scholarly journals STUDIES ON TUBERCLE BACILLUS-HISTIOCYTE RELATIONSHIP

1962 ◽  
Vol 115 (3) ◽  
pp. 475-489 ◽  
Author(s):  
Jacob Fong ◽  
Dennis Chin ◽  
Sanford S. Elberg
Keyword(s):  
Passive Transfer ◽  
Immune Serum ◽  
Resistance Factor ◽  
Polymorphonuclear Leucocytes ◽  
Tubercle Bacillus ◽  
Cell Resistance ◽  
Cellular Resistance ◽  
Immune Lymphocytes ◽  
Active Replication ◽  
Induction Of Resistance

Studies of passive transfer of cellular resistance, as manifested by refractoriness to necrotization with virulent tubercle bacilli, have shown that immune histiocytes or immune lymphocytes were effective transferring agents; immune polymorphonuclear leucocytes and immune serum as well as comparable cells from normal animals lacked this capacity. Comparisons of immune histiocytes and immune lymphocytes showed that the former cells were more efficient; this was indicated by (a) the smaller numbers of immune histiocytes needed for passive transfer, (b) the longer duration of cellular resistance in recipients given histiocytes than in those given lymphocytes, (c) the greater capacity of histiocytes to effect serial passive transfer, and (d) the ability of histiocytic but not lymphocytic lysates to transfer cellular resistance. Experiments to establish the mechanism of passive transfer of cellular resistance showed that there was no active induction of resistance in recipients through transfer of bacillary antigens contained in immune histiocytes; in fact, the results of serial passive transfers with immune histiocytes suggested an active replication of the "cell resistance factor."

scholarly journals STUDIES ON TUBERCLE BACILLUS-MONOCYTE RELATIONSHIP

1957 ◽  
Vol 105 (1) ◽  
pp. 25-37 ◽  
Author(s):  
Jacob Fong ◽  
Patricia Schneider ◽  
Sanford S. Elberg ◽  
Keyword(s):  
Culture Filtrate ◽  
Immune Cells ◽  
Immune Serum ◽  
Normal Serum ◽  
Tubercle Bacillus ◽  
Cellular Resistance ◽  
Normal Cells ◽  
Serum Factors ◽  
Virulent Strains ◽  
Homologous Antiserum

Studies of virulent, attenuated, and avirulent strains of tubercle bacilli have demonstrated the proficiency of virulent strains to effect degeneration of normal monocytes cultivated in the presence of normal serum. Attenuated strains were less active in this respect, and avirulent bacilli failed to induce monocytic degeneration. Comparison of the effects of virulent H37Rv with O.T., P.P.D., and a culture filtrate of H37Rv revealed a similarity in action of H37Rv and its filtrate. The action of O.T. and P.P.D. differed from that of H37Rv in that the greatest effect of H37Rv was upon normal cells as opposed to the effect of O.T. and P.P.D. upon immune cells. Additionally, it was demonstrated that immune serum (anti-BCG) protected immune cells against H37Rv but not against O.T. or P.P.D. The protection of immune cells by heterologous antisera (anti-Salmonella and anti-ovalbumin) as well as by homologous antiserum (anti-BCG) against the degenerative effects of H37Rv indicated a non-specificity in action of serum factors. The ability of the monocytes of animals immunized with BCG and the failure of monocytes of animals immunized with Salmonella rutgers to withstand parasitization with H37Rv, when both types of monocytes were cultivated in immune (anti-BCG) serum, indicated a specificity of cellular resistance.

scholarly journals STUDIES OF TUBERCLE BACILLUS-HISTIOCYTE RELATIONSHIPS

1963 ◽  
Vol 118 (5) ◽  
pp. 727-742 ◽  
Author(s):  
Jacob Fong ◽  
Dennis Chin ◽  
Herta M. Vickrey
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Animal Species ◽  
Agar Medium ◽  
Immune Serum ◽  
Blood Agar ◽  
Tubercle Bacillus ◽  
Immune Mouse ◽  
Cellular Resistance ◽  
Immune Rabbit

