Endotoxin and asthma: friends or foes?

Abstract

The role of endotoxin (ET) depends on the conditions of the body exposure. ET or lipopolysaccharide (LPS) of gram-negative flora is able either to be protective from the risk of allergic diseases and asthma, or to perform as a pathogenetic factor to aggravate the course of asthma. Environmental ET can inhibit development of asthma, reduce bronchial hyperactivity and airway inflammation, decrease IgE by stimulating the Т1 immune response and inhibiting Т2. The ET protection from the development of asthma may be abolished by anthropogenic pollution of the environment with industrial and household wastes; qualitative and quantitative disruption of macro- and microbiocenoses, immune systems associated with mucous membranes; and various genetic, epigenetic, and metabolic determinants of the body response to ET. The pathogenic effect of ET in asthma is related with the pro-inflammatory effect of ET on the development of chronic inflammation. ET may contribute to the pathogenesis of all known asthma endotypes and phenotypes. The efficacy of methods for reducing the effect of ET on asthma is limited, and these methods require further research.