LPS-induced platelet response and rapid shock in mice: contribution of O-antigen region of LPS and involvement of the lectin pathway of the complement system

Zhao, Lijuan; Ohtaki, Yuko; Yamaguchi, Kohei; Matsushita, Misao; Fujita, Teizo; Yokochi, Takashi; Takada, Haruhiko; Endo, Yasuo

doi:10.1182/blood-2002-01-0252

Cited by 92 publications

(77 citation statements)

References 39 publications

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“…Recently it was demonstrated that LPS being inducers of the anaphylactoid shock bind MBL in vitro [22]. Our data are in agreement with this observation.…”

Section: Discussionsupporting

confidence: 83%

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Role of the complement‐lectin pathway in anaphylactoid reaction induced with lipopolysaccharide in mice

et al. 2003

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We show that Proteus vulgaris O25 (PO25) lipopolysaccharide (LPS) induced an anaphylactoid reaction not only in wild-type and in lipid A non-responding mice but also in recombinase-activating gene-2-deficient (RAG-2 -/-) and in mast cell-deficient (W/Wv) animals. Western blot analysis indicated that PO25 LPS bound to Ra-reactive factor (RaRF), the complex of mannan-binding lectins (MBL) and MBL-associated serine proteases. Binding of RaRF to PO25 LPS led to the activation of C4 component without participation of either C1 or Ig, via the lectin pathway. Relative concentration of RaRF and hemolytic activity in mouse serum decreased rapidly during the process of anaphylactoid reaction. A significant drop of MBL-A, but not MBL-C level was observed. Administration with antiserum to RaRF prevented animals from death as a consequence of the inhibition of interaction of RaRF with the carbohydrate target and complement activation. These results indicate that complementlectin pathway activation is responsible for the anaphylactoid reaction induced with LPS in muramyldipeptide-primed mice. RaRF also activated fibrinogen in vitro suggesting the involvement of the coagulation system in the process investigated.

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“…Recently it was demonstrated that LPS being inducers of the anaphylactoid shock bind MBL in vitro [22]. Our data are in agreement with this observation.…”

Section: Discussionsupporting

confidence: 83%

“…Certain LPS, such as those of PO25 and KO3, induce severe anaphylactoid symptoms in mice [10,13]. This reaction has been hypothesized to be connected with LP activation [22]. Shibazaki et al demonstrated that administration of KO3 LPS causes rapid accumulation and degradation of platelets in liver and lung.…”

Section: Discussionmentioning

confidence: 99%

Role of the complement‐lectin pathway in anaphylactoid reaction induced with lipopolysaccharide in mice

et al. 2003

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“…We evoked complement activation in mice by i.p. administration of LPS (15). Serum IL-1b and IL-18 levels 3 h after LPS treatment were significantly higher than were those in untreated mice.…”

Section: /2mentioning

confidence: 74%

Cutting Edge: The NLRP3 Inflammasome Links Complement-Mediated Inflammation and IL-1β Release

Laudisi

Spreafico

Evrard

et al. 2013

The Journal of Immunology

174

127

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The complement system is a potent component of the innate immune response, promoting inflammation and orchestrating defense against pathogens. However, dysregulation of complement is critical to several autoimmune and inflammatory syndromes. Elevated expression of the proinflammatory cytokine IL-1β is often linked to such diseases. In this study, we reveal the mechanistic link between complement and IL-1β secretion using murine dendritic cells. IL-1β secretion occurs following intracellular caspase-1 activation by inflammasomes. We show that complement elicits secretion of both IL-1β and IL-18 in vitro and in vivo via the NLRP3 inflammasome. This effect depends on the inflammasome components NLRP3 and ASC, as well as caspase-1 activity. Interestingly, sublethal complement membrane attack complex formation, but not the anaphylatoxins C3a and C5a, activated the NLRP3 inflammasome in vivo. These findings provide insight into the molecular processes underlying complement-mediated inflammation and highlight the possibility of targeting IL-1β to control complement-induced disease and pathological inflammation.

