Preliminary report: complement activation in wasp-sting anaphylaxis

Linden, P.-W. G. Van Der; Hack, C. E.; Kerckhaert, J.; Struyvenberg, A; Zwan, J. C. van der

doi:10.1016/0140-6736(90)92272-j

Cited by 62 publications

(24 citation statements)

References 19 publications

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“…According to reports on C1q increased vasopermeability and loss of proteins into the interstitial space are not responsible for decreased serum levels in anaphylactic shock [6, 11]. This is in accordance with our results on MBL.…”

Section: Discussionsupporting

confidence: 82%

“…It is believed that complement activation in anaphylactic shock occurs via the classical pathway, as serum C1q levels decrease after antigenic challenge [6, 11]. In this study we demonstrate that the lectin pathway might be involved as well, since serum MBL levels decreased in our mouse model of anaphylaxis.…”

Section: Introductionsupporting

confidence: 49%

“…It is believed that this activation occurs via the classical pathway, as serum C1q levels are diminished [6, 11]. We observed that also the lectin pathway of complement activation is involved, as sera taken after challenge from mice showed a decreased capacity to cleave C4 as well as diminished MBL levels, suggesting lectin pathway activation or, at least, MBL consumption or redistribution during anaphylaxis.…”

Section: Discussionmentioning

confidence: 56%

“…During anaphylactic shock the complement system is activated [5, 6, 11]. It is believed that this activation occurs via the classical pathway, as serum C1q levels are diminished [6, 11].…”

Section: Discussionmentioning

confidence: 99%

“…Common allergens like house dust and Aspergillus fumigatus lead to the generation of the anaphylatoxins C3a, C4a and C5a when incubated with human serum [4]. Elevated levels of the anaphylatoxin C3a have been found in a cardiac anaphylaxis model in the guinea pig [5] and in the blood of patients undergoing immediate hypersensitivity reactions [6]. Pre-treatment with soluble complement receptor 1, which binds C3b and C4b and inhibits further C3a generation, ameliorated the symptoms [7], whereas inhibition of C3a inactivation prolonged the anaphylactic reaction [5].…”

Section: Introductionmentioning

confidence: 99%

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Investigations on the Involvement of the Lectin Pathway of Complement Activation in Anaphylaxis

Windbichler

Echtenacher

Takahashi

et al. 2006

Int Arch Allergy Immunol

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Background: Systemic anaphylaxis is the most severe form of immediate hypersensitivity reaction. The activation of the complement system occurs during anaphylactic shock. The purpose of this study was to determine in a mouse model whether the lectin pathway of complement activation is involved in anaphylaxis. Methods: To see whether the lectin pathway is involved in anaphylactic shock, serum mannan-binding lectin (MBL) levels were measured after passive anaphylaxis. Also MBL expression and binding to potential ligands were investigated. To determine whether complement or mast cell activation is essential for hypothermia in anaphylactic shock, mouse strains deficient in MBL-A and MBL-C, C1q, factors B and C2, C5, C5aR, or mast cells were tested. Results: After antigenic challenge a marked drop in body temperature as well as a rapid decrease in serum MBL levels were observed. The decrease of serum MBL levels in shock could not be attributed to MBL binding to immune complexes or tissues, but an interaction of MBL with mast cell-derived proteoglycans was seen. In contrast to mast cell-deficient mice, none of the complement-deficient mouse strains were protected from shock-associated hypothermia. Conclusions: These results indicate that neither MBL nor activation of the complement cascade is crucial for the induction of anaphylaxis. In contrast mast cell activation is associated with the development of hypothermia and possibly the observed decrease in serum MBL levels.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionsupporting

confidence: 49%

Section: Discussionmentioning

confidence: 56%

“…During anaphylactic shock the complement system is activated [5, 6, 11]. It is believed that this activation occurs via the classical pathway, as serum C1q levels are diminished [6, 11].…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Investigations on the Involvement of the Lectin Pathway of Complement Activation in Anaphylaxis

Windbichler

Echtenacher

Takahashi

et al. 2006

Int Arch Allergy Immunol

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Poisons of Animal Origin

Wedin

Keyler

Bilden

2009

General, Applied and Systems Toxicology

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A great number of species in the animal kingdom possess means by which they subdue prey or defend against predators. Human encounters with these species may result in bites or stings that produce local injury or systemic toxicity ranging from local pain and varying degrees of tissue injury to systemic illness, organ failure and even death. Most of these animals deliver a dose of venom when they bite or sting, but some produce or accumulate toxin in their flesh that may produce illness if ingested. Venoms are generally complex mixtures of proteins and enzymes, but few are very well understood. Antivenoms have been produced to treat exposures to some species, but treatment generally consists of supportive measures and treatment of symptoms. This chapter presents an overview of some of more common animal species found throughout the world, the toxic syndromes they produce and current therapeutic strategies.

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Complement‐mediated immune mechanisms in allergy

et al. 2023

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Allergic conditions are associated with canonical and noncanonical activation of the complement system leading to the release of several bioactive mediators with inflammatory and immunoregulatory properties that regulate the immune response in response to allergens during the sensitization and/or the effector phase of allergic diseases. Further, immune sensors of complement and regulator proteins of the cascade impact on the development of allergies. These bioactive mediators comprise the small and large cleavage fragments of C3 and C5. Here, we provide an update on the multiple roles of immune sensors, regulators, and bioactive mediators of complement in allergic airway diseases, food allergies, and anaphylaxis. A particular emphasis is on the anaphylatoxins C3a and C5a and their receptors, which are expressed on many of the effector cells in allergy such as mast cells, eosinophils, basophils, macrophages, and neutrophils. Also, we will discuss the multiple pathways, by which the anaphylatoxins initiate and control the development of maladaptive type 2 immunity including their impact on innate lymphoid cell recruitment and activation. Finally, we briefly comment on the potential to therapeutically target the complement system in different allergic conditions.

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Preliminary report: complement activation in wasp-sting anaphylaxis

Cited by 62 publications

References 19 publications

Investigations on the Involvement of the Lectin Pathway of Complement Activation in Anaphylaxis

Investigations on the Involvement of the Lectin Pathway of Complement Activation in Anaphylaxis

Poisons of Animal Origin

Complement‐mediated immune mechanisms in allergy

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