Inability of Rat Anaphylatoxin to Induce Histamine Release in Rats

Konno, Satoshi; Tsurufuji, Susumu

doi:10.1254/jjp.38.185

Cited by 3 publications

(3 citation statements)

References 23 publications

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“…As reported in other asthma models, C3a and C5a participate in shifting Th2 and Th1 balance respectively but blocking or antagonizing C5a shift response to Th2 [13] and Th2 shift results in elevated Th2 adaptive response followed by airway inflammation [42]. These anaphylatoxins can induce ASM contraction [20, 58, 59], mucus secretion [60, 61], increased microvascular permeability [62, 63] [17, 24], vasodilation [64, 65], leukocyte migration and activation, and degranulation of mast cells [66], which are the hallmarks features of asthma. Further, the most important, neutralization of anaphylatoxin activity through the use of blocking antibodies, genetic targeting or by using specific antagonist of various complement factors or their receptors has been shown to attenuate allergic inflammation, and AHR in mice, and guinea pigs [67, 68].…”

Section: Discussionmentioning

confidence: 99%

Complement components as potential therapeutic targets for asthma treatment

Khan

Nicolls

Surguladze³

et al. 2014

Respiratory Medicine

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Summary Asthma is the most common respiratory disorder, and is characterized by distal airway inflammation and hyperresponsiveness. This disease challenges human health because of its increasing prevalence, severity, morbidity, and the lack of a proper and complete cure. Asthma is characterized by TH2–skewed inflammation with elevated pulmonary levels of IL-4, IL-5, and IL-13 levels. Although there are early forays into targeting TH2 immunity, less-specific corticosteroid therapy remains the immunomodulator of choice. Innate immune injury mediated by complement components also act as potent mediators of the allergic inflammatory responses and offer a new and exciting possibility for asthma immunotherapy. The complement cascade consists of a number of plasma- and membrane-bound proteins, and the cleavage products of these proteins (C3 and C5) regulate the magnitude of adaptive immune responses. Complement protein are responsible for many pathophysiological features of asthma, including inflammatory cell infiltration, mucus secretion, increases in vascular permeability, and smooth muscle cell contraction. This review highlights the complement-mediated injury during asthma inflammation, and how blockade of active complement mediators may have therapeutic application.

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Section: Discussionmentioning

confidence: 99%

Complement components as potential therapeutic targets for asthma treatment

Khan

Nicolls

Surguladze³

et al. 2014

Respiratory Medicine

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“…While CVF caused a transient significant fall in MABP although not below the renal autoregulatory capacity in the normal filtrating kidney [28], in the hydronephrotic kidney model no pressure changes were observed. The interspecies differences in blood pressure re-sponses could be due to minor anaphylatoxin dependent release of histamine in rats [29], while other species liberate higher amounts of histamine, secondary to anaphylatoxins, which lowers MABP [30,3 11. The difference in systemic blood pressure between the two models used in this study might be due to different fluid substitution to sustain a normal haematocrit.…”

Section: Discussionmentioning

confidence: 99%

Effects of systemic complement activation on renal circulation of rats

Schlottmann

Gulbins

Rauterberg

et al. 1994

Eur J Clin Investigation

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In a variety of immunopathological diseases activation of the complement cascade occurs either systemically or localized in the kidney. To elucidate the functional impact of complement activation upon the renal microcirculation, we administered cobra venom factor of Naja naja kaouthia (CVF) i.v. into thiobarbital anaesthetized female rats. CVF is a potent activator of the alternative pathway of complement by forming the C3-convertase CVF, Bb which cannot be downregulated by the natural inhibitor factors H and I and thereby leads to generation of the anaphylatoxins C3a and C5a and formation of the membrane attack complex (MAC). We utilized creatinine clearance and flowmeter measurements in the normal kidney and intravital microscopy of the split hydronephrotic rat kidney model to observe the microvascular changes. Bolus injection of CVF (100 U kg-1) resulted in an immediate reduction of RBF (-68% after 10 min), which remained decreased during the entire experiment (90 min). Systemic blood pressure was significantly reduced only in the early period (-23% of control: 126 mmHg after 10 min). After an initial anuric phase of 30 min duration, the glomerular filtration rate was significantly diminished by 47%. White cell count was decreased by about 50% after the experiments. Application of the competitive thromboxane A2-antagonist, BM 13505, reversed all renal and systemic CVF-effects. Continuous infusion of the competitive leukotriene D4-antagonist, ICI 198615, attenuated the late renal CVF-effects (i.e. 30 min after injection of CVF). Depletion of polymorphonuclear cells (PMN) attenuated the CVF-effects similar to BM 13505. Intravenous administration of CVF in the hydronephrotic kidney model resulted in a massive constriction of the interlobar and arcuate artery, with a fall in glomerular blood flow comparable to the reduction of RBF in the normal kidney. Diameters of the afferent arterioles--most sensitive to many vasoconstricting agents--were not significantly altered. Our results suggest that injection of CVF and the liberation of high amounts of the anaphylatoxins, C3a and C5a, induces the release of TXA2, which contributes to the early renal effects and the formation of cysteinyl-leukotrienes which play an important role in the late phase of systemic complement activation. Utilizing the split hydronephrotic kidney model we demonstrated the predominant action of complement activation on the large preglomerular vessels for the first time. PMN are seemingly involved in the liberation of secondary mediators which appear to reduce renal blood flow and glomerular filtration.

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“…Tsurufuji and co-workers have developed various modifica tions of his original method by employing a variety of characteristic stimuli involving foreign substances such as carrageenan [17], carboxymethylcellulose [18], zymosan [19][20][21][22] and more complex allergic mecha nisms [23]. Those studies made it evident that the airpouch method has definite advantages in supplying a suitable space for the induction of inflammatory re sponses and in measuring chemical mediators and plasma exudation quantitatively.…”

Section: Discussionmentioning

confidence: 99%

Passive Air-Pouch Anaphylaxis in Rats

Hirao²,

Kohno³

et al. 1989

Int Arch Allergy Immunol

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Induction of an experimental passive anaphylaxis of the air-pouch type, passive air-pouch anaphylaxis, was carried out in an attempt to induce a reproducible anaphylaxis model suitable for quantitative studies. Rats were injected subcutaneously with 10 ml of air into the dorsal skin to make an air-pouch and with 2 ml of antiserum at an appropriate dilution for passive sensitization, and then 5 ml of air was removed. The challenge with 5 ml of antigen solution into the air-pouch 48 h later provoked mast cell degranulation and increased vascular permeability induced by released histamine. Treatment with monovalent hapten prior to the antigen challenge almost completely inhibited histamine release and plasma exudation to levels similar to those in the nonsensitized group. In this model, mast cell-dependent late-phase allergic reaction, such as leukocyte migration or the increase of plasma exudation following mast cell degranulation, was not observed.

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Inability of Rat Anaphylatoxin to Induce Histamine Release in Rats

Cited by 3 publications

References 23 publications

Complement components as potential therapeutic targets for asthma treatment

Complement components as potential therapeutic targets for asthma treatment

Effects of systemic complement activation on renal circulation of rats

Passive Air-Pouch Anaphylaxis in Rats

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