Journal
PHYSIOLOGICAL RESEARCH
Volume 66, Issue -, Pages S147-S157Publisher
ACAD SCIENCES CZECH REPUBLIC, INST PHYSIOLOGY
DOI: 10.33549/physiolres.933672
Keywords
Lipopolysaccharide; Pulmonary surfactant; Inhibition; Alveolar type II cells; Lung injury
Categories
Funding
- project Biomedical Center Martin [26220220187]
- project Center for Experimental and Clinical Respirology
- EU sources
- [VEGA 1/0469/16]
- [APVV-0435-11]
- [APVV-15-0075]
- [GUK 10/2017]
- [GUK 113/2017]
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The respiratory system is constantly exposed to pathogens which enter the lungs by inhalation or via blood stream. Lipopolysaccharide (LPS), also named endotoxin, can reach the airspaces as the major component of the outer membrane of Gram-negative bacteria, and lead to local inflammation and systemic toxicity. LPS affects alveolar type II (ATII) cells and pulmonary surfactant and although surfactant molecule has the effective protective mechanisms, excessive amount of LPS interacts with surfactant film and leads to its inactivation. From immunological point of view, surfactant specific proteins (SPs) SP-A and SP-D are best characterized, however, there is increasing evidence on the involvement of SP-B and SP-C and certain phospholipids in immune reactions. In animal models, the instillation of LPS to the respiratory system induces acute lung injury (ALI). It is of clinical importance that endotoxin-induced lung injury can be favorably influenced by intratracheal instillation of exogenous surfactant. The beneficial effect of this treatment was confirmed for both natural porcine and synthetic surfactants. It is believed that the surfactant preparations have anti-inflammatory properties through regulating cytokine production by inflammatory cells. The mechanism by which LPS interferes with ATII cells and surfactant layer, and its consequences are discussed below.
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