free radicals in the isolated blood-perfused guinea-pig lung. It seemed like the neutrophils were sequestered due to mechanical forces rather than activation, since the model turned out to be a sensitive method for measuring microvascular and respiratory variables in a wellcontrolled environment with all cellular interactions maintained in the tissue. Haemodialysis treatment was simulated in this model, but the connection of a dialysis membrane in the perfusion system did not seem to activate neutrophils to the extent that they generate oxygen free radicals or alter capillary permeability. Nevertheless inappropiate sequestration of neutrophils can be hannful in several diseases and therapeutic modulation of leukocyte sequestration can therefore be of interest IL-8 is a chemokine involved in the inflammatory response, mainly attracting neutrophils to the site of intlannnation. Different cells including endothelial cells produce IL-8. In this study we stimulated endothelial cells with the inflannnatory cytokines IL-1ß or TNF-α to simulate the inflammatory response. It resulted in an increased expression of adhesion molecules as well as dramatically increased secretion and production of IL-8. The present study showed that cytokine-induced IL-8 secretion and production could be inhibited by the innnunomodulatory cytokine IFN-γ and anti-intlannnatory glucocorticosteroids. Steroids and intetferons are used therapeutically in the treatment of autoimmune and inflammatory disorders, although the exact mechanisms of inhibition are not fully elucidated. Taken together, results from ELISA, flow cytornetry and RT-PCR suggested that IFN-γ and corticosteroids inhibit synthesis rather than intracellular transport of IL-8. Their inhibitory effect is probably mediated by the transcription factor NF-K'B, since this factor is probably involved in the cytokineinduced production of IL-8. Basal production of IL-8 by endothelial cells was inhibited by IFN-γ but not by glucocorticosteroids suggesting that the basal production may be mediated through systems other than NF-κB. In conclusion, this thesis reports that leukocytes can sequester in the pulmonary capillaries due to factors other than adhesion molecules and without affecting the microvasculature. However, when leukocyte sequestration involves IL-8, interfemns and glucocorticostemids might present novel opportunities for therapeutic amelioration of deleterious effects associated with leukocyte sequestration.

    List of papers
    1. An isolated blood-perfused guinea-pig lung model for simultaneous registration of haemodynamic, microvascular and respiratory variables
    Open this publication in new window or tab >>An isolated blood-perfused guinea-pig lung model for simultaneous registration of haemodynamic, microvascular and respiratory variables
    1997 (English)In: Acta Physiologica Scandinavica, ISSN 0001-6772, E-ISSN 1365-201X, Vol. 159, no 4, p. 293-302Article in journal (Refereed) Published
    Abstract [en]

    We have developed an optimized isolated lung perfusion system, which possesses several advantages. Firstly, studies of microvascular, respiratory, haematological and biochemical variables are combined in one model. Secondly, blood perfusion resulted in less oedema formation than buffer-perfused lungs, and high Po2 through ventilation with room air. Finally, data for the variables can be displayed, controlled and recorded in real time using a computerized system permitting subsequent processing (e.g. filtering without destroying original data). In this paper we discuss the basic behaviour of the model in terms of vascular resistance, vascular permeability, respiration and neutrophil sequestration. In addition, the effects of oleic acid, histamine and histamine receptor blockers were tested, and two methods of calculating vascular permeability are discussed. The way in which different anaesthetics affect the neutrophil content of lung tissue and blood was also investigated. In the model, oleic acid increased pulmonary vascular resistance and permeability, whereas histamine did not affect either permeability or the pre/postcapillary vascular resistance ratio. However, histamine receptor blockers increased this ratio, indicating that there was endogenous histamine release. The neutrophil content of the isolated lungs was increased, but this did not affect the variables measured. There was also accumulation of neutrophils in the lungs of blood donor animals, due to CO2 sedation. However, CO2 sedation proved to be superior to pentobarbital or ketamine anaesthesia in maintaining the levels of neutrophils circulating in the blood. In conclusion, this model seems to be sensitive and to yield reproducible results regarding the physiology or pathophysiology of the lung.

