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Results for “Immune Adherence Reaction”

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At least 19 recordsLinked to original sources
PubMed2001

Leishmania immune adherence reaction in vertebrates.

In normal human blood, C3-opsonized Leishmania promastigotes immune adhere to erythrocytes, a mechanism believed to enhance their clearance from blood and phagocytosis. Given the potential importance of this reaction in host defence against infection, the promastigote-erythrocyte interaction was studied in blood of individuals from one avian and 12 mammalian genera; [111In]-labelled promastigotes were found to bind only to primate erythrocytes. Nevertheless, previous experiments coincubating platelets isolated from nonprimate mammals with C3-opsonized promastigotes led to promastigote-platelet adherence. To ascertain whether this is a natural mechanism in nonprimate Leishmania infection, normal blood from members of Leishmania animal models of interest, dog, guinea-pig, hamster, mouse and rabbit, was infected ex vivo with promastigotes. Within 1 min of blood contact, the promastigote surface was loaded with platelets, rapidly evolving into large aggregates. These results confirm the physiological nature of the reaction and demonstrate that promastigote-erythrocyte and promastigote-platelet binding are the first parasite-host cell encounters after Leishmania invasion of primates and nonprimate mammals, respectively. Leishmania immune adherence shares the characteristics of the nonanticipatory immune systems, and we consider it should be viewed as an innate vertebrate host effector mechanism.

Animals↗
PubMed1981

[Therapeutic action of proteolytic enzymes and antibiotics in experimental staphylococcal infection. The effect of lincomycin, chymotrypsin and their combinations on the level of autoplaque-forming cells in the blood and the immune adherence reaction of staphylococci].

The effect of lincomycin, chymotrypsin and their combination on the blood count of the plaque-autoforming cells (PAFC) and immune adhesion (IA) of staphylococci was studied on mice with staphylococcal infection. The infected mice were divided into 4 groups: nontreated, lincomycin treated, chymotrypsin treated, and lincomycin + chymotrypsin treated. The doses of lincomycin and chymotrypsin were 150 and 2 mg/kg, respectively. The mice were decapitated by the 3rd, 7th, 14th or 21st day of the infection and treatment and the blood was collected for the count of the PAFC and IA. A decrease in the rate of IA with a simultaneous increase in the PAFC count was found in the untreated mice and the mice treated with lincomycin alone. The use of chymotrypsin and its combination with lincomycin stimulated IA and lowered the level of autosensibilization.

Animals↗
PubMed1977

The immune adherence phenomenon in experimental candidiasis.

The immune adherence reaction was shown in experimental candidiasis. This phenomenon has not been previously described for candidiasis, to the best of our knowledge. Forty-eight sera of guinea pigs inoculated with a single or several inoculations of live Candida albicans were tested at different time intervals after inoculation for anti C. albicans antibodies detectable by the immune adherence reaction. From the 14th day after inoculation, a positive immune adherence reaction was observed with titer and strength increasing as time passed after inoculation and as the number of inoculations increased. All the sera were tested parallely in agglutination and indirect mast cell degranulation tests. The significance of the data obtained is discussed.

Agglutination Tests↗
PubMed1976

[Immune status of indefinitely surviving rat renal allograft recipients after short course of ALS-treatment Detection of a serum blocking factor by allorosette formation inhibition test (author's transl)].

53 LBNF1 kidneys were grafted into L-rats. 24 untreated recipients served as control and survived 16.1 +/- 1.7 days. 14 recipients were treated with 4 ml alloantiserum (ADS) each, and the other 15 animals with 4 ml ALS each. 9 and 10 of these 14 and 15 animals survived for more than 4 months. We performed GvH-reaction with spleen cells of these 19 animals. It showed normal cellular immune response. After splenectomy first donor specific skin was transplanted, 18 days later second skin of same origin (LBNF1) and 18' days after third party skin (LBufF1). The first grafts survived 13.1 +/- 1.9 days in the recipients of ADS treatment and 12.2 +/- 1.2 days in the recipients of ALS. Second skin grafts were rejected delayed in the former recipients as the first grafts, in the later more accelerated than the first grafts. The third grafts survived as the controls. Before and after skin grafting we could not detect lymphocytotoxin and hemagglutinin. The sera of animals with ADS therapy inhibited the spontaneous allorosette formation to 46.0 +/- 4.4% and of ALS therapy 37.7 +/- 9.2%. Our results suggest that after ALS treatment blocking antibodies were produced in the recipients and they cause the enhancement of kidney allograft.

Animals↗
PubMed1975

Immunological studies on the localization of phosphatidylglycerol in the membranes of Mycoplasma hominis.

Phosphatidylglycerol is the main component (87%) of the membrane phospholipids of Mycoplasma hominis. It is immunologically active. Antibodies directed against phosphatidylglycerol were detected in rabbits intravenously immunised with native M. hominis or isolated M. hominis membranes. The intravenous method of immunisation was chosen in order to select for a response to surface antigenic determinants. Anti-phosphatidylglycerol antibodies were induced in rabbits by intravenously injecting the flocculated complexes of methylated bovine serum albumin and a phosphatidylglycerol/phosphatidylcholine/cholesterol mixture. These antibodies were specifically bound to intact M. hominis, as shown by complement fixation and Coombs tests. Native M. hominis were not agglutinated by anti-phosphatidylglycerol antibodies; but after partial digestion of the membrane proteins with Pronase, the mycoplasmas were heavily agglutinated by the anti-phosphatidylglycerol antibodies. The same amount of anti-phosphatidylglycerol antibodies was bound to intact M. hominis, containing 600 mug of phosphatidylglycerol as to 6 mug of phosphatidylglycerol in the optimal configurational arrangement of a mixed phosphatidylglycerol/phosphatidylcholine/cholesterol micelle. It is concluded that the major part of the phosphatidylglycerol in native M. hominis membranes is masked, probably by membrane proteins, and is not accessible to the anti-phosphatidylglycerol antibodies.

Agglutination Tests↗