Exacerbations of allergic asthma

Exacerbations of asthma result in an acute decrement in lung function and can be caused by many inhaled environmental or infectious insults. Asthma exacerbations are an important clinical problem and contribute significantly to use of healthcare resources, quality of life and challenges in asthma management [103-105]. Both bacterial and viral infections are major factors associated with exacerbations of allergic asthma (review [106]), although the specific components of these pathogens which results in a worsening clinical status have not been extensively studied. Severe asthmatics can present with relatively high numbers of neutrophils in the airways [24]. Therefore, the mechanisms leading to exacerbations of asthma could be related to either enhanced allergic inflammation (TH2) or recruitment of neutrophils (Th1) into the airways, or both. Given the potential of TLR signaling to both enhance allergic responses and promote neutrophil recruitment, it is reasonable to propose an involvement of these receptors in exacerbations. Not surprisingly, studies with inhaled endotoxin have revealed that endotoxin, and its receptor TLR4, can be associated with exacerbations of allergic asthma [74, 107-109]. Similarly, administration of Mycoplasma pneumoniae to allergic mice during the challenge phase can exacerbate their allergic responses [110]. This effect is due at least in part, to lipopeptides of this organism that are recognized by both TLR2 and TLR6 [79, 111]. Streptococcus is another common respiratory pathogen associated with exacerbations of asthma [112]. Although the lipoteichoic acid (LTA) component of the cell wall of streptococcus is a known ligand for TLR2 [113], a specific role for TLR signaling in exacerbations of allergic asthma related to streptococcal infection has not been established. In addition to these bacteria, common viral pathogens, including respiratory syncytial virus (RSV), are associated with exacerbations of childhood asthma. RSV has recently been shown to induce signaling through TLR4 [114]. It is therefore of interest that polymorphisms in TLR4 are associated with the severity of RSV-induced bronchiolitis in infants [115]. The links between susceptibility to commonly encountered pathogens, TLRs and exacerbations of existing airway disease are an area of active investigation.

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