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“…resulting in the induction of anaphylactoid shock. [24][25][26][27][28] The lethal toxicity of CAWS 8) and O9 LPS [29][30][31] is similar with respect to the following. 1) Lethal toxicity occurs 15-60 min after intravenous injection.…”

Section: )mentioning

confidence: 99%

Candida albicans Derived Fungal PAMPS, CAWS, Water Soluble Mannoprotein-.BETA.-Glucan Complex Shows Similar Immunotoxicological Activity with Bacterial Endotoxin from Escherichia coli O9

Tada

Nagi-Miura

Adachi

et al. 2006

Biological & Pharmaceutical Bulletin

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Shock is a serious clinical problem because of high mortality. There are many mechanisms inducing shock and major mechanisms related to immune dysfunction are anaphylaxis, septic shock, and endotoxin shock. Shock is usually difficulty to treat, because it is a systemic response involving not only changes in immunological parameters but inducing dysfunction of circulation, coagulation and fibrinolysis. 1) There have been many studies establishing and analyzing animal models of shock. We have also long been analyzing septic and endotoxic shock from various points of view such as, the detoxification of endotoxin by lysozyme, modulation of antibiotic action by lysozyme, 2,3) development of a monoclonal anti-CD14 antibody and its application, 4,5) and establishing an endogenous septic shock model using non-steroidal anti-inflammatory drugs. 6,7) In the course of studying early diagnosis of deep seated fungal infection we have found a limulus factor G activating activity in a water soluble polysaccharide fraction rich in mannan, named Candida albicans water soluble fraction (CAWS), released from Candida albicans, and it strongly caused acute anaphylaxis-like shock in mice. 8)The pathogenic yeast Candida albicans, a commensal of the human digestive tract and vaginal mucosa, is now one of the most common microbes of bloodstream infections in immunocompromised or intensive-care patients.9) The invasive mycoses including candidiasis, aspergillosis and cryptococcosis are increasingly becoming associated with immunosuppressive therapies and immunodeficiency associated with infections of the human immunodeficiency virus. The associated crude mortality is extensively high (38 to 75%), despite appropriate treatment with anti-fungal drugs.10-13) Sepsis, which is caused by a Gram-negative bacterial infection, has also increased for the reasons described above and the associated mortality is markedly high. 14)We previously obtained a water-soluble fraction (CAWS), prepared from the culture supernatants of Candida albicans grown in a completely synthetic medium. CAWS is mainly composed of a complex of mannoprotein and b-1,3-, b-1,6-glucans.15,16) CAWS exhibits various potential biological activities, such as cytokine synthesis by leukocytes, platelet aggregation, lethal toxicity like anaphylactoid shock, induction of coronary arteritis in various strains of mice, and so on. [17][18][19][20] However, the detailed mechanisms of these biological activities are unclear.It is reported that the intravenous injection of lipopolysaccharide from Escherichia coli O9, which possesses the mannose homopolysaccharide (MHP) as the O-antigen region, induced anaphylactoid shock within 15-60 min, but not lipopolysaccharide (LPS) from Escherichia coli O111, which possesses a heterosaccharide (not containing mannose). 21,22) The characteristics of this shock differ from those of the well-known endotoxic shock with respect to time until shock occurs and can be evoked in LPS-hyposensitive mice, like C3H/HeJ strain, 23) with a defect in Toll-like recept...

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LPS-induced platelet response and rapid shock in mice: contribution of O-antigen region of LPS and involvement of the lectin pathway of the complement system

Cited by 92 publications

References 39 publications

Role of the complement‐lectin pathway in anaphylactoid reaction induced with lipopolysaccharide in mice

Role of the complement‐lectin pathway in anaphylactoid reaction induced with lipopolysaccharide in mice

Cutting Edge: The NLRP3 Inflammasome Links Complement-Mediated Inflammation and IL-1β Release

Candida albicans Derived Fungal PAMPS, CAWS, Water Soluble Mannoprotein-.BETA.-Glucan Complex Shows Similar Immunotoxicological Activity with Bacterial Endotoxin from Escherichia coli O9

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