TY - JOUR
T1 - Human β-Defensin-2 Induction in Nasal Mucosa after Administration of Bacterial Lysates
AU - Guaní-Guerra, Eduardo
AU - Negrete-García, María Cristina
AU - Montes-Vizuet, Rosalía
AU - Asbun-Bojalil, Juan
AU - Terán, Luis M.
N1 - Funding Information:
The authors are grateful to the Department of Otorhinolaryngology (Instituto Nacional de Enfermedades Respiratorias) and Dr. Alejandro Jimenez Chobillon for providing nasal tissue for this study. Eduardo Guaní Guerra received a grant from the National Council for Science and Technology (CONACyT).
PY - 2011/4
Y1 - 2011/4
N2 - Background and Aims: The airway epithelium produces antimicrobial peptides (AMPs) that prevent colonization of host tissues by a wide range of pathogens. Human β-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.
AB - Background and Aims: The airway epithelium produces antimicrobial peptides (AMPs) that prevent colonization of host tissues by a wide range of pathogens. Human β-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.
KW - Antimicrobial peptides
KW - Bacterial lysates
KW - Defensins
KW - Host defense
KW - Immunostimulants
KW - Nasal mucosa
UR - http://www.scopus.com/inward/record.url?scp=79959742240&partnerID=8YFLogxK
U2 - 10.1016/j.arcmed.2011.04.003
DO - 10.1016/j.arcmed.2011.04.003
M3 - Artículo
C2 - 21722813
SN - 0188-4409
VL - 42
SP - 189
EP - 194
JO - Archives of Medical Research
JF - Archives of Medical Research
IS - 3
ER -