The biology of bacterial colonization and invasion of the respiratory mucosa

Abstract

Despite being regularly exposed to particulate matter during breathing, which contains bacteria from the commensal flora in the nasopharynx and from the environment, the healthy lung is kept sterile by efficient defence mechanisms. Bacterial infections of the respiratory mucosa represent a dynamic interaction, to which both host and bacterial factors contribute.The abnormal host defences associated with chronic respiratory infections (e.g. cystic fibrosis and other forms of bronchiectasis) serve to emphasize their permissive role. The bacteria that cause bronchial infections possess a wide array of potential virulence factors that contribute to their pathogenicity. Many of these factors influence the mucociliary system, an important first-line defence mechanism. The multiplication, spread and persistence of bacteria within the bronchial lumen, and consequent damage to the epithelium, stimulates a chronic inflammatory response, which also impairs mucociliary clearance and damages lung tissue.A greater understanding of host-bacterial interactions during mucosal infections should in the future lead to the development of new therapies and treatment strategies.

Predisposing factors to bacterial colonization in chronic obstructive pulmonary disease

“…It is well known that the lower airways of healthy individuals are not colonized by bacteria [18], whereas patients with COPD are frequently infected by bacteria [3,4], possibly because of impairment of the mucociliary system [19]. However, several aspects of the problem, such the percentage of COPD patients with significant bacterial colonization, the spectrum of pathogens colonizing the lower respiratory tract [20] and predisposing factors to bacterial colonization, are unclear.…”

Induced sputum eosinophils and neutrophils and bronchiectasis severity in allergic bronchopulmonary aspergillosis

“…In bronchiectasis, chronic infection leads to epithelial damage, release of IL-8 and migration of neutrophils into the airways [4]. Activated neutrophils release myeloperoxidase (MPO), reactive oxygen species [4] and collagenases [5]. This results in chronic airway inflammation and degradation of the connective tissue matrix, leading to bronchiectasis.…”

“…Chronic airway inflammation underlies the disordered airway function found in asthma and bronchiectasis [3,4]. In asthma, T-helper type 2 lymphocytes (Th2) release interleukin (IL)-5 and orchestrate the eosinophil and mast cell inflammatory infiltrate.…”

“…In asthma, T-helper type 2 lymphocytes (Th2) release interleukin (IL)-5 and orchestrate the eosinophil and mast cell inflammatory infiltrate. In bronchiectasis, chronic infection leads to epithelial damage, release of IL-8 and migration of neutrophils into the airways [4]. Activated neutrophils release myeloperoxidase (MPO), reactive oxygen species [4] and collagenases [5].…”

Dinámica y patología del barrido mucociliar como mecanismo defensivo del pulmón y alternativas farmacológicas de tratamiento

“…Infecciones virales pueden aumentar la expresión de ecto-ATPasas que agotan el ATP extracelular, inhibiendo la secreción de Cl -y aumentando la viscosidad del moco 3 . La respuesta inmune del hospedero a infecciones inespecíficas también puede alterar el barrido mucociliar 3,60 . La producción de leucotrienos, citoquinas, quimioquinas y la secreción de especies reactivas de oxígeno en el sitio de infección generan inflamación y daño en el epitelio, exponiendo terminales nerviosas sensitivas a ser estimuladas más fácilmente 9 .…”