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We rapport an original observation of adverse reaction (Arthus reaction) during a dust mite hyposensitisation with a aluminum hydroxide absorbed extract. We precise the way of beginning. In discussion, we try to precise the preliminary symptoms of such reaction to prevent it.
The Arthus' reaction in the middle ear cavity was studied using histochemical technique. The deposition of immune complex on the basement membrane and the immune complex in the middle ear effusion were the initial features of these animal models. But, these immune complexes were clearly removed from the tympanic cavity during the early phase of reaction. Immune complexes were supposed to be just a initiation of otitis media with effusion. The tubal dysfunction and local immunity of middle ear mucosa caused by the Arthus' reaction seemed to be responsible for the chronicity and relapsing of otitis media with effusion respectively.
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The active Arthus reaction can be inhibited by hypovolemic shock or the infusion of catecholamines. A reevalution of previous work with platelet antiserum indicates that shock rather than thrombocytopenia was responsible for preventing the active Arthus reaction. Immunofluorescent studies of the inhibited Arthus sites reveal that immune precipitates are not present in the extravascular tissues. Since leukocyte aggregates can be seen within venules at the inhibited sites, and they phagocytize BSA-anti-BSA complexes, their failure to migrate out of the vessels is due to the absence of complexes in the extravascular spaces. (Am J Pathol 78:159-170, 1975)
The active Arthus reaction was completely inhibited in rabbits made thrombocytopenic with platelet antiserum. Platelets or some platelet factor is necessary for the development of immune vasculitis in this model. Since the classic Arthus reaction depends on the union of extravascular antigen with intravascular antibody, it is probable that the missing platelet factor is an agent that alters vascular permeability.
Active Arthus reactions were provoked by injections of 100 micrograms horseradish peroxidase (HRP), 10 micrograms HRP and 100 micrograms bovine serum albumin (BSA) into the skin of sensitized guinea pigs. Labeling indices (LI) of epidermal basal cells were measured 1, 4, 8, 24, 48 and 72 h later by the in vivo 3H-thymidine labeling technique, and compared with those obtained with injections of antigens into the skin of non-sensitized guinea pigs. From 1-8 h after the induction of an active Arthus reaction, the LI of epidermal basal cells of the skin injected with 100 micrograms HRP decreased to a remarkably low value. On the other hand, those obtained with the reaction against 10 micrograms HRP were significantly high. At 24 h after the reaction, LI were as high as those obtained in non-sensitized guinea pigs with control intradermal injections, though the former persisted high until 48 h after the injection. In addition, decreased LI of the epidermal basal cells were observed in the skin 4 h after intradermal injections of immune complexes. It was suggested that DNA synthetic activity of the epidermis increases in a mild active Arthus reaction, while the activity may be suppressed in a severe active Arthus reaction up to 8 h after provocation.
An electron microscopic study of a mild reversed passive Arthus reaction (RPAR) was performed using a horeradish peroxidase (HRP)-anti-HRP system to demonstrate the biological usefulness of the process which exists to clear tissue of immune complexes. To disclose the antigen, HRP, the biopsy material was subjected to a peroxidase reaction. HRP was mainly detected within irregular electron-dense precipitates which were considered insoluable HRP-anti-HRP immune complexes. Neutrophils were found to phagocytose and digest the deposited immune complexes in a similar way as described previously. But there was no vascular and other tissue damage. This study provides morphological evidence that the process of clearing tissues of immune complexes need not be harmful to the host.
The Arthus reaction was studied in guinea pigs passively immunized with human diphtheria antitoxin. Diphtheria toxoid was given intradermally 24 hours following the intravenous administration of antitoxin and the subsequent reactions were graded and measured. The intensity of Arthus reactions was dependent upon the relative amounts of precipitating antitoxin and toxoid used. Severe lesions were caused by intravenous sensitization with 0.48 mg. precipitating antitoxin N and intradermal challenge with 0.05 or 0.17 toxoid N. Reactions of lesser intensity were caused by smaller amounts of antitoxin and toxoid. The nature of the antibody used for sensitization was of importance in the severity of Arthus reactions. In contrast to the behavior of precipitating antitoxin, amounts of non-precipitating antitoxin equivalent to 0.48 mg. N did not cause severe Arthus reactions when 0.05 or 0.17 mg. toxoid N was given intradermally. Precipitating antitoxic whole serum is altered by heating at 56 degrees C. for 5 hours so that its precipitability is lost without any appreciable loss of antitoxic strength. This modified antitoxin produced Arthus reactions of only intermediate severity in guinea pigs sensitized with 0.48 mg. antitoxin N. When fractions of precipitating antitoxic serum were obtained using a cold ethanol technique described by Deutsch (16), a mixture of the purified gamma(2)-globulin and the crude albumin fraction heated together at 56 degrees C. for 5 hours behaved similarly to whole serum. However, gamma(2)-globulin alone was not affected by the heating procedure, remained precipitable by toxoid, and was able to cause a severe Arthus reaction following sensitization with 0.48 mg. antitoxin N.
