The Role of Heat Shock Protein 70 kDa in Asthma.
Marina Alexandrovna ShevchenkoEkaterina ServuliZarema AlbakovaLeonid KanevskiyAlexander SapozhnikovPublished in: Journal of asthma and allergy (2021)
Asthma is a complex chronic disorder of the airways, affecting immune and structural cells and inducing both protein and tissue remodeling. Heat shock proteins 70 kDa (HSP70s) are highly conserved members of the stress-induced family, possessing precisely described chaperone activity. There is growing evidence of a tight relationship between inflammatory diseases of different origins and the elevation of local HSP70 expression and secretion. Although extracellular HSP70 does not serve as a common marker of asthma, elevated HSP70 levels have been detected in the peripheral blood serum and sputum of patients with asthma, as well as in the bronchoalveolar lavage fluid of mice with induced allergic airway inflammation. Possessing diverse immunomodulating properties, extracellular HSP70 can manifest different activities in airway inflammatory processes and asthma, acting either as a pro-inflammatory trigger, or an anti-inflammatory agent. This review will discuss the effects and possible mechanisms concerning HSP70 implication in airway inflammation regulation in asthma. We examine ATPase and chaperone activities of HSP70 as potential modulators of immune responses in asthma. Given the crucial role of a chronic inflammatory response in asthma, understanding the effects of HSP70 on immune and structural cells may reveal new perspectives for the therapeutic control of inflammation.
Keyphrases
- heat shock protein
- heat shock
- chronic obstructive pulmonary disease
- lung function
- allergic rhinitis
- inflammatory response
- heat stress
- stress induced
- peripheral blood
- immune response
- oxidative stress
- induced apoptosis
- mycobacterium tuberculosis
- cystic fibrosis
- anti inflammatory
- metabolic syndrome
- genome wide
- risk assessment
- blood brain barrier
- type diabetes
- single cell
- diabetic rats
- signaling pathway
- lipopolysaccharide induced
- pulmonary tuberculosis