Pathobiochemie und Chirurgie: Neue Ansätze zur Diagnostik und Therapie schwerer entzündlicher Erkrankungen

Jochum, Marianne; Witte, J.; Duswald, Karl-Heimo; Inthorn, D.; Welter, Harald; Fritz, Hans

doi:10.1007/978-3-642-70648-6_10

Cited by 4 publications

(2 citation statements)

References 18 publications

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“…One of the well-known actions of lipopolysaccharides in host organisms is the induction of proteolytic enzyme release by leukocyte degranulation [34], an event recently shown to be mediated by tumor necrosis factor and not by interleukin-1, as previously believed. Proteolytic release of peptides, which in turn act proteolytically on other proenzymes, represents the mechanism by which the cascades of blood coagulation and fibrinolysis as well as the complement and kallikrein/kinin system are activated [75].…”

Section: Discussionmentioning

confidence: 82%

Repression of alpha2-macroglobulin and stimulation of alpha1-proteinase inhibitor synthesis in human mononuclear phagocytes by endotoxin

Ganter¹,

Bauer²,

SCHULZ-HUOTARI³

et al. 1987

Eur J Biochem

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Mononuclear phagocytes are a bone-marrow-derived subgroup of white blood cells which circulate as monocytes and, after differentiation into macrophages, become resident in many tissues. By synthesizing the important proteinase inhibitors a,-macroglobulin and al-proteinase inhibitor mononuclear phagocytes contribute to the control of proteolysis both in blood and tissues. Applying a culture system which enables human blood monocytes to differentiate into macrophages in vitro, synthesis of a,-macroglobulin and al-proteinase inhibitor was studied. The normal course of monocyte -macrophage maturation is accompanied by a strong increase of specific a,-macroglobulin synthesis and a concomitant slight decrease of al-proteinase inhibitor. a,-Macroglobulin can be designated as a marker protein of the monocyte/macrophage differentiation. Endotoxin (Salmonella ryphi) in a concentration as low as 100 ng/ml strongly represses a,-macroglobulin synthesis both in monocytes and macrophages. Furthermore, endotoxin completely abolishes the induction of a,-macroglobulin synthesis during the course of normal monocyte in vitro cultivation, indicating that endotoxin is a strong inhibitor of the monocyte -macrophage maturation. In contrast to a,-macroglobulin, al-proteinase inhibitor synthesis is strongly stimulated by endotoxin in monocytes as well as in macrophages.The cells of the mononuclear phagocyte system derive from stem cells in the bone marrow, linking monoblasts, promonocytes, monocytes and the heterogeneous tissue macrophages (for review see [l -31). Cells of this lineage develop over several days in the marrow and circulate as monocytes in the peripheral blood for a few further days before migrating into different tissues, where they remain resident for up to several months as macrophages. Macrophages are present in the liver (as Kupffer cells), lung (as alveolar macrophages), bone (as osteoclasts) and several other tissues. The development of the blood monocytes into macrophages is accompanied by marked morphological and biochemical changes and is designated as terminal maturation. Differentiation of monocytes into macrophages can be studied in vitro by cultivation of purified populations of human peripheral blood monocytes within hydrophobic Teflon foils in the presence of human serum [4]. In vitro maturation closely resembles differentiation in vivo [5].Secretory products of mononuclear phagocytes are involved in several macrophage functions, such as immunoregulation and the killing of bacteria (for review see [3,61). Several proteinase inhibitors were found to belong to the proteins secreted by mononuclear phagocytes including azCorrespondence to J. Bauer, Medizinische Universitatsklinik, Hugstetter StraSe 55, D-7800 Freiburg, Federal Republic of Germany This work is dedicated to Prof. Dr Georg Wilhelm Lohr on the occasion of his 65th birthday.Abbreviations. E~M , a2-macroglobulin, q P I , ccl-proteinase inhibitor; RPMI, Roswell Park Memorial Institute 1640 medium. macroglobulin (azM) [7] and a]-proteinase inhibitor (a...

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Section: Discussionmentioning

confidence: 82%

Repression of alpha2-macroglobulin and stimulation of alpha1-proteinase inhibitor synthesis in human mononuclear phagocytes by endotoxin

Ganter¹,

Bauer²,

SCHULZ-HUOTARI³

et al. 1987

Eur J Biochem

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“…Ziel dieser Mal3nahmen war es im allgemeinen, die zum Teil fiberschieBend freigesetzten Substanzen oder Rekationsprodukte durch Hemmsubstanzen oder durch Antik6rper zu neutralisieren [18]. Ziel dieser Mal3nahmen war es im allgemeinen, die zum Teil fiberschieBend freigesetzten Substanzen oder Rekationsprodukte durch Hemmsubstanzen oder durch Antik6rper zu neutralisieren [18].…”

Section: Therapie Des Septischen Schocksunclassified

Blutung, Schock und Sepsis

Graeff

Deckardt

1989

Arch Gynecol Obstet

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Hemorrhage and sepsis may lead to multiple organ system failure caused by a redistribution of cardiac output and a reduction of tissue perfusion. The pathophysiologic changes caused by hemorrhage are frequently prevented by rapid diagnosis of the cause of the bleeding (e.g., vessel injury or coagulation disorder) and its therapy. The pathophysiologic changes in sepsis are mediated by toxins which affect almost every organ system. Knowledge of the predisposing factors, rapid recognition of signs and symptoms, and understanding of the underlying pathobiochemical and pathophysiologic changes are mandatory in the successful therapy of septic shock. The main therapeutic principle remains removal of the focus.

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Blutung, Schock und Sepsis

Graeff

Deckardt

1989

Gynäkologie Und Geburtshilfe 1988

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Pathobiochemie und Chirurgie: Neue Ansätze zur Diagnostik und Therapie schwerer entzündlicher Erkrankungen

Cited by 4 publications

References 18 publications

Repression of alpha2-macroglobulin and stimulation of alpha1-proteinase inhibitor synthesis in human mononuclear phagocytes by endotoxin

Repression of alpha2-macroglobulin and stimulation of alpha1-proteinase inhibitor synthesis in human mononuclear phagocytes by endotoxin

Blutung, Schock und Sepsis

Blutung, Schock und Sepsis

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