Expression of TNF-α, TGF-β, IP-10 and IL-10 mRNA in kidneys of hamsters infected with pathogenic Leptospira

• Main Authors: Alisa Lowanitchapat, Sunchai Payungporn, Amornpun Sereemaspun, Pattama Ekpo, Duangporn Phulsuksombati, Yong Poovorawan, Chintana Chirathaworn
• Other Authors: Chulalongkorn University
• Format: Article
• Published: 2018
• Subjects: Immunology and Microbiology; Medicine
• Online Access: https://repository.li.mahidol.ac.th/handle/123456789/29199
• Institution: Mahidol University

Leptospirosis is a worldwide zoonosis caused by pathogenic Leptospira. Although several components of this organism have been identified, the molecular mechanisms underlying pathogenesis of this infectious disease are still poorly understood. Besides, direct injury by microbial factors, cytokines produced in response to infection have been proposed to be involved in pathogenesis of leptospirosis. In this study, cytokine gene expression in kidneys was investigated. Hamsters were injected with pathogenic Leptospira interrogans serovar Pyrogenes and were sacrificed on days 3, 5 and 7 after infection. RNA was extracted from kidney tissues. Real-time PCR was performed to demonstrate expression of TNF-α, TGF-β, IP-10 and IL-10 mRNA in kidneys.TNF-α, TGF-β and IP-10 expression could be demonstrated since day 3 post-infection whereas IL-10 expression was detected later on day 5. Leptospira infection resulted in not only expression of a proinflammatory cytokine, TNF-α, but also a T cell chemokine, IP-10. Detection of IP-10 suggested the involvement of T cell recruitment in the immune response or pathology in infected kidneys. Expressions of anti-inflammatory cytokines, TGF-β and IL-10 were also observed. However, the level of TGF-β expression was prominent since day 3 post-infection whereas IL-10 expression was clearly observed on day 5. Further experiments will provide additional information whether there is a correlation between the expression of these cytokines and pathologies found in an affected organ. © 2009 Elsevier Ltd.