In vitro immunomodulatory effects of pentoxifylline

Rieneck, Klaus; Diamant, Marcus; Haahr, P. M.; Schönharting, Martin; Bendtzen, Klaus

doi:10.1016/0165-2478(93)90022-t

Cited by 56 publications

(22 citation statements)

References 24 publications

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“…Under certain conditions of altered physiology, the neutrophil leukocytes may lead to tissue injury. PTX additionally reduces leukocytosis and neutrophilia, and inhibits the phagocytic activities of monocytes, macrophages and neutrophils as well as degranulation in the latter [44]. We observed that retinas of the group treated with PTX were protected from light-induced retinal injury.…”

Section: Discussionmentioning

confidence: 68%

“…PTX probably acts primarily by inhibiting tumor necrosis factor (TNF), but other cytokines, such as interleukin (IL)-1β, IL-2, IL-6, IL-8, IL-10, γ-interferon and transforming growth factor β, vascular endothelial growth factor as well as adhesion molecules are also implicated. PTX acts as a phosphodiesterase inhibitor and thereby elevates the levels of cyclic adenosine monophosphate [44]. It has also been reported that PTX reduces the local generation of free radicals and infiltration of PMNL and phospholipase A2 activities [15].…”

Section: Discussionmentioning

confidence: 99%

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Effects of Vitamin E, Pentoxifylline and Aprotinin on Light-Induced Retinal Injury

Yılmaz

Aydemir²,

Özercan³

et al. 2007

Ophthalmologica

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Purpose: A considerable amount of clinical and experimental evidence exists suggesting the involvement of reactive oxygen species (ROS) in the etiology of light-induced retinal injury. The aim of this study was to investigate the protective role of vitamin E, pentoxifylline (PTX) and aprotinin against light-induced retinal injury in guinea pigs. Methods: Thirty adult male guinea pigs were divided into 5 groups of 6 animals each. The first group was used as control. The guinea pigs were kept in cyclic light for 2 weeks before the experiments. The animals were maintained in 12-hour light-dark cycles, before and after exposure to intense white fluorescent light, for as long as 12 h and then returned to cyclic light. Groups 3–5 received intraperitoneal injections of vitamin E, PTX and aprotinin, respectively. One eye of each animal was selected for histopathological evaluation and the other for biochemical assay. Retinal malondialdehyde (MDA) levels and the thickness of the outer nuclear layers were measured. Results: The compounds had the following relationships: vitamin E more than PTX more than aprotinin in preventing light-induced retinal damage. All 3 gave significant protection against the formation of MDA. Retinas of all 3 treatment groups had been protected from light-induced injury. Conclusion: The intraperitoneal vitamin E, PTX and aprotinin supplementations may strengthen the antioxidant defense system because of decreased ROS, and these agents may play a role in treating light-induced retinal injury.

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Section: Discussionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Effects of Vitamin E, Pentoxifylline and Aprotinin on Light-Induced Retinal Injury

Yılmaz

Aydemir²,

Özercan³

et al. 2007

Ophthalmologica

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“…shown to inhibit LPS induced TNF-a production in rats, LPS induced sequestration of neutrophils and protected animals from LPS induced mortality [22]. PTX inhibits TNF-a and lymphotoxin production and PTX and the analogues have previously been shown to inhibit both TNF-a and lymphotoxin gene expression [11,23]. PTX modulates meningeal inflammation in experimental Haemophilus influenzae type B meningitis in rabbits [24].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of LPS and Plasmodium falciparum Induced Cytokine Secretion by Pentoxifylline and Two Analogues

