These echographic findings may suggest the diagnosis of granulomatous epididymo-orchitis in the appropriate clinical setting, and help to avoid unnecessary orchiectomy for benign disease.
The authors investigated the production of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) by phytohaemagglutinin (PHA)-stimulated T-lymphocytes from 21 untreated patients with acute brucellosis. PHA-stimulated T-lymphocytes from acute brucellosis patients showed normal IL-2 production but defective IFN-gamma production (brucellosis patients 531 +/- 103 pg mL-1 vs. healthy controls 1024 +/- 212 pg mL-1) after 72 h of culture. This altered pattern of IL-2 and IFN-gamma production by T-lymphocytes was observed in seven brucellosis patients whose T-lymphocytes exhibited a normal proliferative response to PHA (61 612 +/- 18 422 cpm) as well as in the 14 patients with a defective T-lymphocyte proliferative response to the PHA after 5 days of culture (19 479 +/- 4409 cpm). After antibiotic therapy, production of the two lymphokines by the PHA-stimulated T-lymphocytes from acute brucellosis patients was similar to that of T-lymphocytes from healthy control subjects. The authors conclude that PHA-stimulated T-lymphocytes from untreated patients with acute brucellosis have defective INF-gamma production but normal IL-2 production.
Researchers have claimed that natural killer (NK) cells are involved in the mechanisms of defense of the host against infections. We have investigated the activity of NK cells in peripheral blood mononuclear cells (PBMNC) from 12 patients for whom acute brucellar infection has been diagnosed and from 14 healthy controls. The sera of eight of the patients were also analyzed 3 months after initiation of a 45-day course of antibiotic treatment, at which time they had no evidence of relapse. PBMNC from patients with acute brucellar infection showed a significantly depressed NK cell activity (P < .01) when compared with those from healthy controls; this depressed activity was not related to a deficient number of NK cells since the numbers of CD56+ and CD16+ cells present in PBMNC were similar in patients and controls. Incubation of PBMNC from patients with acute brucellar infection with recombinant interleukin-2, but not with interferon-gamma, can correct this impaired cytotoxic activity. In treated patients, there was a significant enhancement (P < .05) and normalization of the previously defective NK cell activity. It is concluded that acute brucellar infection is associated with a deficient cytotoxic activity of NK cells that can be overcome by in vitro incubation with interleukin-2 and that reverts to normal after antibiotic treatment.
T lymphocytes from 21 untreated patients with acute brucellosis were tested for their proliferative response to polyclonal mitogens. The purified T lymphocytes from these patients showed a defective proliferative response to plant lectins and anti CD3 monoclonal antibodies with respect to the response observed in T lymphocytes from 21 healthy controls (p < 0.05). This defective proliferative response was not corrected by the exogenous addition of interleukin-2 or tumor necrosis factors alpha or beta to the culture medium. After antibiotic therapy, the proliferative response to the mitogens in T lymphocytes was found to be similar to that of the healthy controls (p > 0.05), and significantly higher than that found before treatment (p < 0.05). It was concluded that T lymphocytes from acute brucellosis patients have a defective proliferative response to membrane mitogenic signals, which disappears when the patients are cured after antibiotic treatment.
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