Host-Etiological Agent Interactions in Intranasally and Intraperitoneally Induced Cryptococcosis in Mice

1980 ◽  
Vol 29 (2) ◽  
pp. 633-641 ◽  
Author(s):  
Thuang S. Lim ◽  
Juneann W. Murphy ◽  
Larry K. Cauley
Keyword(s):  
Etiological Agent ◽  
Delayed Type Hypersensitivity ◽  
In Vivo Model ◽  
Spleen Cells ◽  
Polysaccharide Antigen ◽  
Cryptococcal Antigen ◽  
Agent Interactions ◽  
Growth Profiles ◽  
Host Parasite

Inbred CBA/J mice were used in developing a defined in vivo model for studying host-parasite relationships in cryptococcosis. Mice were infected either intranasally or intraperitoneally with 10 3 viable Cryptococcus neoformans cells. At weekly intervals over a 92-day period, C. neoformans growth profiles in the lungs, spleens, livers, and brains of the infected animals were determined. In addition, humoral and delayed-type hypersensitivity responses and cryptococcal antigen levels were assayed in these mice. Intranasally infected mice developed strong delayed-type hypersensitivity reactions in response to cryptococcal culture filtrate (CneF) antigen, and there was good correlation between acquisition of delayed-type hypersensitivity and the reduction of C. neoformans cell numbers in infected tissues. In contrast, intraperitoneally infected mice displayed greater numbers of C. neoformans cells in tissues and had somewhat suppressed delayed-type hypersensitivity responses to CneF antigen. Anticryptococcal antibodies were not detected in intranasally or intraperitoneally infected mice, but cryptococcal polysaccharide antigen titers were relatively high in both groups. The transfer of sensitized spleen cells from intranasally infected mice to syngeneic naive recipient mice resulted in the transfer of delayed-type hypersensitivity responsiveness to cryptococcal antigen in the recipients. The intranasally induced infection in mice was similar to the naturally acquired infection in humans; therefore we are proposing that this murine-cryptococcosis model would be useful in gaining a greater understanding of host-etiological agent relationships in this disease.

scholarly journals Evidence for mouse Th1- and Th2-like helper T cells in vivo. Selective reduction of Th1-like cells after total lymphoid irradiation.

1989 ◽  
Vol 170 (5) ◽  
pp. 1495-1511 ◽  
Author(s):  
H Bass ◽  
T Mosmann ◽  
S Strober
Keyword(s):  
T Cells ◽  
Selective Reduction ◽  
Adoptive Cell Transfer ◽  
Delayed Type Hypersensitivity ◽  
Cell Mediated Immunity ◽  
Spleen Cells ◽  
Total Lymphoid Irradiation ◽  
Early Return ◽  
Th1 And Th2

Purified CD4+ BALB/c spleen T cells obtained 4-6 wk after total lymphoid irradiation (TLI) helped normal syngeneic B cells to produce a vigorous antibody response to TNP keyhole limpet hemocyanin in adoptive cell transfer experiments. However, the same cells failed to transfer delayed-type hypersensitivity to the adoptive hosts as measured by a foot pad swelling assay. In addition, purified CD4+ cells from TLI-treated mice were unable to induce graft vs. host disease in lethally irradiated allogeneic C57BL/Ka recipient mice. In response to mitogen stimulation, unfractionated spleen cells obtained from TLI mice secreted normal levels of IL-4 and IL-5, but markedly reduced levels of IL-2 and INF-gamma. A total of 229 CD4+ clones from spleen cells of both normal and TLI-treated mice were established, and the cytokine secretion pattern from each clone was analyzed. The results demonstrate that the ratio of Th1- and Th2-like clones in the spleens of normal BALB/c mice is 1:0.6, whereas the ratio in TLI mice is approximately 1:7. These results suggest that Th2-like cells recover rapidly (at approximately 4-6 wk) after TLI treatment and account for the early return of antibody helper activity and secretion of IL-4 and IL-5, but Th1-like cells recover more slowly (in approximately 3 mo) after irradiation, and this accounts for the deficit in cell-mediated immunity and the reduced amount of IL-2 and IFN-gamma secretion.

scholarly journals An antigen-specific signal is required for the activation of second-order suppressor T cells in the regulation of delayed-type hypersensitivity to 2,4,6-trinitrobenzene sulfonic acid.