    Keywords
    anaesthesia; capillary permeability; histamine; histamine receptor blockers; MPO; oleic acid; pulmonary resistance
    National Category
    Medical and Health Sciences
    Identifiers
    urn:nbn:se:liu:diva-81852 (URN)10.1046/j.1365-201X.1997.00103.x (DOI)
    Available from: 2012-09-24 Created: 2012-09-24 Last updated: 2017-12-07Bibliographically approved
    2. Leukocyte sequestration in isolated guinea pig lungs during extracorporeal circulation: effects on microvascular function
    Open this publication in new window or tab >>Leukocyte sequestration in isolated guinea pig lungs during extracorporeal circulation: effects on microvascular function
    2000 (English)In: Blood Purification, ISSN 0253-5068, E-ISSN 1421-9735, Vol. 18, no 2, p. 121-127Article in journal (Refereed) Published
    Abstract [en]

    Neutrophils accumulate in patient lungs during clinical hemodialysis and in isolated blood-perfused guinea pig lungs due to the contact between blood and extracorporeal system. However, it is unclear how these sequestered and partly activated neutrophils affect the lung microvasculature. We, therefore, studied pulmonary vascular resistance, vascular permeability, gas exchange, and oxygen free radical production in isolated guinea pig lungs during perfusion with whole blood containing partly ‘activated’ neutrophils in comparison with perfusions using leukopenic blood. We also connected a Cuprophan hemodialysis membrane to the whole-blood perfusion system in order to investigate whether a dialyzer, which may further activate leukocytes, affects lung microvascular permeability, vascular resistances, and reactive oxygen species production. The sequestered neutrophils did not seem to markedly affect the lung microvascular function, since neither the leukocyte-free perfusion nor the hemodialysis membrane altered any of the measured variables as compared with whole-blood perfusion in a system without a dialyzer. We conclude that neutrophils, whether activated by a perfusion system or by a dialysis membrane, can accumulate in isolated lungs without adversely affecting the microvascular function.

    Keywords
    oxygen free radicals, isolated lung, capillary permeability, hemodialysis
    National Category
    Natural Sciences
    Identifiers
    urn:nbn:se:liu:diva-49687 (URN)10.1159/000014435 (DOI)10838471 (PubMedID)
    Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2017-12-12Bibliographically approved
    3. Corticosteroids and interferons inhibit cytokine-induced production of IL-8 by human endothelial cells
    Open this publication in new window or tab >>Corticosteroids and interferons inhibit cytokine-induced production of IL-8 by human endothelial cells
    2000 (English)In: Cytokine, ISSN 1043-4666, E-ISSN 1096-0023, Vol. 12, no 4, p. 355-360Article in journal (Refereed) Published
    Abstract [en]

    IL-8, secreted by endothelial cells at the site of inflammation, participates in recruitment and transmigration of leukocytes. IL-8 may also have pathophysiological consequences in inflammatory and immunological disorders. We have investigated the effect of interferons (IFNs) and glucocorticosteroids (GCs) on cytokine induced secretion and production of IL-8 by human umbilical endothelial cells (HUVEC). There was a low spontaneous secretion of IL-8 by unstimulated HUVEC which increased after 6 or 24 h of stimulation with the pro-inflammatory cytokines TNF-α or IL-1β. IFN-γ as well as the GCs, Dexamethasone and Budesonide, inhibited TNF-α induced IL-8 secretion in a dose-dependent manner. IFNs may have a general modulating effect, since IFN-α also inhibited the TNF-α-induced IL-8 secretion. There was a slight, but significant, increase in the content of intracellular IL-8 in stimulated HUVEC. However, there was no difference between stimulation with IL-1β or TNF-α alone or in combination with IFNs or GCs, whereas inhibition of IL-8 secretion with monensin increased IL-8 content suggesting that IFNs and GCs inhibit synthesis rather than secretion of IL-8. In conclusion, IFNs or GCs may be useful for inhibiting IL-8 production by endothelial cells and could thus be used for therapeutic modulation of the inflammatory response.

    National Category
    Medical and Health Sciences
    Identifiers
    urn:nbn:se:liu:diva-47672 (URN)10.1006/cyto.1999.0557 (DOI)
    Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2017-12-13Bibliographically approved
    4. Modulation of Cytokine-Induced Production of IL-8 in Vitro by Interferons and Glucocorticosteroids
    Open this publication in new window or tab >>Modulation of Cytokine-Induced Production of IL-8 in Vitro by Interferons and Glucocorticosteroids
    2004 (English)In: Inflammation, ISSN 0360-3997, E-ISSN 1573-2576, Vol. 28, no 2, p. 77-88Article in journal (Refereed) Published
    Abstract [en]