Immunization of mice or guinea pigs with BCG rendered all or most of the histiocytes of these animals resistant to necrotization by virulent H37Rv; this cellular resistance was mediated by immune serum. Immune mouse histiocytes (from BCG-immunized animals) were able to induce cellular resistance in normal homologous and heterologous (rabbit) animal species; mouse histiocytic ribosomes were also tested in the homologous species and found to be active. Immune guinea pig histiocytes (from BCG-immunized guinea pigs) were ineffective in transferring cellular resistance to either homologous or heterologous (mouse and rabbit) animal species. Immune rabbit histiocytes were capable of inducing cellular resistance in mice and guinea pigs; rabbit histiocytic ribosomes were also tested in normal mice and found to be active in induction of cellular resistance. Recipient guinea pig histiocytes (from guinea pigs inoculated with immune rabbit histiocytes) were capable of inducing cellular resistance in normal guinea pigs and rabbits. Cultivation of lysed immune histiocytes of all three animal species on glycerol-blood agar medium failed to reveal any viable BCG; this provided one additional bit of evidence against the idea that induction of cellular resistance is due to viable bacilli.

scholarly journals Immunity to syphilis: passive transfer in rabbits using serial doses of immune serum.

1976 ◽  
Vol 13 (5) ◽  
pp. 1402-1407 ◽  
Author(s):  
R S Weiser ◽  
D Erickson ◽  
P L Perine ◽  
N N Pearsall
Keyword(s):  
Passive Transfer ◽  
Immune Serum

A study upon passive immunity in experimental trichiniasis

Parasitology ◽  
1938 ◽  
Vol 30 (2) ◽  
pp. 156-166 ◽  
Author(s):  
James T. Culbertson ◽  
Samuel S. Kaplan
Keyword(s):  
Trichinella Spiralis ◽  
Passive Transfer ◽  
Immune Serum ◽  
Passive Immunity ◽  
Therapeutic Value ◽  
Protection Against Infection

Protection against infection with Trichinella spiralis is conferred upon mice by the passive transfer to them of a specific immune serum from rabbits. A smaller percentage of mice treated with the immune serum die, and fewer larvae invade the muscles of the treated mice than among control animals. The action of the antibody of the immune serum appears to be directed specifically against the ingested larvae which are maturing to adult worms in the intestine of the infected animals. The results obtained thus far indicate that an immune serum would have little therapeutic value in the later stages of the disease.

Passive transfer of acquired resistance to Schistosoma mansoni in laboratory mice

Parasitology ◽  
1975 ◽  
Vol 70 (3) ◽  
pp. 347-358 ◽  
Author(s):  
A. Sher ◽  
S. R. Smithers ◽  
Pamela Mackenzie
Keyword(s):  
Schistosoma Mansoni ◽  
Partial Resistance ◽  
Primary Infection ◽  
Acquired Resistance ◽  
Passive Transfer ◽  
Immune Serum ◽  
Laboratory Mice ◽  
Humoral Factors ◽  
Effector Mechanism

Serum taken from mice 12–15 weeks after a primary infection of Sehistosoma mansoni transfers to normal recipients a partial resistance to subsequent schistosome challenge. The transfer of immunity is evident not oniy in the reduced recovery of mature parasites from the liver, but also in the diminished numbers of invading schistosomula recovered from the lungs. Since the recipients of immune serum exhibit a level of resistance equivalent on average to 47 % of that found in actively immunized animals, the results suggest that humoral factors play a major role in the effector mechanism of schistosome immunity.

