Journal ArticleDOI
Suggested importance of monokines in pathophysiology of endotoxin shock and malaria
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There are many similarities in the pathophysiology of gram-negative infections and in acute falciparum malaria, and the notion that macrophage derived mediators may be responsible, at least in part, for the pathology observed in malaria is suggested.Abstract:
There are many similarities in the pathophysiology of gram-negative infections and in acute falciparum malaria. Particularly, noteworthy is the detection of circulating inflammatory mediators in animals receiving endotoxin and in animals infected with malarial parasites. These observations have lead to the notion that macrophage derived mediators may be responsible, at least in part, for the pathology observed in malaria.read more
Citations
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Cytokine storm and sepsis disease pathogenesis
TL;DR: The pathophysiology of the cytokine storm is summarized; the type, effects, and kinetics of cytokine production are described; and new promising therapeutic strategies focusing on the endothelium, as a source and a target of cytokines are described.
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Human malarial disease: a consequence of inflammatory cytokine release
TL;DR: The evidence is considered that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen.
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Tumor-Necrosis Factor and other Cytokines in Cerebral Malaria: Experimental and Clinical Data
TL;DR: Evidence is presented here that tumor necrosis factor/cachectin (TNF), is of crucial importance in the pathogenesis of cerebral malaria and metabolic parameters of CM and its main lesion in both mouse and human, correspond to the known properties of TNF.
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How TNF was recognized as a key mechanism of disease
TL;DR: This review summarizes the origins of the insight that excess production of pro-inflammatory cytokines caused a constellation of changes that contribute to pathophysiology of disease.
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The pathophysiology of falciparum malaria.
Ian A. Clark,William B. Cowden +1 more
TL;DR: It is plausible that this will be demonstrable in severe falciparum malaria, and it is argued that it can best be understood in terms of excessive stimulation of normally useful pathways mediated by inflammatory cytokines, the prototype being tumor necrosis factor (TNF).
References
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An endotoxin-induced serum factor that causes necrosis of tumors
TL;DR: It is proposed that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages.
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Possible importance of macrophage-derived mediators in acute malaria.
TL;DR: It is proposed that these macrophage-derived mediators may be important in the glucocorticoid antagonism, bone marrow depression, fever, hypergammaglobulinemia, splenomegaly, elevation of serum amyloid A, consumptive coagulopathy, and shock syndrome with associated organ damage which can accompany malaria.
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Protection of mice against babesia and plasmodium with bcg.
TL;DR: It is suggested that Mycobacterium bovis strain BCG protects by increasing the release of non-antibody soluble mediators of immunity postulated to cause the death of B.microti inside red cells2.
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Cerebral arteriolar damage by arachidonic acid and prostaglandin G2
TL;DR: Application of arachidonic acid or prostaglandin G(2) to the brain surface of anesthetized cats induced cerebral arteriolar damage and increased prostaglandsin synthesis produces cerebral vascular damage by generating free oxygen radicals.
Journal Article
Endogenous pyrogens made by rabbit peritoneal exudate cells are identical with lymphocyte-activating factors made by rabbit alveolar macrophages.
TL;DR: Results are consistent with the idea that EP and LAF are identical, and analysis for LAF activity showed an identical microheterogeneity.