    Interleukin-8 (IL-8) has been implicated in the pathogenesis of inflammation and cancer. Intracellular levels of cytokine-induced IL-8 in human umbilical vein endothelial cells (HUVEC) were modulated using interferons and steroids to further elucidate their mechanism. Basal and cytokine-induced production of IL-8 was studied using a novel ELISA application, flow cytometry, and RT-PCR. The intracellular amount of IL-8 increased after 6-h stimulation with TNF- (30%) or IL-1ß (55%) which was doubled when Golgi transport was disrupted using monensin. IFN-γ decreased the intracellular amount of IL-8 by 60% in both unstimulated and TNF--stimulated cells, but only when secretion was blocked using monensin. Dexamethasone inhibited the TNF--induced production by 33%, but had no effect in unstimulated cells. Our study indicated that both, dexamethasone and IFN inhibit TNF--induced upregulation of IL-8 at the mRNA level. It could be speculated that they inhibit IL-8 production by affecting different gene regulatory mechanisms.

    National Category
    Medical and Health Sciences
    Identifiers
    urn:nbn:se:liu:diva-24058 (URN)10.1023/B:IFLA.0000033023.76110.51 (DOI)3617 (Local ID)3617 (Archive number)3617 (OAI)
    Available from: 2009-10-07 Created: 2009-10-07 Last updated: 2017-12-13Bibliographically approved
  • 4.
    Nyhlén, Kristina
    et al.
    Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
    Gautam, Chamilly
    Hospital Pharmacy, University Hospital, Linköping, Sweden.
    Andersson, Rolf
    Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
    Uppugunduri, Srinivas
    Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
    Modulation of Cytokine-Induced Production of IL-8 in Vitro by Interferons and Glucocorticosteroids2004In: Inflammation, ISSN 0360-3997, E-ISSN 1573-2576, Vol. 28, no 2, p. 77-88Article in journal (Refereed)
    Abstract [en]

    Interleukin-8 (IL-8) has been implicated in the pathogenesis of inflammation and cancer. Intracellular levels of cytokine-induced IL-8 in human umbilical vein endothelial cells (HUVEC) were modulated using interferons and steroids to further elucidate their mechanism. Basal and cytokine-induced production of IL-8 was studied using a novel ELISA application, flow cytometry, and RT-PCR. The intracellular amount of IL-8 increased after 6-h stimulation with TNF- (30%) or IL-1ß (55%) which was doubled when Golgi transport was disrupted using monensin. IFN-γ decreased the intracellular amount of IL-8 by 60% in both unstimulated and TNF--stimulated cells, but only when secretion was blocked using monensin. Dexamethasone inhibited the TNF--induced production by 33%, but had no effect in unstimulated cells. Our study indicated that both, dexamethasone and IFN inhibit TNF--induced upregulation of IL-8 at the mRNA level. It could be speculated that they inhibit IL-8 production by affecting different gene regulatory mechanisms.

  • 5.
    Nyhlén, Kristina
    et al.
    Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
    Linden, Margareta
    Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
    Andersson, Rolf
    Department of Cell & Molecular Biology, Astra Draco AB, Lund, Sweden.
    Uppugunduri, Srinivas
    Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
    Corticosteroids and interferons inhibit cytokine-induced production of IL-8 by human endothelial cells2000In: Cytokine, ISSN 1043-4666, E-ISSN 1096-0023, Vol. 12, no 4, p. 355-360Article in journal (Refereed)
    Abstract [en]

    IL-8, secreted by endothelial cells at the site of inflammation, participates in recruitment and transmigration of leukocytes. IL-8 may also have pathophysiological consequences in inflammatory and immunological disorders. We have investigated the effect of interferons (IFNs) and glucocorticosteroids (GCs) on cytokine induced secretion and production of IL-8 by human umbilical endothelial cells (HUVEC). There was a low spontaneous secretion of IL-8 by unstimulated HUVEC which increased after 6 or 24 h of stimulation with the pro-inflammatory cytokines TNF-α or IL-1β. IFN-γ as well as the GCs, Dexamethasone and Budesonide, inhibited TNF-α induced IL-8 secretion in a dose-dependent manner. IFNs may have a general modulating effect, since IFN-α also inhibited the TNF-α-induced IL-8 secretion. There was a slight, but significant, increase in the content of intracellular IL-8 in stimulated HUVEC. However, there was no difference between stimulation with IL-1β or TNF-α alone or in combination with IFNs or GCs, whereas inhibition of IL-8 secretion with monensin increased IL-8 content suggesting that IFNs and GCs inhibit synthesis rather than secretion of IL-8. In conclusion, IFNs or GCs may be useful for inhibiting IL-8 production by endothelial cells and could thus be used for therapeutic modulation of the inflammatory response.

