Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Complement C3a”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,261 records · Page 70Linked to original sources
PubMed2006

[Transfusion-induced immunomodulation and infectious complications].

Transfusions are not without risk. One of the side effects of transfusions is the development of transfusion-induced immunomodulation (TRIM)--primarily immunosuppression, but also a strong proinflammatory effect. This may be the cause of acute lung injury (TRALI), multiorgan failure (MOF), transfusion related acute-graft-versus-host-disease (TR AGvHD), as well as of the development of secondary nosocomial infections, mostly pulmonary infections, sepsis and wound infections, and also of elevated number of tumour relapses in oncological patients. The causes of TRIM development are the induction of microchimerism, different cells and also soluble factors--complement components, such as C3a, soluble HLA-I and HLA-II molecules (HLA--human leukocyte antigen), soluble Fas ligand (sFasL), and others. The immunosuppressive potential of blood products grows with the time of their storage and becomes highest in non-leukoreduced blood products stored for a long time. In view of possible adverse effects of a transfusion, the expected benefit should be balanced against possible risks.

Cross Infection↗
PubMedDate not supplied

Contributions to the study of the favouring role of chronic urinary infections in inducing and starting drug-allergic-type reactions.

A randomized study in a group of 87 patients with drug-allergic-type reactions (DAtR) manifested by urticaria and or angioedema, revealed in 55 patients (63.2%) the presence of chronic urinary infections (CUI), significantly different (p less than 0.001) from the control group (80 patients without DAtR) in which the incidence of CUI was only 20% (16 patients). Among the drugs observed to induce allergic-type reactions were substances such as penicillins and aspirin which are not used in CUI. It was therefore assumed that it is not their frequent use in CUI (as is the case with antibacterial drugs and contrast iodide substances) that leads to DAtR but rather more the CUI proper. The assumption that CUI are risk factors for the occurrence of DAtR is discussed and the following mechanisms are suggested in support of this assumption: enhancement of IgE secretion (by the drugs as allergens--complete or haptens--or by the inhibiting effects of some antibiotics on the T suppressor cells): nonimmunological mast cell degranulation (by the bacterial wall products--lectins and proteoglycans--or by the endotoxines with complement activation generating anaphylatoxines C3a and C5a): neurovegetative changes induced by infectious diseases.

Chronic Disease↗
PubMed1995

Continuous hemofiltration as blood purification in sepsis.

Continuous hemofiltration was first described as a new form of renal replacement for critically ill patients in the late 1970s. Since then, it has undergone remarkable technical and conceptual modifications and has become a widely used form of dialytic therapy in the ICU. More recent insights into the pathogenesis of sepsis and the role of soluble molecules in the mediation of organ injury during septic shock have led to a resurgence of the concept of blood purification during life-threatening infection. Recent studies have confirmed that cytokine extraction occurs in vivo in humans during continuous hemofiltration and that other smaller, potentially noxious molecules such as platelet-activating factor, complement factors C5a and C3a, and thromboxane are also removed from the circulation of septic patients or animals. Experimental studies have shown that continuous hemofiltration has beneficial hemodynamic effects in septic animals and that such effects may correlate with the intensity of ultrafiltration. Cardiac function also appears to improve and myocardial depressant factors are removed from the circulation. Continuous hemofiltration offers some promise as an adjunctive form of treatment in severe sepsis.

Animals↗
PubMed1998

Complement and contact activation in term neonates after fetal acidosis.

AIMS: To evaluate complement and contact activation after fetal acidosis. METHODS: Fifteen term neonates with hypoxic-ischaemic encephalopathy after umbilical arterial pH < 7.10 were compared with 15 healthy neonates with umbilical arterial pH > 7.20. Determinations of the complement function and C1-inhibitor activity were performed as kinetic tests 22-28 hours after birth. C1q, C1-inhibitor, and factor B concentrations were determined by radial immunodiffusion and those of C3a, C5a, and factor XIIa by enzyme immunoabsorbent assay. RESULTS: Median complement function (46 vs 73%), C1q (4.3 vs 9.1 mg/dl), and factor B (5.2 vs 7.7 mg/dl) decreased after fetal acidosis. The activated split products C3a (260 vs 185 micrograms/l), C5a (5.0 vs 0.6 micrograms/l), and factor XIIa (3.2 vs 1.3 micrograms/l) increased in the neonates after fetal acidosis. No differences were found in the concentration and activity of C1-inhibitor. CONCLUSIONS: Complement and contact activation occurred in the newborns with hypoxic-ischaemic encephalopathy. Activation of these systems generates mediators which can trigger inflammation and tissue injury.

