Depression Of Cell-mediated Immune Response Research Articles

Natural killer cell activity in experimental paracoccidioidomycosis of the Syrian hamster.

The study evaluated the activity of NK cells during the course of experimental infection of hamsters with Paracoccidioides brasiliensis. Eighty hamsters were infected with P. brasiliensis by intratesticular route and sacrificed at 24h, 48h, 96h, 1, 2, 4, 8 and 11 weeks of infection and compared to 40 noninfected hamsters employed as controls. These animals were submitted to the study of NK cytotoxic activity by a single-cell assay and humoral immune response by immunodiffusion and ELISA tests. The production of macrophage migration inhibitory factor in the presence of Phytohemagglutinin and P. brasiliensis antigen and histopathology of the lesions were evaluated at 1, 4, 8 and 11 weeks of infection. The infected animals displayed significantly high levels of NK activity during the four weeks of infection that decreased from the 8th week on when compared to controls. This impairment of NK activity was associated with depression of cell-mediated immune response and with increase in the extension of the histopathologic lesions. There was an inverse correlation between NK cell activity and specific antibody levels. The results suggest that after initial activation, NK cells were unable to control the fungus dissemination. The impairment of NK activity in the late stages of the infection might be related to immunoregulatory disturbances associated with paracoccidioidomycosis.

Immune response of adult rats is altered by administration of diazepam in the first postnatal week

The potential innnunotoxic risk of perinatal treatment with diazepam was investigated using early postnatal administration of the drug to the rat and monitoring the immune response until the age of 24 months. Rats given a single dose of diazepam 10 mg/kg SC on the seventh postnatal day revealed at the age of 6 months a depression of cell-mediated immune response, and at the age of 12 months significant decrease of humoral immune response. The latter persisted until senescence (age 24 months). Also, a repeated dosage of diazepam (3 x 5 mg/kg/day SC on postnatal days 5 to 7) induced a significant depression of humoral immune response in 7-month-old rats. The results demonstrate that both the humoral and cell-mediated immune response of adult rats can be altered by administering diazepam in early postnatal life.

Cryptococcal Cellulitis in Congenital Lymphedema

A 27-year-old woman with intestinal lymphangiectasia and congenital lymphedema developed cryptococcal cellulitis as a result of her underlying depressed cell-mediated immune responsiveness. Prompt therapy with amphotericin B and 5-fluorocytosine resulted in an excellent outcome. The authors believe that the increasing population of patients with depression of cell-mediated immune response will lead to an increase in the frequency with which cryptococcal cellulitis is seen and emphasize that proper evaluation of a patient with presumptive cellulitis includes consideration of fungal, as well as bacterial, etiology.

Effect of anti-PGE antibody on cell-mediated immune response in thermally injured mice.

Prostaglandin E (PGE) production is elevated in burn-injured individuals and has been implicated as a mechanism in thermal injury-induced immunosuppression. Profound depression of cell-mediated immune response (CMIR) is a characteristic effect of burn injury, and was evaluated using the popliteal lymph node assay for graft-versus-host and host-versus-graft responsiveness in mice. Preservation of CMIR after burn injury was observed in animals treated with 40 mg/kg ibuprofen and in mice given anti-PGE antibody. It appears that PGE is a central immunoregulatory mediator of suppressed CMIR following thermal injury and that treatment resulting in inhibition of PGE production or neutralization of PGE with anti-PGE antibody prevented burn-induced immunosuppression.

In vitro effect of interleukin 2 on depression of cell-mediated immune response after surgery.

Effect of exogenous interleukin 2 (IL 2) on the postoperative depression of cell-mediated immune response in vitro was studied in 8 patients with benign lesion and 11 patients with various carcinoma, undergoing major surgical procedures. When peripheral blood mononuclear cells (PBM) were obtained from patients 3 days after surgery, the proliferative response of PBM in mixed lymphocyte culture (MLC) was significantly decreased, as compared to that before operation. The depressed proliferative response was significantly increased and improved to the preoperative level, when exogenous IL 2 was added at a concentration of 50 per cent in culture. The defective generation of cytotoxic cells in MLC 3 days after operation was also significantly augmented and improved to the preoperative range by addition of 25 per cent IL 2 in culture. IL 2 produced minimal increase in these responses when PBM were obtained preoperatively. There was no significant difference between each value in these responses obtained from patients with benign lesion and carcinoma. These results show that PBM from patients who had undergone major surgery were responsive to exogenous IL 2. The postoperative depression of cell-mediated immune response may be reversible with exogenous IL 2.

Asymptomatic hapatic disease in blood donors with hepatitis B antigenemia.

In the routine screening of blood donors, 30 asymptomatic donors were found to be positive for hepatitis-B antigen (HB Ag). They had no history suggestive of hepatitis in the past. None had antibody to HB Ag (HB Ab). Three were heroin addicts. All 30 donors were found to have demonstrable biochemical and histologic abnormalities of the liver. However, they have remained asymptomatic throughout the periods of HB antigenemia, which have ranged from 13 to 72 weeks. The immunoglobulins were normal in all of the donors. The cell-mediated immune response (CMIR), as tested by leukocyte migration inhibition, was normal in 16 subjects and was only slightly depressed in four, indicating that depression of CMIR is not the cause of this clinical state. Long-term observation of these individuals will be continued, with regular biochemical and histologic assessment to determine the natural course of this condition.