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Antisera were raised in rabbits against the half-saturated ammonium sulfate soluble fraction of rat saliva. With these antisera, at least four antigens were demonstrated by immunodiffusion in the saliva and in a saline extract of the parotid gland; three of these antigens were also found in a saline extract of the submaxillary gland. Two of the four antigens were salivary gland specific, the other two being shared by the liver,pancreas and testis. The immunofluorescent pattern indicates that these antigens originate from the acinar epithelium of the salivary glands and probably constitute products of secretion and/or cellular turnover.

Using Mancini's single radial immunodiffusion technique, the excretion of a liver specific saline soluble antigen was semiquantitatively assayed in the urine of rats with thioacetamine induced hepatic necrosis. The relative amounts of antigen detected in the urine were found to roughly correlate with the extent of necrotic liver parenchyma. It is suggested that a quantitative approach to histuria may provide clinically relevant information on the activity of pathologic processes associated with release of organ specific antigens from degenerative and necrotic lesions into the circulation (histemia) and thence into the urine.

Placenta-specific antigens and alpha-fetoprotein were detected in the urine of rats with induced abnormal pregnancies. Moreover, in those cases, in which the presumptive diagnosis of intrauterine fetal death or resorption was made, urinary excretion of placental antigens persisted for at least 5 days.

Liver antigens were detected in the urine of 4 of 42 patients with various liver diseases. The urine of 25 healthy subjects and patients with diseases not affecting the liver was devoid of antigens in detectable amounts. The presence of hepatic antigens in the urine did not correlate with severity of jaundice and SGOT levels but correlated with parenchymal necrosis and was associtated with a high mortaltiy.

Acute sialoadenitis, ascribed to local formation of immune complexes, develops in sensitized rats after a single intraductal challenge with the sensitizing antigen. Multiple intraductal challenges induce a state of non-reactivity of the organ characterized by a lack of inflammatory reaction to the sensitizing antigen. This non-reactivity is antigen-specific, since introduction of ovalbumin, after multiple intraductal instillations of bovine serum albumin (BSA), elicits an inflammatory response in animals immunized with the two antigens. At the same time, instillation of BSA into the contralateral gland, which has not been challenged, causes acute adenitis. Anti-BSA antibodies are detected in the serum and parotid saliva at the time of refractoriness of the gland. The phenomenon is a transient one since the faculty of the salivary gland to respond by an inflammatory reaction recovers after a challenge-free period. These experiments bring to light a new phenomenon, the possible mechanisms of which are discussed. [ABSTRACT FROM AUTHOR]

One to eight injections of BSA or saline were given into the gingiva of sensitized or non-sensitized rats. The mucous membrane of untreated rats was found to be mildly inflamed. A single injection of BSA or saline caused moderate to severe gingivitis. The severity and incidence of gingivitis decreased with increasing number of injections of BSA or saline into the mucosa. This phenomenon of induced "local non-reactivity" is similar to that observed in the parotid gland after multiple introductions of antigen. [ABSTRACT FROM AUTHOR]

Instillations of bovine serum albumin into the parotid gland of rats elicit a local and systemic immune response, the former being the more pronounced response. With increasing number of intraductal instillations of antigen, the titers of antibodies in the saliva and serum rise progressively. [ABSTRACT FROM AUTHOR]

Rats were passively immunized by an intraperitoneal injection of homologous anti-BSA serum and their salivary glands were challenged 20 min or 24 hours later with BSA by the intraductal route. Immune complex sialoadenitis developed only when challenge was early. It is concluded that immunoglobulins are transferred from the circulation into the salivary glands and are relatively rapidly cleared by a mechanism yet unknown, possibly by salivary flow. [ABSTRACT FROM AUTHOR]

The parotid gland and knee joint of immunized ruts were challenged with the sensitizing antigen. Sialoadenitis developed in over half of these rats alter one and three challenges via the parotid duct. On the other hand, most glands were normal after five, seven and eight intraductal challenges in spite of the presence of precipitating antibodies in the serum and hemagglutinating antibodies in the parotid saliva; in only a few animals did chronic destructive adenitis ensue. This contrasted with the incidence and severity of synovitis, which increased with the number of intra-articular injections of antigen, The non-reactivity of the gland is antigen specific in as much as acute adenitis resulted from intraductal instillation of a second antigen following multiple challenges with another one in rats sensitized with two antigens. The results evince a difference in the local reactivity between the salivary gland and synovial membrane. [ABSTRACT FROM AUTHOR]