A Skin Reaction in Guinea Pig Homograft Donors with a Cell-free Substance from Recipient Lymph Nodes

Nature ◽  
1962 ◽  
Vol 193 (4821) ◽  
pp. 1198-1199 ◽  
Author(s):  
A. E. POWELL ◽  
OTIS RAY ◽  
D. WHITENACK ◽  
C. A. HUBAY ◽  
W. D. HOLDEN
Keyword(s):  
2013 ◽  
Vol 81 (4) ◽  
pp. 1152-1163 ◽  
Author(s):  
Vladimir Savransky ◽  
Daniel C. Sanford ◽  
Emily Syar ◽  
Jamie L. Austin ◽  
Kevin P. Tordoff ◽  
...  

ABSTRACTNonhuman primates (NHPs) and rabbits are the animal models most commonly used to evaluate the efficacy of medical countermeasures against anthrax in support of licensure under the FDA's “Animal Rule.” However, a need for an alternative animal model may arise in certain cases. The development of such an alternative model requires a thorough understanding of the course and manifestation of experimental anthrax disease induced under controlled conditions in the proposed animal species. The guinea pig, which has been used extensively for anthrax pathogenesis studies and anthrax vaccine potency testing, is a good candidate for such an alternative model. This study was aimed at determining the median lethal dose (LD50) of theBacillus anthracisAmes strain in guinea pigs and investigating the natural history, pathophysiology, and pathology of inhalational anthrax in this animal model following nose-only aerosol exposure. The inhaled LD50of aerosolized Ames strain spores in guinea pigs was determined to be 5.0 × 104spores. Aerosol challenge of guinea pigs resulted in inhalational anthrax with death occurring between 46 and 71 h postchallenge. The first clinical signs appeared as early as 36 h postchallenge. Cardiovascular function declined starting at 20 h postexposure. Hematogenous dissemination of bacteria was observed microscopically in multiple organs and tissues as early as 24 h postchallenge. Other histopathologic findings typical of disseminated anthrax included suppurative (heterophilic) inflammation, edema, fibrin, necrosis, and/or hemorrhage in the spleen, lungs, and regional lymph nodes and lymphocyte depletion and/or lymphocytolysis in the spleen and lymph nodes. This study demonstrated that the course of inhalational anthrax disease and the resulting pathology in guinea pigs are similar to those seen in rabbits and NHPs, as well as in humans.


1976 ◽  
Vol 10 (3) ◽  
pp. 223-231 ◽  
Author(s):  
L. D. Olson ◽  
R. L. Schueler ◽  
G. M. Riley ◽  
L. G. Morehouse

Streptococcal lymphadenitis with macroscopic abscesses was induced in guinea-pigs when an isolate of Lancefield's group C streptococci of guinea-pig origin was sprayed orally. The disease was also produced in guinea-pigs when another isolate was injected sublingually but not when it was sprayed orally. Treatment with prednisolone did not increase the susceptibility to the latter isolant when sprayed orally. Abscesses could not be induced in the cervical lymph nodes of guineapigs exposed by injecting group E streptococci sublingually, although the organism was isolated from the cervical lymph nodes 2 days after inoculation. Neither could abscesses be induced by injecting these streptococci sublingually in guinea-pigs treated with prednisolone.


1951 ◽  
Vol 107 (12) ◽  
pp. 487-493 ◽  
Author(s):  
R. Hadek
Keyword(s):  

1982 ◽  
Vol 72 (2) ◽  
pp. 306-315 ◽  
Author(s):  
Yoichiro Moriya ◽  
Jiro Koyama
Keyword(s):  