1983 ◽  
Vol 158 (3) ◽  
pp. 932-945 ◽  
Author(s):  
M Tsurufuji ◽  
B Benacerraf ◽  
M S Sy
Keyword(s):  
T Cells ◽  
Sulfonic Acid ◽  
Suppressor Cells ◽  
Delayed Type Hypersensitivity ◽  
Trinitrobenzene Sulfonic Acid ◽  
Spleen Cells ◽  
Suppressor T Cells ◽  
Histocompatibility Complex

Suppressor T cells (Ts-1) induced with trinitrophenyl (TNP)-conjugated syngeneic spleen cells (TNP-SC) can be enriched on antigen-coated plates and are afferent suppressors. In addition, these suppressor cells produced soluble suppressor factors (TsF) that were active in vivo. Therefore, the Ts-1 cells in the TNP system are very similar to the Ts-1 cells in other systems we have studied earlier. Further characterization of these TsF-1 revealed that TsF-1 obtained from TNP-SC-induced Ts-1 is major histocompatibility complex restricted in its activity. Injection of TNP-specific TsF-1 into naive mice did not induce Ts-2 unless additional corresponding antigen was provided. Moreover, the Ts-2 cells induced by administration of both TsF-1 and trinitrobenzene sulfonic acid were antigen specific rather than antiidiotypic.

Establishment of an in vivo model for KCNJ5 dependent hyperaldosteronism

2015 ◽  
Vol 122 (03) ◽  
Author(s):  
U Lichtenauer ◽  
PL Schmid ◽  
A Oßwald ◽  
I Renner-Müller ◽  
M Reincke ◽  
...  
Keyword(s):  
In Vivo Model

An in vivo Model for the Assessment of Acute Fibrinolytic Capacity of the Endothelium

1997 ◽  
Vol 78 (04) ◽  
pp. 1242-1248 ◽  
Author(s):  
David E Newby ◽  
Robert A Wright ◽  
Christopher A Ludlam ◽  
Keith A A Fox ◽  
Nicholas A Boon ◽  
...  
Keyword(s):  
Blood Flow ◽  
Substance P ◽  
Sodium Nitroprusside ◽  
Plasma Concentrations ◽  
In Vivo Model ◽  
Forearm Circulation ◽  
Von Willebrand ◽  
Local Release ◽  
Willebrand Factor

SummaryThe effects on blood flow and plasma fibrinolytic and coagulation parameters of intraarterial substance P, an endothelium dependent vasodilator, and sodium nitroprusside, a control endothelium independent vasodilator, were studied in the human forearm circulation. At subsystemic locally active doses, both substance P (2-8 pmol/min) and sodium nitroprusside (2-8 μg/min) caused dose-dependent vasodilatation (p <0.001 for both) without affecting plasma concentrations of PAI-1, von Willebrand factor antigen or factor VIII:C activity. Substance P caused local increases in t-PA antigen and activity (p <0.001) in the infused arm while sodium nitroprusside did not. At higher doses, substance P increased blood flow and t-PA concentrations in the noninfused arm. We conclude that brief, locally active and subsystemic infusions of intraarterial substance P cause a rapid and substantial local release of t-PA which appear to act via a flow and nitric oxide independent mechanism. This model should provide a useful and selective method of assessing the in vivo capacity of the forearm endothelium to release t-PA acutely.

Closure of Fetoscopic Access Sites with Amniotic Extracellular Matrix Scaffolds in an In Vivo Model

2006 ◽  
Vol 66 (S 01) ◽  
Author(s):  
N Ochsenbein-Kölble ◽  
J Jani ◽  
G Verbist ◽  
L Lewi ◽  
K Marquardt ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
In Vivo Model ◽  
Extracellular Matrix Scaffolds
Sign in / Sign up

Export Citation Format

Share Document