Enhanced bronchial responsiveness during and following lower
respiratory tract infections is a major clinical problem, but its pathogenesis is poorly understood.
Brain-derived neurotrophic factor (
BDNF), which can be released by platelets and leukocytes, has been identified as a mediator of bronchial hyperresponsiveness. It is unknown whether the release of
BDNF is altered during lower
respiratory tract infections of the adult. In this clinical pilot study, 16 patients (35-80 years old) with the diagnosis of an acute bacterial lower
respiratory tract infection and elevated serum concentrations of
c-reactive protein (>100 microg/ml) and
procalcitonin (>0.1 ng/ml) were examined on admission to the hospital and 1 week after
antibiotic treatment. Sixteen age- and sex-matched controls were examined in the same time period.
BDNF concentrations in serum and platelets, but not in plasma, were markedly reduced in patients on the day of admission (median <25% of the controls). Analysis of the platelet marker
serotonin (5-HT) suggested that the decrease of platelet
BDNF is part of a non-specific release of platelet-derived mediators in this condition. Clinical improvement was accompanied by a restoration of serum and platelet
BDNF concentrations which returned to control levels after 1 week of treatment. Cell culture experiments revealed that bacterial
lipopolysaccharide (LPS) enhanced the release of
BDNF by peripheral blood mononuclear cells of the patients at both time points. In conclusion, these data suggest that lower
respiratory tract infections might be associated with an augmented release of
BDNF by platelets and mononuclear cells.