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Abstract:
Asthma and chronic obstructive pulmonary disease (COPD) have both been
historically associated with significant morbidity and financial burden.
These diseases can be induced by several exogenous factors, such as
pathogen associated molecular patterns (PAMPs) (e.g., allergens and
microbes). Endogenous factors, including reactive oxygen species, and
damage-associated molecular patterns (DAMPs) recognized by toll-like
receptors (TLRs), can also result in airway inflammation. Asthma is
characterized by the dominant presence of eosinophils, mast cells, and
clusters of differentiation (CD)4(+) T cells in the airways, while CORD
typically results in the excessive formation of neutrophils,
macrophages, and CD8+ T cells in the airways. In both asthma and CORD,
in the respiratory tract, TLRs are the primary proteins of interest
associated with the innate and adaptive immune responses; hence,
multiple treatment options targeting TLRs are being explored in an
effort to reduce the severity of the symptoms of these disorders.
TLR-mediated pathways for both CORD and asthma have their similarities
and differences with regards to cell types and the pro inflammatory
cytotoxins present in the airway. Because of the complex TLR cascade, a
variety of treatments have been used to minimize airway hypersensitivity
and promote bronchodilation. Although unsuccessful at completely
alleviating CORD and severe asthmatic symptoms, new studies are focused
on possible targets within the TLR cascade to ameliorate airway
inflammation.