If a guinea-pig R is sensitized by the transplantation of a skin homograft from a guinea-pig D , the intradermal injection into R of antigenic matter from D provokes an inflammatory response of delayed onset ( direct reaction ) that is outwardly and histologically similar to a tuberculin reaction. A reaction of the same kind is provoked when living cells expressed from the regional lymph nodes of R are injected intradermally into D ( transfer reaction ). The transfer reaction is interpreted as a local passive transfer of the state of reactivity dis­closed by the direct reaction. When due allowance is made for the sharing of antigens by members of outbred populations of guinea-pigs, both direct and transfer reactions are immunologically specific (§§ 2.3, 2.4, 3.1). The direct reaction can be provoked by cellular extracts (§ 2.3) as well as by living cells (§ 2-4). Its intensity is strongly correlated with the strength of the homograft reaction (§ 8). After sensitization by a single set of skin homografts, direct reactivity persists for a period of the order of hundreds of days (§ 4). ‘Hyperimmunization’ by the repeated injection of D cells into R is accompanied by a decline of direct reactivity (§ 6). The transfer reaction can be mediated through blood leucocytes (§ 3.2) and peritoneal exudate cells (§ 3.3) as well as by cells from lymph nodes. Although the regional node is the first node to be activated by a regional homograft, activity spreads thereafter to other nodes (§ 3.4). After the intravenous injection into R of 40 million lymphoid cells from D , transfer reactivity can be demonstrated in the leucocytes of R within 3 days (§ 3.2). Sensitized cells killed by heating, freezing or drying do not mediate the transfer reaction (§ 7.1). Extracts of leucocytes disrupted in the presence of deoxyribonuclease (Lawrence’s ‘transfer factor’) cannot deputize for living cells in the transfer reaction (§ 7.3), and evidence that such extracts can transfer direct reactivity to normal guinea-pigs is equivocal (§ 7.4). Disrupted leucocytes and especially blood platelets of syngeneic (‘isologous’) origin can give rise to violent non-specific delayed inflammatory reactions which resemble tuberculin reactions superficially but differ from them histologically (§ 7.3). Direct and transfer reactions were combined in an experiment in which cells or antigenic extracts from D were mixed with sensitized cells from R and then injected into a normal guinea-pig syngeneic with R (§ 3.5). Thus both direct and transfer reactions seem to depend essentially upon the local engagement of antigen with sensitized cells. Neither direct nor transfer reactions were affected by the administration of high doses of hydrocortisone (§ 5). It has not been possible to demonstrate direct or transfer reactions in mice, but the transfer reaction in rabbits is violent and prolonged (§ 3.0). (Other workers have demon­ strated direct reactivity in man.) The evidence, taken in the round, suggests that the delayed cutaneous inflammatory reactions revealed by the direct and transfer tests are manifestations of the homograft reaction, and not of an immunological reaction associated with some different iso-antigenic system. It thus supports the analogy long since drawn between the homograft and tuberculin reactions, and upholds the contention that the ‘second set’ homograft reaction reveals a pre-existing and not are-awakened (anamnestic) sensitivity (§ 8).


1985 ◽  
Vol 101 (4) ◽  
pp. 1442-1454 ◽  
Author(s):  
P Cowin ◽  
H P Kapprell ◽  
W W Franke

Desmosomal plaque proteins have been identified in immunoblotting and immunolocalization experiments on a wide range of cell types from several species, using a panel of monoclonal murine antibodies to desmoplakins I and II and a guinea pig antiserum to desmosomal band 5 protein. Specifically, we have taken advantage of the fact that certain antibodies react with both desmoplakins I and II, whereas others react only with desmoplakin I, indicating that desmoplakin I contains unique regions not present on the closely related desmoplakin II. While some of these antibodies recognize epitopes conserved between chick and man, others display a narrow species specificity. The results show that proteins whose size, charge, and biochemical behavior are very similar to those of desmoplakin I and band 5 protein of cow snout epidermis are present in all desmosomes examined. These include examples of simple and pseudostratified epithelia and myocardial tissue, in addition to those of stratified epithelia. In contrast, in immunoblotting experiments, we have detected desmoplakin II only among cells of stratified and pseudostratified epithelial tissues. This suggests that the desmosomal plaque structure varies in its complement of polypeptides in a cell-type specific manner. We conclude that the obligatory desmosomal plaque proteins, desmoplakin I and band 5 protein, are expressed in a coordinate fashion but independently from other differentiation programs of expression such as those specific for either epithelial or cardiac cells.


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