Oxidative damage markers and inflammatory cytokines are altered in patients suffering with post-chikungunya persisting polyarthralgia

Abstract

Redox homoeostasis is necessary for the maintenance of living systems. Chikungunya viral infection manifests into joint inflammation and debilitating polyarthralgia affecting the life style of the patient badly. The disease pathophysiology is poorly understood and there is a lack of targeted therapeutics. The pathogenic role of free radicals in arthritis is well established. This study aims for the first time to evaluate the status of several standard oxidative stress markers and their correlation in chikungunya patients suffering with polyarthralgia. Expression of Siglec-9 on monocytes; which can modulate oxidative stress is studied along with intracellular reactive oxygen species (ROS), cellular lipid and protein damage markers in chikungunya patients with/without persisting polyarthralgia along with healthy controls. Furthermore, plasma NO level, antioxidant status was investigated along with some inflammatory cytokines namely IL-6, IFN-γ, CXCL-9, IL-10 and TGFβ1. Interestingly, all oxidative damage markers are altered significantly in groups but their alteration levels vary in patients with/without persisting polyarthralgia. Siglec-9 expression level is increased in patients revealing cellular response to manage oxidative stress with respect to controls. Correlation studies reveal that intracellular ROS correlates well with most of the studied parameters but the correlation coefficient (Pearson r) differs with disease manifestation demonstrating strong role of these factors in a pro-oxidant milieu. The presence of free radicals increases the availability of neoantigens continuously, which possibly further cascades oxidative damage and development of persisting polyarthralgia.

Keywords:

• Chikungunya
• cytokines
• intracellular ROS
• oxidative damage
• persisting polyarthralgia
• Siglec-9

Acknowledgements

The authors are indebted to all patients and healthy donors for participating in this study. Authors are thankful to Prof (Dr) Bibhuti Saha for providing clinical insight.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was funded by Department of Biotechnology, Government of West Bengal, India [File No.:232/BT(Estt)/RD-24/2014]. Nilotpal Banerjee received Research Fellowship from Department of Biotechnology, Government of West Bengal. Sumi Mukhopadhyay also acknowledges funding from Young Scientist Scheme of Science & Engineering Research Board, Government of India [File No. YSS/2014/000934].