Abstract:
Leptospirosis is a worldwide zoonosis caused by spirochetes of the genus Leptospira. The spectrum of human disease caused by leptospires is extremely wide, ranging from sub-clinical infection to a severe syndrome of multi-organ infection with high mortality. Leptospirosis pathogenesis mechanisms are not clearly understood. Various enzymes and toxins have been identified and suggested to be involved in tissue damage. In addition, it has been demonstrated that immune response to Leptospira may induce pathologies in infected organs. Cytokine and chemokine induction by Leptospira or Leptospira components have been demonstrated. Various Leptospira components have been studied; however, the most widely studied components are outer membrane proteins, especially LipL32. Most studies on cytokine induction by Leptospira were done in vitro. In this study, the expression of mRNA of TNF-α, TGF-β, Il-10 and IP-10 in kidneys and livers, the commonly affected organs in Leptospirosis were investigated. Leptospira interrogans serovar Pyrogenes was intraperitoneally injected into Golden Syrian Hamsters. Kidney and liver tissues were collected at 3, 5 and 7 days after injection. RNA was extracted from tissues for RT-PCR to demonstrate cytokine/chemokine expression. The expression of LipL32 in kidneys and livers was also investigated since it has been demonstrated that this protein induced cytokine/chemokine expression. This study demonstrated that LipL32 was expressed in both kidneys and livers of infected hamsters. The level of LipL32 expression was similar in both tissues. However, the pattern of cytokine mRNA expression was different. IL-10 and IP-10 expression was induced in kidneys whereas they were undetectable in livers. TNF-α and TGF-β expression was enhanced in livers from infected hamsters. Further studies such as localization of cytokine expression in order to demonstrate the correlation with pathologies in kidneys and livers and the study of expression of other Leptospira components will provide further information not only on the immune response to Leptospira but also on pathogenesis of this infectious disease.
