Disease relevance of Arthus Reaction

• These data indicate a dominant role for the C5aR and its ligand in the reverse passive Arthus reaction in the lung and a synergistic role together with other inflammatory mediators in immune complex-mediated peritonitis and skin injury [1].
• When L-652,731 was added to the antibody employed in the reversed passive Arthus reaction, the injury resulting from immune complex-induced vasculitis was significantly attenuated [2].
• The compounds inhibited the reversed passive Arthus reaction in rats and arachidonic acid-induced dermatitis in mice, models in which leukocyte infiltration is responsible for the inflammatory reaction [3].
• Effect of chlorpromazine on the development of experimental glomerulonephritis and Arthus reaction [4].
• These results indicate potent anti-inflammatory activities of a new C5a receptor antagonist and provide more evidence for a key early role for C5a in sepsis and the reverse Arthus reaction [5].

High impact information on Arthus Reaction

• The classical model for this immunopathological cascade, the Arthus reaction, was reinvestigated with a murine strain deficient in Fc receptor expression [6].
• Impaired inflammatory responses in the reverse arthus reaction through genetic deletion of the C5a receptor [1].
• C5aR- deficient mice exhibit decreased migration of neutrophils and decreased levels of TNF-alpha and interleukin 6 in the peritoneal reverse passive Arthus reaction compared to their wild-type littermates [1].
• In contrast, the Arthus reaction was induced in FcRgamma(+) MRL/lpr mice, but not in FcRgamma(-/-) MRL/lpr mice [7].
• The cutaneous reverse Arthus reaction requires intercellular adhesion molecule 1 and L-selectin expression [8].

Chemical compound and disease context of Arthus Reaction

• Likewise, chlorpromazine prevented passive reverse Arthus reaction in the skin [4].
• In the reversed passive Arthus reaction in the rat, the suppressive activity of colchicine is at least 50 times that of indomethacin and 100 times that of phenylbutazone [9].
• In a rat skin lesion model, GP-1-515 significantly reduced cutaneous neutrophil infiltration following an intradermal injection of carrageenan or zymosan-activated plasma, or induction of a reverse passive Arthus reaction [10].
• In addition, we provided evidence for C3-independent C5aR triggering, which may explain why the cutaneous Arthus reaction develops normally in C3(-/-) mice [11].
• Conversely, coumarin reduced the volume of exudate in the Arthus reaction whereas the cellular infiltrate remained unaltered [12].

Biological context of Arthus Reaction

• In all cases a dose-dependent inhibition of chemotaxis was observed, more striking in the case of CaPP elicited cells which were more reactive than cells collected after the induction of the Arthus reaction [13].
• Effects of dapsone on passive Arthus reaction and chemotaxis and phagocytosis of polymorphonuclear leukocytes [14].
• Trasylol, ovomucoid, tranexamic acid and soybean inhibitor decrease the vascular permeability as measured by extravasation of 131I-albumin when injected with the antibody at induction of a reverse passive Arthus reaction in the rat skin [15].
• Rats with electrolytic anterior hypothalamic lesions showed a suppressed Arthus reaction, delayed skin hypersensitivity, and antibody production at 7, 14 and 21 days after immunization with bovine serum albumin (BSA) in complete Freud's adjuvant (CFA) [16].

Anatomical context of Arthus Reaction

• Macrophages induce the inflammatory response in the pulmonary Arthus reaction through G alpha i2 activation that controls C5aR and Fc receptor cooperation [17].
• Reduced infiltration of neutrophils and mast cells was observed in the peritoneal Arthus reaction and was associated with the decreased production of tumor necrosis factor alpha and interleukin-6 [18].
• 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 [19].
• Mipragoside treatment significantly reduced (p < 0.05 vs placebo) the conjunctival vasopermeability induced by reverse passive Arthus reaction as well as successfully reduced the eosinophil levels in the conjunctival epithelium (p < 0.01 vs placebo) elicited by compound 48/80 [20].
• Immunoreactive leukotriene B4 (iLTB4), detected in the pleural cavity following induction of a reverse passive Arthus reaction (RPAR), was inhibited by the mixed lipoxygenase-cyclooxygenase inhibitors, phenidone and BW 755C, but not by cyclooxygenase inhibitors or by chlorpheniramine or methysergide [21].

Gene context of Arthus Reaction

• PURPOSE: To determine the role of interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) in the induction of uveitis by a reverse passive Arthus reaction (RPAR) [22].
• A codominant role of Fc gamma RI/III and C5aR in the reverse Arthus reaction [23].
• With the use of the reversed passive Arthus reaction in the skin, local administration of SOD, but not of catalase, blocked the early phase of the tissue injury, as quantitated by the leakage of homologous albumin [24].
• To assess the contribution of P-selectin glycoprotein ligand-1 (PSGL-1) and selectins in the pathogenetic process, the cutaneous reverse-passive Arthus reaction was examined in mice treated with monoclonal antibodies (mAb) to PSGL-1 or P- and/or E-selectin [18].
• 1. Initiation of a peritoneal Arthus reaction by deposition of immune-complexes results in vascular leakage, polymorphonuclear leukocyte (PMN) infiltration, and tumour necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) production [25].

Analytical, diagnostic and therapeutic context of Arthus Reaction

• Neither ICAM-1 mRNA nor expression, assessed by immunocytochemistry, was increased above control levels in rats during the pleural Arthus reaction [26].
• The efficacy of three such inhibitors that have been in clinical trials (zileuton, A-78773 and ZD2138) were evaluated in: 1) ex vivo whole blood assay, 2) dermal Arthus reaction, and 3) functional airway response [27].
• Pretreatment with a single subcutaneous injection of nicotine (0.4 or 0.8 mg/kg) 30 or 60 min. before antigen challenge attenuated the passive skin Arthus reaction immunological inflammation [28].

References