Acidosis↗
PubMed1991

Plasma levels and mode of excretion of the anaphylatoxins C3a and C4a in renal disease.

Plasma levels of the anaphylatoxins C3a and C4a were examined in patients suffering with various renal diseases. Raised levels were observed in a considerable number of patients; although such elevation could be ascribed to in vivo complement activation in cases of immune complex glomerulonephritis, we found that raised plasma C4a levels appeared to be related to impaired renal function, suggesting that C4a anaphylatoxin is cleared by the kidneys. No such relationship was found in the case of the anaphylatoxin C3a suggesting the possible existence of another mechanism of elimination of C3a.

Adult↗
PubMed1996

Investigation of mechanism-based inhibitors of complement targeting the activated thioester of human C3.

An intramolecular thioester bond in complement protein C3 is vital for covalent attachment of C3b (the proteolytically activated form of C3) to biological surfaces and for activation of the complement system. Proteolytic removal of C3a from C3 activates the thioester in the C3b fragment. Activated C3b primarily forms ester bonds with hydroxyl groups of carbohydrates on complement activating surfaces, but it has also been shown to react with the hydroxyl group of tyrosine and with specific Ser and Thr residues on IgG and on complement protein C4b. To examine the reactivity of the thioester, several families of hydroxylated compounds were examined. Reactivity of a series of substituted phenols varied over two orders of magnitude and demonstrated a linear correlation between reactivity and the Hammett substituent constants. Hydroxylated drugs including members of the L-DOPA/epinephrine family and hydroxamic acids also were examined. Compounds were identified that were 20,000 times more reactive than carbohydrates. These compounds were found to inhibit both the classical and alternative pathways of complement activation. Although the specificity of the thioester for its natural biological targets appears to be determined by many structural features, the data presented here demonstrate that increasing the nucleophilic character of the target hydroxyl group can increase the potency of a synthetic inhibitor many orders of magnitude.

Complement C3↗
PubMed1997

Regulation of B cell functions by C3a and C3a(desArg): suppression of TNF-alpha, IL-6, and the polyclonal immune response.

Regulation of the humoral immune response by fragments of complement component C3 has been shown to play an important role in host defense. In this study, we investigated expression of the C3a receptor (C3aR) by human B cells and the effects of C3a and C3a(desArg) on IgG, TNF-alpha, and IL-6 production in Staphylococcus aureus Cowan strain I (SAC)/IL-2-activated B cells. Here we report that tonsil-derived human B cells express a C3aR that is indistinguishable at both the protein (by flow cytometry) and mRNA (by reverse transcription-PCR) levels from that on human neutrophils or on C3aR-transfected mouse L cells. Incubation of SAC/IL-2-activated B cells with C3a or C3a(desArg) resulted in a dose-dependent suppression of the polyclonal immune response. Under these same experimental conditions, IL-6 and TNF-alpha release was suppressed in a dose-dependent manner. Kinetic studies with SAC/IL-2-activated B cells revealed that C3a must be present at initiation of the culture to exert its suppressive effect on IgG and IL-6 production. These results demonstrate that tonsil-derived B cells express the C3aR and that C3a as well as C3a(desArg) have a direct immunomodulatory effect on these cells.

Adolescent↗
PubMed1984

Radioimmunoassay for anaphylatoxins: a sensitive method for determining complement activation products in biological fluids.

