The American journal of otology · 1997
Impaired interferon production by leukocytes from patients with Bell palsy and lack of findings suggestive for a systemic viral involvement.
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Pitkäranta A, Hovi T, Peltomaa M, Pyykkö I, Julkunen I
Аннотация
HYPOTHESIS: This study aimed to test the hypothesis that viral and other microbial infections cause Bell palsy and to use the interferon (IFN) alpha/beta-induced MxA protein as an indicator of systemic viral infection.
BACKGROUND: Bell palsy has been previously associated with several viral infections. Recently, after this study was completed, herpes simplex virus DNA was detected in the endoneurial fluid of some patients with Bell palsy.
METHODS: Serum and blood mononuclear cells were obtained from 30 patients with Bell palsy and 12 control subjects. The sera were tested for antibodies to 21 microbes. Mononuclear cells were assayed for (a) MxA protein using immunoblotting and (b) capacity to produce IFN in short-term culture after stimulation with influenza A virus.
RESULTS: No significant differences were seen in serum antibodies or MxA protein between the patients and controls. The geometric mean of leukocyte IFN production in the convalescent phase of Bell palsy patients was higher than in the acute phase but remained still at significantly lower levels as compared with the control group (p < 0.05). In three patients there was no detectable IFN production.
CONCLUSIONS: These results provide no evidence for a systemic viral involvement in Bell palsy, but the observed decreased IFN-producing capacity at the onset of Bell palsy could be a sign of transient immunosuppression or of an abnormal frequency of leukocyte subpopulations in the disease.
BACKGROUND: Bell palsy has been previously associated with several viral infections. Recently, after this study was completed, herpes simplex virus DNA was detected in the endoneurial fluid of some patients with Bell palsy.
METHODS: Serum and blood mononuclear cells were obtained from 30 patients with Bell palsy and 12 control subjects. The sera were tested for antibodies to 21 microbes. Mononuclear cells were assayed for (a) MxA protein using immunoblotting and (b) capacity to produce IFN in short-term culture after stimulation with influenza A virus.
RESULTS: No significant differences were seen in serum antibodies or MxA protein between the patients and controls. The geometric mean of leukocyte IFN production in the convalescent phase of Bell palsy patients was higher than in the acute phase but remained still at significantly lower levels as compared with the control group (p < 0.05). In three patients there was no detectable IFN production.
CONCLUSIONS: These results provide no evidence for a systemic viral involvement in Bell palsy, but the observed decreased IFN-producing capacity at the onset of Bell palsy could be a sign of transient immunosuppression or of an abnormal frequency of leukocyte subpopulations in the disease.