Variants of Plasmodium berghei resistant to passive transfer of immune serum

1968 ◽  
Vol 22 (3) ◽  
pp. 338-345 ◽  
Author(s):  
N.T. Briggs ◽  
B.T. Wellde ◽  
E.H. Sadun
Keyword(s):  
Plasmodium Berghei ◽  
Passive Transfer ◽  
Immune Serum

scholarly journals Antibody-Mediated Disease Remission in the Mouse Model of Lyme Borreliosis

2006 ◽  
Vol 74 (8) ◽  
pp. 4817-4825 ◽  
Author(s):  
Stephen W. Barthold ◽  
Emir Hodzic ◽  
Stefan Tunev ◽  
Sunlian Feng
Keyword(s):  
T Cell ◽  
Mouse Model ◽  
Lyme Borreliosis ◽  
Dna Analysis ◽  
Passive Transfer ◽  
Immune Serum ◽  
Scid Mice ◽  
Disease Remission ◽  
Vascular Walls ◽  
Deficient Mice

ABSTRACT In the mouse model of Lyme borreliosis, the host immune response during infection with Borrelia burgdorferi results in the remission of carditis and arthritis, as well as global reduction of spirochete numbers in tissues, without elimination of infection (28). These events were recapitulated by passive transfer of immune serum from infected immunocompetent mice or T-cell-deficient mice to severe combined immunodeficient (SCID) mice. Previous studies have shown that immune serum is reactive against arthritis-related protein (Arp) and that Arp antiserum induces arthritis remission (16). However, although immune serum from T-cell-deficient mice induced disease remission, it was not reactive against Arp, suggesting that antibody to another antigen may be responsible. T-cell-deficient mouse immune serum was reactive to decorin binding protein A (DbpA). Therefore, DbpA antiserum was tested to determine its ability to induce disease remission in SCID mice. Antisera to Arp or DbpA induced both carditis and arthritis remission but did not significantly reduce spirochete numbers in tissues, based upon quantitative flaB DNA analysis, nor did treatment affect RNA levels of several genes, including arp and dbpA. Immunohistochemical labeling of spirochetes in hearts and joints during disease remission induced by adoptive transfer of lymphocytes, passive transfer of immune serum, or passive transfer of DbpA antiserum revealed that such treatment resulted in elimination of spirochetes from heart base and synovium but not vascular walls, tendons, or ligaments. These results suggest that Arp and DbpA antibodies may be active as disease-resolving components in immune serum but antibody against other antigens may be involved in reductions of spirochetes in tissues.

scholarly journals Passive Transfer of Antibodies Protects Immunocompetent and Immunodeficient Mice against Lethal Ebola Virus Infection without Complete Inhibition of Viral Replication

2001 ◽  
Vol 75 (10) ◽  
pp. 4649-4654 ◽  
Author(s):  
Manisha Gupta ◽  
Siddhartha Mahanty ◽  
Mike Bray ◽  
Rafi Ahmed ◽  
Pierre E. Rollin
Keyword(s):  
Virus Infection ◽  
Viral Replication ◽  
Ebola Virus ◽  
Protective Efficacy ◽  
Hemorrhagic Fever ◽  
Passive Transfer ◽  
Immune Serum ◽  
Immunodeficient Mice ◽  
Ebola Hemorrhagic Fever ◽  
Ebola Virus Infection

ABSTRACT Ebola hemorrhagic fever is a severe, usually fatal illness caused by Ebola virus, a member of the filovirus family. The use of nonhomologous immune serum in animal studies and blood from survivors in two anecdotal reports of Ebola hemorrhagic fever in humans has shown promise, but the efficacy of these treatments has not been demonstrated definitively. We have evaluated the protective efficacy of polyclonal immune serum in a mouse model of Ebola virus infection. Our results demonstrate that mice infected subcutaneously with live Ebola virus survive infection and generate high levels of anti-Ebola virus immunoglobulin G (IgG). Passive transfer of immune serum from these mice before challenge protected upto 100% of naive mice against lethal Ebola virus infection. Protection correlated with the level of anti-Ebola virus IgG titers, and passive treatment with high-titer antiserum was associated with a delay in the peak of viral replication. Transfer of immune serum to SCID mice resulted in 100% survival after lethal challenge with Ebola virus, indicating that antibodies alone can protect from lethal disease. Thus antibodies suppress or delay viral growth, provide protection against lethal Ebola virus infection, and may not require participation of other immune components for protection.

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