Activation of the blood complement system generates bioactive fragments called anaphylatoxins. The three anaphylatoxins C3a, C4a, and C5a are released during "classical pathway" activation while only C3a and C5a are released when the "alternative pathway" of complement is activated. Radioimmunoassays were designed to individually detect and quantitate the activation fragments C3a, C4a, and C5a in biological fluids without interference from the precursor molecules C3, C4, and C5. Kinetics of complement activation in fresh human serum exposed to the activators zymosan, heat-aggregated immunoglobulin, or cobra venom factor were monitored using the radioimmunoassay technique. For the first time, activation of components C3, C4, and C5 was followed simultaneously in a single serum sample. Analysis of the patterns and extent of anaphylatoxin formation during activation in serum may be used to screen for deficiencies or defects in the complement cascade. Levels of the anaphylatoxins in freshly drawn serum were much higher than levels detected in EDTA-plasma. Detection limits of anaphylatoxins in plasma are governed by background levels of 152 +/- 69, 155 +/- 33, and 5.4 +/- 6.6 ng/ml for C3a, C4a, and C5a, respectively. Detection of low-level complement activation in patient's blood, urine, or synovial fluid, using anaphylatoxin formation as an indicator, may prove useful in signaling numerous forms of inflammatory reactions. The demonstration of anaphylatoxins in clinical samples is being recognized as a valuable diagnostic tool in monitoring the onset of immune disease.

Anaphylatoxins↗
PubMed1996

Respiratory dysfunction and white cell activation following cardiopulmonary bypass: comparison of membrane and bubble oxygenators.

OBJECTIVE: Cardiopulmonary bypass induces respiratory dysfunction postoperatively, with activation of both the complement system and white cells implicated. This study compared the effects of bubble and membrane oxygenators for cardiopulmonary bypass in terms of respiratory dysfunction and markers of white cell activation and endothelial damage. METHODS: Fifty patients undergoing cardiopulmonary bypass were randomly allocated either membrane or bubble oxygenation. Respiratory function was assessed serially by arterial oxygen tension and alveolar-arterial oxygen gradient. Complement activation was measured by serial sampling of serum C3a levels. White cell activation was assessed by serial measurement granulocyte elastase; other markers investigated were levels of thromboxane B2, von Willebrand factor and malondialdehyde. All sample measurements were made preoperatively, early and late during bypass, 4-6 h postoperatively and then on the 1st, 2nd and 6th postoperative day. All samples were corrected for haemodilution, and differences between groups tested non-parametrically. RESULTS: In both groups of patients there was a highly significant fall (P < 0.001) in arterial oxygen tension accompanied by a highly significant rise (P < 0.0001) in aleveolar-arterial oxygen gradient at 18 h compared to preoperative values persisting until 6 days postoperatively. Levels of C3a increased significantly in both groups at 10 min post bypass, increased further at 60 min peaking at 4-6 h post bypass. Granulocyte elastase serum levels increased significantly at 10 min postoperatively in both groups compared to control levels, remaining elevated till 48 h, but returning to control levels by 6 days. There was a small difference (P < 0.04) between the groups at 4-6 h only. Levels of von Willebrand factor increased significantly at 60 min post bypass in both groups, remaining elevated 6 days postoperatively. Levels of malondialdehyde increased at 10 min post bypass, remaining elevated until 6 days post bypass. Thromboxane levels showed no significant changes. For all markers measured, there were no significant differences between the groups other than those already indicated. CONCLUSIONS: This study demonstrated marked respiratory dysfunction, complement activation and white cell activation in patients undergoing cardiopulmonary bypass with either bubble or membrane oxygenators. There was marked variability in the response of individual patients with either oxygenation technique, but overall no significant differences between the groups.

Blood Gas Analysis↗
PubMed1997

Postoperative inflammatory response after autologous and allogeneic blood transfusion.

BACKGROUND: Allogeneic blood transfusions cause immunosuppression. The aim of this study was to determine whether complement anaphylatoxins, cytokines, or both are released in the recipient, after blood transfusions in general, and after autologous blood transfusions in particular. METHODS: Thirty-one patients having total hip joint replacement surgery were randomized to receive either allogeneic red blood cells (n = 15) or predeposited autologous whole blood transfusion (n = 16). Plasma concentrations of the anaphylatoxins C3a and C5a, the terminal C5b-9 complement complex, and cytokines IL-6 and IL-8 in the recipients were repeatedly analyzed before, during, and after surgery. RESULTS: Significantly increased concentrations of IL-6 and IL-8 appeared in both groups, with a significantly greater increase in the autologous blood group. Patients in both groups developed a moderate but significant increase of C3a without a significant difference between them. C5a and terminal C5b-9 complement complex were not greatly changed. CONCLUSIONS: The study showed a greater increase in cytokine concentration after autologous blood transfusion than after allogeneic blood transfusion. The lower response in the latter may result from transfusion-induced suppression of cellular immunity.

