Heat shock protein 60 and asthma treatment 10.5372/1905-7415.0604.084

Background: Asthma is a chronic and complex airway inflammatory disease characterized by airway hyperresponsiveness. Current asthma therapies are limited to specific disease manifestations, highlighting the importance of developing treatments with broader treatment applications. CD4⁺ T lymphocytes, which produce a characteristic repertoire of cytokines, play a critical role in the development of airway inflammation, mucus production, and airway hyper-responsiveness in asthma. Recently, it has been demonstrated that Heat Shock Protein 60 (HSP60) could mediate CD4⁺ T lymphocyte differentiation, suggesting that HSP60 can be targeted in the development of novel anti-asthma medications, especially for the treatment of severe disease or refractory patients.

Objective: This review summarizes the current knowledge regarding the relationship between HSP60 and asthma.

Method: We conducted a literature search using the MEDLINE (PubMed), SCOPUS and OVID/LWWW databases using the keywords “HSP”, “HSP60”, “HSP60 signaling pathway”, “TLR”, “TLR2 signaling pathway”, “asthma”, and “CD4⁺ T Lymphocytes”. Only articles published in English were included in the review.

Results: HSP60 was shown to either inhibit or exacerbate asthma through different mechanisms. However, the deleterious effects of HSP60 on asthma likely surpassed any beneficial inhibitory effects.

Conclusion: HSP60 can be expected to be developed into a new treatment target for asthma that may be of great interest to medical scientists and clinicians.