  • 6.
    Persson, Karin
    et al.
    Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences.
    Whiss, Per A.
    Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences.
    Nyhlén, Kristina
    Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences.
    Jacobsson-Strier, Monica
    Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
    Glindell, Maria
    Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
    Andersson, Rolf G. G.
    Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
    NO donors and ACE inhibitors act in concert to inhibit human ACE activity and platelet aggregation in vitroManuscript (preprint) (Other academic)
    Abstract [en]

    This study investigates the effects of exogenous and endogenous nitric oxide (NO) on human circulating and endothelial angiotensin-converting enzyme (ACE) activity, and platelet aggregation. The NO donor S-nitroso N-acetylpenicillamine SNAP (10-8-10-6 M) significantly and dose-dependently inhibited serum ACE activity. The concomitant addition of SNAP to ACE inhibitor-treated (captopril or enalaprilat) serum, further reduced ACE activity. In cultured endothelial cells from human umbilical veins (HUVEC), both SNAP and 3-morpholinosydnonimine (SIN-1) significantly reduced ACE activity. An additative effect was seen with a combined treatment of captopril and SNAP. Treatment with the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) did not affect ACE activity. Thrombin inhibited endothelial ACE activity, an effect that was abolished when cells were pretreated with L-NMMA. ADP-induced platelet aggregation was inhibited with SNAP, SIN-1 and nitroglycerine (GTN). Captopril did not affect aggregation, while a high concentration of enalaprilat (10-4 M) reduced it. The concomitant addition of 10-5 M ACE inhibitor to NO donor-treated platelets resulted in a further reduction of platelet aggregation. This effect was most evident with SIN-I and enalaprilat. In conclusion, both exogenous and endogenous NO inhibit human ACE activity. NO donors and ACE inhibitors act in concert to inhibit ACE and platelet aggregation. 

  • 7.
    Persson, Karin
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Pharmacology .
    Whiss, Per
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Pharmacology .
    Nyhlén, Kristina
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Nursing Science.
    Jacobsson-Strier, M.
    Glindell, M.
    Andersson, Rolf
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Pharmacology .
    Nitric oxide donors and angiotensin-converting enzyme inhibitors act in concert to inhibit human angiotensin-converting enzyme activity and platelet aggregation in vitro2000In: European Journal of Pharmacology, ISSN 0014-2999, E-ISSN 1879-0712, Vol. 406, no 1, p. 15-23Article in journal (Refereed)
    Abstract [en]

    This study investigates the effects of exogenous and endogenous nitric oxide (NO) on human circulating and endothelial angiotensin-converting enzyme activity and platelet aggregation. The NO donor S-nitroso-N-acetylpenicillamine (10-8-10-6 M) significantly and dose-dependently inhibited serum angiotensin-converting enzyme activity. The concomitant addition of S-nitroso-N-acetylpenicillamine to angiotensin-converting enzyme inhibitor-treated (captopril or enalaprilat) serum, further reduced angiotensin-converting enzyme activity. In cultured endothelial cells from human umbilical veins (HUVECs), both S-nitroso-N-acetylpenicillamine and 3-morpholinosydnonimine (SIN-1) significantly reduced angiotensin-converting enzyme activity. An additative effect was seen with a combined treatment of captopril and S-nitroso-N-acetylpenicillamine. Treatment with the NO synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA) did not affect angiotensin-converting enzyme activity. Thrombin inhibited endothelial angiotensin-converting enzyme activity, an effect that was abolished when cells were pretreated with L-NMMA. Adenosine 5'-diphosphate (ADP)-induced platelet aggregation was inhibited with S-nitroso-N-acetylpenicillamine, SIN-1 and nitroglycerine. Captopril did not affect aggregation, while a high concentration of enalaprilat (10-4 M) reduced it. The concomitant addition of 10-5 M angiotensin-converting enzyme inhibitor to NO donor-treated platelets resulted in a further reduction of platelet aggregation. This effect was most evident with SIN-1 and enalaprilat. In conclusion, both exogenous and endogenous NO inhibit human angiotensin-converting enzyme activity. NO donors and angiotensin-converting enzyme inhibitors act in concert to inhibit angiotensin-converting enzyme and platelet aggregation. Copyright (C) 2000 Elsevier Science B.V.

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