Adult↗
PubMed1990

[Complement activation by killed polyvalent bacterial vaccine on the pleurodesis].

Broncasma Berna (B.B.) prepared from killed polyvalent bacterial vaccine is used as a pleural irritant for pleurodesis on patients with spontaneous pneumothorax. The effects of B.B. on the complement system in vivo after injections into pleural spaces were investigated. Five patients with spontaneous pneumothorax underwent intrapleural injections of B.B. Increased body temperatures with positive C-reactive proteins and increased polymorphonuclear leukocyte counts in peripheral blood were observed in all patients. Serum levels of complement components (Clq, Cls, C4, C3 and B), hemolytic activity of complement (CH50) and plasma levels of C3a were gradually elevated after intrapleural injections of B.B. Analysis of pleural fluids from 4 patients showed that levels of C3a and C5a were increased compared with plasma levels, and an accumulation of polymorphonuclear leukocytes were observed. These findings suggest that intrapleural injections of B.B. activate the complement system and cause inflammatory reactions accompanied by an increase of C3a and C5a and an accumulation of polymorphonuclear leukocytes. Such inflammatory reactions might inversely induce the synthesis of complement components and promote the migration of polymorphonuclear leukocytes from bone marrow. The deposit of fibrin during these inflammatory processes might contribute to the development of pleurodesis. These inflammatory reactions might be mediated through the activation of the classical complement pathway by B.B.

Adult↗
PubMed1995

The extracellular neutral cysteine proteinase of Entamoeba histolytica degrades anaphylatoxins C3a and C5a.

We have shown previously that the extracellular cysteine proteinase of Entamoeba histolytica trophozoites activates the alternative pathway of complement by specifically cleaving C3. This unique mechanism of complement activation leads to passive lysis of nonpathogenic, but not of pathogenic strains. In an attempt to investigate the relationship between the cleavage of complement components C3 and C5 and the pathogenesis of amebiasis, we investigated the production of the anaphylatoxins C3a and C5a, which have diverse effects on the host immune response. The concentration of proteinase required to cleave purified C5 was at least 5 to 10 times that needed for C3 cleavage, but these levels are easily obtainable as demonstrated by cleavage of 125I-labeled C5 during incubation with purified trophozoites. When the C3a-like cleavage fragments were purified by gel filtration, they were found to be extensively degraded during a 1-h incubation of C3 with the proteinase. Subsequent evaluations of the C3a- and C5a-like cleavage products generated earlier in the reaction using immunoblots and cellulose acetate electrophoresis revealed rapid degradation, even during incubation periods as short as 5 min. Because C-terminal fragments as small as 20 amino acid residues can mimic the biologic functions of C3a or C5a, we tested cleavage products for activity. In sensitive bioassays, including guinea pig platelet aggregation for C3a activity and chemotaxis for C5a activity, we demonstrated that proteolysis renders these molecules inactive. These studies suggest that the extracellular cysteine proteinase of E. histolytica, which is capable of activating the complement system, may also provide a mechanism to circumvent normal host immunity by inactivating the proinflammatory factors C3a and C5a.

Anaphylatoxins↗
PubMed1993

Complement activation by polymethyl methacrylate minimized by end-point heparin attachment.

After intraocular lens implantation, despite good clinical results, many cataract patients develop a chronic uveitis, caused by an inflammatory response to the implant. One way to improve the biocompatibility of the intraocular lens is to modify the surface by end-point heparin attachment. This study shows that complement activation caused by poly(methyl methacrylate) can be diminished by end-point heparin attachment, as demonstrated by a significant reduction in the generation of C3a and fluid phase terminal complement complexes. It suggests that assessment of complement activation is a good indicator of the biocompatibility of intraocular lenses.

Biocompatible Materials↗
PubMed1980

Pulmonary injury induced by C3a and C5a anaphylatoxins.

