The effect of bronchodilation and spirometry on fractional exhaled nitric oxide (FeNO50), bronchial NO flux (JawNO) and alveolar NO concentration (CANO) in children and young adults.

OBJECTIVE: Fractional exhaled nitric oxide (FeNO), bronchial nitric oxide (JawNO) and alveoar nitric oxide (CANO) are biomarkers of eosinophilic inflammation, usually measured simultaneously with spirometry and bronchodilation. Our aim was to investigate the effect of bronchodilation and spirometry on FeNO, CANO and JawNO in children and young adults with well-controlled asthma and in healthy volunteers. METHODS: FeNO was measured in 95 subjects (62 controls, 33 asthmatics). CANO and JawNO were assessed in 41 of the subjects (35 healthy, 6 asthmatics.) Measurements were performed before spirometry (1), right after spirometry (2), 20 min after the first spirometry and bronchodilation (3), right after the post-bronchodilation spirometry (4) and 30 min after the last spirometry (5). RESULTS: The presence of well-controlled asthma was not associated with different pattern of reaction after spirometry and bronchodilation. A statistically significant difference was observed only between FeNO4 and FeNO5, as well as between CANO1 and CANO3 (19.14 ± 1.68 vs 20.62 ± 1.85 ppb, p = 0.001 and 4.42 ± 0.40 vs 3.09±0.32 ppb, p = 0.001, respectively). CONCLUSIONS: Spirometry and bronchodilation have an insignificant effect on FeNO and JawNO. Even if a slight change occurs in FeNO and JawNO, this does not modify clinician's decision and therapeutic strategy. CANO values (CANO1) are significantly decreased 20 min after spirometry and bronchodilation.

In vivo induction of the autophagic machinery in human bone marrow cells during Leishmania donovani complex infection.

Autophagy is a homeostatic process promoting cell survival in periods of stress. The induction of the autophagic machinery has also been implicated in both innate and adaptive immunity. Leishmania donovani, which is the causative pathogen of visceral leishmaniasis, is an intracellular parasite that invades and multiplies in bone marrow macrophages. We describe the induction of host cell autophagic machinery during acute natural bone marrow infection by L. donovani complex, detected by LC3B immunoblot. The successful treatment with liposomal amphotericin B resulted in the resolution of this phenomenon. Even though the role of autophagy in parasite biology has been previously studied, our findings show for the first time the in vivo host cell LC3B conversion as a marker of the induction of the autophagic machinery during infection with Leishmania parasite in real time conditions.