1997

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Jakobsen PH, Koch C, Bendtzen K. Inhibition of LPS and Plasmodium falciparum Induced Cytokine Secretion by Pentoxifylline and Two Analogues. Scand J Immunol 1997;45:546-550 Pentoxifylline and the two analogues HWA138 and HWA448, at concentrations exceeding 60 mg/ml, inhibited malaria antigen or lipopolysaccharide (LPS) induced TNF-a and IL-1a secretion, but not IL-6 secretion, from human peripheral blood mononuclear cells in vitro. HWA448 had lower inhibitory activity in vitro than pentoxyfylline and HWA138. A small enhancement of cytokine secretion was induced by pentoxifylline and the two analogues at low concentrations. The drugs did not affect cell viability. Pentoxifylline, HWA138 and HWA448 also inhibited LPS induced TNF production in vivo in female CF1xBalb/c mice. The drugs were inhibitory at 0.5-1 mg per mouse when mixed with LPS, and 1 mg per mouse of the drugs was inhibitory when injected 1 h before LPS challenge. HWA448 had similar inhibitory activities in vivo compared to pentoxifylline and HWA138, possibly because of the longer serum half-life of HWA448. The pentoxifylline analogues may have lower toxicity than pentoxifylline itself and may therefore be useful in future treatment of diseases induced by endotoxic substances.

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“…Employing PTX at concentrations between 0.2 and 0.5 m M , which has been shown to modulate activation of leukocytes [31, 32], endothelial cells [32, 33], and cancer cells [34], we found that PTX (0.5 m M ), like the intracellularly permeable dibutyric cAMP (0.1 m M ), could significantly enhance tRA-induced growth inhibition of HL-60 cells as measured by 3 H-thymidine incorporation assay (fig. 2a), and augment tRA-induced differentiation of HL-60 cells as determined by an increase in cells showing NBT reduction (fig.…”

Section: Resultsmentioning

confidence: 99%

Pentoxifylline Synergizes with All-Trans Retinoic Acid to Induce Differentiation of HL-60 Myelocytic Cells, but Suppresses tRA-Augmented Clonal Growth of Normal CFU-GM

Yang

Chao²,

Shaio

1998

Acta Haematol

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All-trans retinoic acid (tRA) has been shown to promote terminal differentiation of promyelocytic leukemia cells, but frequently induce hyperleukocytosis and pulmonary leakage syndrome. Employing pentoxifylline (PTX), a phosphodiesterase inhibitor which could raise intracellular cAMP and modulate leukocyte activation, we sought to investigate if PTX could enhance tRA-induced promyelocytic leukemic cell differentiation but suppress tRA-augmented growth and activation of human granulocytes. tRA could significantly suppress clonal growth of U937 and HL-60 leukemic cells but enhanced the CFU-GM formation of normal bone marrow cells (22 ± 6 vs. 90 ± 16 CFU/well). PTX significantly augmented tRA suppression of clonal growth of U937 and HL-60 leukemic cells but suppressed tRA-augmented CFU-GM formation of normal bone marrow cells (90 ± 16 vs. 25 ± 9 CFU/well). In addition, PTX enhanced tRA-induced growth inhibition and differentiation of promyelocytic HL-60 leukemic cells, but suppressed respiratory burst activation by the immature granulocytic HL-60 cells and suppressed CD11b adhesion molecule expression by mature granulocytes. PTX similar to dibutyric cAMP promoted HL-60 myelocytic leukemic cell differentiation and growth inhibition, whereas PTX, in contrast to dibutyric cAMP which could augment phorbol myristate acetate (PMA)-elicited respiratory burst activity by immature granulocytes, suppressed the PMA-elicited respiratory burst activity by immature and mature granulocytes. PTX did not raise the intracellular cAMP level of HL-60 cells, but partly suppressed the dibutyric cAMP-elicited elevation of intracellular cAMP level. Results from these studies suggest that PTX might act through different signaling pathways to enhance tRA-induced myelocytic leukemic cell differentiation but prevent from hyperreactive normal granulopoiesis and granulocyte activation.

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In vitro immunomodulatory effects of pentoxifylline

Cited by 56 publications

References 24 publications

Effects of Vitamin E, Pentoxifylline and Aprotinin on Light-Induced Retinal Injury

Effects of Vitamin E, Pentoxifylline and Aprotinin on Light-Induced Retinal Injury

Inhibition of LPS and Plasmodium falciparum Induced Cytokine Secretion by Pentoxifylline and Two Analogues

Pentoxifylline Synergizes with All-Trans Retinoic Acid to Induce Differentiation of HL-60 Myelocytic Cells, but Suppresses tRA-Augmented Clonal Growth of Normal CFU-GM

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