Homogeneous anaphylatoxins C3a (human or porcine), C5a (porcine), and the porcine classic anaphylatoxin, a mixture of C5a and C5a des Arg, isolated from complement-activated serum, were shown to induce acute pulmonary injury in the guinea pig following intrabonchial instillation. The gross physiologic response to these factors is characterized by respiratory distress with rapid, shallow breathing. Administration of 8--17 micrograms/kg of porcine classic anaphylatoxin proved lethal in 50% of the animals treated. The acute response (less than 20 minutes after instillation) of pulmonary tissue to insult by the anaphylatoxins is characterized by constriction of the smooth muscle walls in both bronchioles and pulmonary arteries and by focal atelectasis. Aggregates of platelets and leukocytes in pulmonary vessels and in other organs such as the chambers of the heart were commonly observed after intrabronchial administration of the anaphylatoxins. Although C3a was never lethal in guinea pigs even when doses as high as 500 micrograms/kg were administered by the intrabronchial route, this anaphylatoxin did induce the same pattern of acute pulmonary injury as C5a. In vitro experiments employing guinea pig platelets indicated that these cells aggregate in the presence of 10(-10) M porcine C5a but are not affected by C3a (human or porcine) even at levels up to 10(-6) M. Hence, platelet aggregation as observed in vivo may be directly affected by C5a, but in the case of C3a, secondary mediators must be involved. Anaphylatoxin preparations were also shown to induce contraction of guinea pig lung strips in vitro: this effect was not inhibited by antihistamines at concentrations that blocked contraction to exogenous histamine. The in vivo response to anaphylatoxin could be blocked with high doses of the antihistamine chlorpheniramine but not by corresponding doses of diphenhydramine.

Anaphylatoxins↗
PubMed2005

C3a expressed in the central nervous system protects against LPS-induced shock.

Complement is implicated in the pathogenesis of inflammatory disorders of the central nervous system (CNS), like multiple sclerosis, Alzheimer's disease, and trauma. The anaphylatoxins C3a and C5a are thought to be the major contributors to complement-mediated inflammation in the CNS, likely mediating their effects via their ability to attract and activate leukocytes and common capacity to augment inflammation. For example, in experimental autoimmune encephalomyelitis, the animal model of multiple sclerosis, CNS-specific expression of C3a in C3a/GFAP transgenic mice renders them prone to massive cellular infiltration of the CNS and increases their mortality. In contrast, other studies have suggested that C3a can function in an anti-inflammatory fashion in the CNS, by inducing neurotrophin production and preventing NMDA-mediated neurotoxicity. To further investigate the seemingly paradoxical role of C3a in acute inflammation of the brain, we studied the pathogenesis of endotoxin shock in C3a/GFAP transgenic, C3a receptor-deficient (C3aR-/-) and C3a/GFAPxC3aR-/- mutant mice. Here we report that C3a/GFAP mice were significantly more resistant to endotoxin-induced lethality than wild-type and C3aR-/- mice. Surprisingly, C3a/GFAPxC3aR-/- hybrids were also significantly protected, indicating that C3a exerts its protective anti-inflammatory effect either directly or via an as yet unidentified non-canonical C3aR.

Animals↗
PubMed1984

Generation of human C3a, C4a, and C5a anaphylatoxins by protein A of Staphylococcus aureus and immobilized protein A reagents used in serotherapy of cancer.

Protein A (SpA) alone or immobilized on bacteria (e.g., Cowan strain I), collodion charcoal, or on Sepharose have been used in serotherapy of cancer in humans and experimental animals. Because SpA forms complexes with IgG that can activate complement, and the physiologic response during treatment often involves hypocomplementemia and reactions that are similar to those induced by anaphylatoxins, we used sensitive and specific radioimmunoassays to test the ability of SpA reagents to generate C3a, C4a, and C5a from human serum. The yield of anaphylatoxins depended on the dose of SpA, with the maximum generation of C3a (47 to 55 micrograms/ml) and C5a (1.4 to 1.9 micrograms/ml) being produced with levels of SpA that were maximally precipitated from serum. Maximum C4a levels (up to 15 micrograms/ml) were obtained at concentrations of SpA equal to or greater than the dose required to give optimal precipitation. The maximum concentrations of anaphylatoxins correspond to essentially quantitative conversions of C3 to C3a, C4 to C4a, and 40% of C5 to C5a after correction for levels found in serum incubated in pyrogen-free saline. Preformed insoluble complexes prepared from either serum or monomeric IgG also were capable of generating anaphylatoxins in fresh whole serum up to levels approximately equal to those observed in serum treated directly with an optimal amount of SpA. The preformed complexes from serum or IgG generated similar high concentrations of anaphylatoxins when carried through four sequential incubations with fresh serum, and complexes that contained approximately 1 microgram SpA were still active. Preincubating the insoluble complexes with chicken anti-SpA serum did not alter their activity. Incubation of serum with collodion charcoal coated with SpA, in a system that models the perfusion technique used to treat cancer, produced complexes that generated significant levels of C3a compared with levels found in serum passaged over albumin charcoal or in untreated serum. The C3a levels in serum from the albumin collodion charcoal were not significantly different from those found in untreated serum. Similar amounts of C3a, C4a, or C5a were observed in serum incubated with differing numbers of bacteria representing a strain of S. aureus rich in cell bound SpA (Cowan strain I) or a strain (Wood 46) deficient in SpA. This suggests that in intact bacteria, cell wall factors other than SpA (e.g., peptidoglycan) are predominantly responsible for generating anaphylatoxins.(ABSTRACT TRUNCATED AT 400 WORDS)