The reversed passive Arthus reaction (RPAR) was performed in the dorsal area of the skin and skeletal muscles of the pelvic girdle of male guinea pigs. Biopsies were taken 3, 24 and 48 hours after antibody administration. In the dermal type of RPAR attention was paid to the structure of striated muscles of the subcutaneous panniculus carnosus. Histological and electron microscopic studies were performed. Changes in the dermal RPAR were more rapid and more intensive than those directly in the muscles. In both types of RPAR the affected muscle fibres demonstrated vacuolar and hyaline degeneration, segmental necrosis, internal nuclei, cellular infiltration, phagocytosis and regeneration in the late phase of reaction. Neutrophils predominated in the infiltrations after 3 hrs but after 24 and 48 hrs the main cells were macrophages and lymphocytes. Ultrastructural studies showed various stages of damage to the mitochondria, dispersion and disruption of the myofibrils and formation of tubular structures. A similar morphological appearance is characteristic of polymyositis (pm) and dermatomyositis (dm) suggesting a similar i.e. immune complex mechanism of muscle fibre damage in RPAR and in pm and dm.
A reversed passive Arthus reaction was induced in guinea pigs using horseradish peroxidase as antigen. An electron microscopic study on the cutaneous localization of the immune complexes was performed applying a peroxidase reaction. Precipitates of immune complexes were found within the walls of small blood vessels and among the collagen bundles in the dermis. The adherence of immune complexes to numerous eosinophils was observed and some of immune complexes were phagocytosed by neutrophils. The adherence of immune complexes to fibroblasts and the deposits of immune complexes in some areas of the basement membrane zone, especially in the zona diffusa, were found in the upper dermis and in the papillae. In the lower layers of the epidermis, we observed immune complexes adhering to the cell membranes of keratinocytes.
The Arthus reaction, passively induced in rat sciatic nerve by local injection of antibody and intravenous injection of antigen, was studied by immunofluorescence, using fluorescein and tetramethylrhodamine isothiocyanate. The reaction in nerve is similar to that occurring in skin. Antigen-antibody complexes formed at the site of the reaction activate complement and attract large numbers of polymorphonuclear leucocytes which then ingest the immune complexes. The significance of the Arthus reaction in relation to diseases of the peripheral nervous system is mentioned.
The ability of antisera to guinea-pig C3 to inhibit the Arthus and local Shwartzman reactions was studied. They were found to reduce the non-haemorrhagic component of the active and reversed passive Arthus reactions and to delay the appearance of the haemorrhage in the active Arthus reaction. Cobra venom factor, however, had no effect on the non-haemorrhagic components of these reactions and only delayed the appearance of the haemorrhage of the active Arthus reaction. There appeared to be a correlation between the serum complement level and the time taken for the haemorrhage to appear, and between the circulating platelet count and the extent of the non-haemorrhagic, oedematous component of the reaction. The haemorrhagic component of the local Shwartzman reaction was not affected by decomplementation with cobra venom factor. The ability of the antisera to inhibit the haemorrhage of the Shwartzman reaction was not dependent on lowering the serum complement titre. However, the haemorrhage was inhibited if the circulating platelet count was also reduced to very low numbers. Antiserum to zymosan alone had the same effect as anti-beta1C/beta1A globulin (zymosan) in blocking the reaction, although it did not alter the complement levels or the platelet counts. The possibility of an immunological cross-reactivity between zymosan and endotoxin in this action is discussed.
A classic Arthus reaction was elicited in normal domestic cats using chicken red blood cells as antigen. The response was quantitated grossly by measuring the area of the resulting skin bleb at several set time intervals and by microscopic examination of biopsies taken at the conclusion of each of the trials. This method produced an intense Arthus reaction in each of the cats tested.
The effect of anti-inflammatory drugs on the biochemical changes in the Arthus reaction have been studied and correlated to changes in the pathology of the reaction. In the Arthus reaction all the non-steroidal anti-inflammatory drugs inhibited the migration of cells into the lesion and reduced the lysosomal enzyme concentration at the Arthus site. The steroids did not inhibit the cellular inflitration or the total lysosomal enzyme concentration in the skin but did reduce the concentration of cathepsin D in the oedema fluid. In addition, prednisolone and, to a lesser extent, hydrocortisone reduced the degree of oedema formation. The results suggest that non-steroidal anti-inflammatory drugs inhibit the Arthus reaction by reducing the cellular infiltration whereas anti-inflammatory steroids act by preventing these cells secreting their lysosomal enzymes and thus causing tissue damage.
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