Human ß-defensin-2 induction in nasal mucosa after administration of bacterial lysates.

BACKGROUND AND AIMS: The airway epithelium produces antimicrobial peptides (AMPs) that prevent colonization of host tissues by a wide range of pathogens. Human ß-defensin 2 (hBD-2) is one of the most well-documented AMPs in humans. Several bacterial products can induce production of this peptide. Bacterial immunostimulants containing bacterial lysates have long been used in the treatment of respiratory infections, but their effects on hBD-2 release have not been investigated. We undertook this study to induce production of hBD-2 after stimulation of the nasal mucosa with bacterial lysates. METHODS: A nasal lavage (NL) was performed in 12 healthy volunteers under basal conditions and after a nasal challenge with separate and subsequent stimuli with either bacterial lysates (20 million), cholecalciferol (400 IU), or sham-challenge with glycerol plus isotonic saline solution. Immunohistochemistry was performed in nasal biopsies 48 h after stimulation with bacterial lysates to identify the presence of hBD-2. RESULTS: Increased levels of hBD-2 (4668.99 ± 2829.33 pg/mL) were measured with ELISA in NL fluids following bacterial challenge. However, hBD-2 concentrations were below the limit of detection in NL fluids at baseline and after the administration of cholecalciferol or the sham-challenge. Through immunohistochemistry, hBD-2 was predominantly localized to the epithelium. CONCLUSIONS: hBD-2 can be induced in the nasal mucosa after administration of bacterial lysates. Stimulation of the innate immune system to produce hBD-2 could be used to prevent or even treat infections caused by respiratory pathogens.

Inmunogenética en tuberculosis pulmonar / Immunogenetics in pulmonar tuberculosis

La predisposición genética a la tuberculosis y enfermeades infecciosas crónicas similares, ha sido tema de numerosos estudios y controversias, debido a la diversidad de resultados obtenidos. En un estudio previo realizado en una población abierta de enfermos, determinando los antígenos de histocompatibilidad se describió una disminución importante en expresión de estos marcadores. También se describió un incremento en la beta 2 microglobulina, péptido asociado estructuralmente a estos antígenos. En este trabajo, se estudiaron 19 familias de tuberculosos (23 enfermos y 58 sanos) los antígenos HLA (incluyendo el locus DQ) y la beta 2 microglobulina, así como, las subpoblaciones de linfocitos T. Encontrando que la coincidencia en enfermos del alelo DQ1 e incremento de la beta 2 microglobulina sérica es altamente significativa (p<0.00001). Estos datos apoyan la existencia de una predisposición genética en la mayoría de los enfermos con tuberculosis.