Anaphylatoxins↗
PubMed1992

The activation of polymorphonuclear neutrophils and the complement system during immunotherapy with recombinant interleukin-2.

The toxicity due to interleukin-2 (IL-2) strongly resembles the clinical picture seen during septic shock. In septic shock activation of polymorphonuclear neutrophils (PMN) and the complement system contribute significantly to the pathophysiology of the condition. We therefore investigated whether similar events contributed to the toxicity observed with IL-2. Four patients received seven cycles of escalating dose IL-2 (18.0 to 72.0 X 10(6) IU m-2 day-1) and 16 were treated with 20 cycles of fixed dose IL-2 (12.0 or 18.0 X 10(6) IU m-2 day-1). Toxicity, as judged by hypotension (P = less than 0.005) and capillary leakage (fall in serum albumin 18.2 vs 4.0 gm l-1; P = less than 0.0005 and weight gain 4.0 vs 1.2 kg; P = less than 0.025) were worse with the esc. dose protocol. PMN became activated following IL-2 with mean peak elastase/alpha 1-antitrypsin (E alpha 1 A) and lactoferrin values of 212 (SEM = 37) and 534 (SEM = 92) ng ml-1 respectively occurring 6 h after the IL-2. Peak values for the esc. dose IL-2 group being generally higher than 500 ng ml-1. Activation of the complement cascade was evidenced by a dose dependent elevation of peak C3a values (fixed dose 9.1 (SEM = 0.6); esc. dose 25.7 (SEM = 6.33); P = less than 0.005) on day 5 of IL-2. There was a significant correlation between C3a levels and the degree of hypotention during the first 24 h after IL-2 (r = 0.91) and parameters of capillary leakage such as weight gain and fall in serum albumin (r = 0.71). These data suggest that activation of PMN initiates endothelial cell damage which subsequently leads to activation of the complement cascade. This latter system then contributes to the haemodynamic changes and capillary leakage seen in IL-2 treated patients.

Carcinoma, Renal Cell↗
PubMed1990

Effect of exercise on complement activity.

Complement measurements of C1, C1q, C2, C3, C4, C5; the anaphylatoxins, C3a, C4a, and C5a; and total hemolytic activity of the classical and alternative pathways were made in 26 experienced adult runners before and after shortterm aerobic exercise. The baseline results were compared with those of nonexercising age-matched controls. In most subjects tested, running resulted in nanogram increases in C3a and C4a with corresponding decreases in the hemolytic activity of C4 (C4H). Baseline values of C3 and C4H were decreased significantly in runners when compared with nonexercising controls. Preliminary studies measuring the effect of exercise on C3a levels were also done in three asthmatic runners. Mean resting and postexercise levels, and exercise-induced increases in C3a anaphylatoxin in the asthmatic subjects were significantly higher than in the nonasthmatic subjects. The findings indicate that short-term exercise results in the activation of C3 and C4 and subsequent generation of C3a and C4a anaphylatoxins, and suggest that both activation of the classical pathway of complement and a selective downregulation of C3 production may occur in persons regularly engaged in aerobic exercise. The exaggerated generation of C3a by asthmatic subjects during exercise raises the possibility that anaphylatoxins play an etiologic role in exercise-induced asthma.

Adult↗