Nnot be regarded as the result of a general depression of metabolism only, but it involves the complex interplay between up-regulation and down-regulation of diverse cellular activities. Hence, efforts should be made in the future to identify and differentiate molecular, biochemical and physiological phenomena in AfricanPLOS ONE | DOI:10.1371/journal.pone.0121224 March 30,23 /Differential Gene Expression in the Liver of the African Lungfishlungfishes incidental to each of the three phases (induction, maintenance and arousal) of aestivation.Author ContributionsConceived and designed the experiments: YKI SFC. Performed the experiments: KCH. Analyzed the data: KCH SFC YKI. Contributed reagents/materials/analysis tools: WPW. Wrote the paper: SFC KCH YKI. Took care of the animals: WPW.
Lyme borreliosis (LB), caused by spirochete Borrelia burgdorferi sensu lato, is a tick-borne infection common in northern hemisphere [1]. Borrelia burgdorferi sensu lato is further classified into several genospecies of which Borrelia burgdorferi sensu stricto (B. burgdorferi), Borrelia garinii and Borrelia afzelii are clinically the most important human pathogens. From the inoculation site in the skin, the bacteria can disseminate to other organs like the heart, joints and the nervous system, and cause a persistent infection in these foci. However, the molecules targeting the spirochete to the various tissues remain incompletely characterized. Animal models, especially with mice, are widely used to study the dissemination and treatment response of LB. B. burgdorferi infected C3H mice develop prominent joint manifestations with joint swelling, periarticular oedema and leukocyte infiltration [2]. Some studies suggest that B. burgdorferi infected and antibiotic treated mice still harbour live but obviously attenuated and non-cultivable bacteria especially in collagen-rich tissues [3?]. Parallel results have been obtained also using dogs and rhesus macaques [6, 7]. We have previously shown that a part of B. burgdorferi infected C3H/He mice treated with ceftriaxone became B. burgdorferi culture positive after immunosuppression by anti-TNF-alpha [8]. In contrast, recent mouse data obtained using intravital microscopy of antibiotic treated mice suggest that persisting B. burgdorferi antigens rather than an on-going infection can be detected in mouse joint after the treatment [9]. Taken together, the above animal data suggest the persistence of some form of B. burgdorferi remnants in animal joints after antibiotic treatment. The molecular mechanisms of this phenomenon are poorly understood. Borrelia burgdorferi sensu lato has several adhesins, which are of critical ICG-001 site importance for the virulence [10, 11]. Two such adhesins are decorin binding proteins A and B (DbpA/B) [12?6]. DbpA/B mediate bacterial PX-478 site attachment to decorin, which is a major component at the extracellular matrix, especially in the joint, skin and endothelial tissue [17?9]. The importance of B. burgdorferi adhesion to decorin is further underlined by the partial resistance of decorin deficient mice to LB [20]. Recent mouse data suggest a role for DbpA in the development of joint manifestations in mice [21, 22]. Interestingly, it is suggested that decorin rich tissues, like the joint, might serve as a protective niche for B. burgdorferi where the bacteria can hide from the immune response [23]. The present study was undertaken to test the hypothesis that DbpA and/or B are required for the development of joi.Nnot be regarded as the result of a general depression of metabolism only, but it involves the complex interplay between up-regulation and down-regulation of diverse cellular activities. Hence, efforts should be made in the future to identify and differentiate molecular, biochemical and physiological phenomena in AfricanPLOS ONE | DOI:10.1371/journal.pone.0121224 March 30,23 /Differential Gene Expression in the Liver of the African Lungfishlungfishes incidental to each of the three phases (induction, maintenance and arousal) of aestivation.Author ContributionsConceived and designed the experiments: YKI SFC. Performed the experiments: KCH. Analyzed the data: KCH SFC YKI. Contributed reagents/materials/analysis tools: WPW. Wrote the paper: SFC KCH YKI. Took care of the animals: WPW.
Lyme borreliosis (LB), caused by spirochete Borrelia burgdorferi sensu lato, is a tick-borne infection common in northern hemisphere [1]. Borrelia burgdorferi sensu lato is further classified into several genospecies of which Borrelia burgdorferi sensu stricto (B. burgdorferi), Borrelia garinii and Borrelia afzelii are clinically the most important human pathogens. From the inoculation site in the skin, the bacteria can disseminate to other organs like the heart, joints and the nervous system, and cause a persistent infection in these foci. However, the molecules targeting the spirochete to the various tissues remain incompletely characterized. Animal models, especially with mice, are widely used to study the dissemination and treatment response of LB. B. burgdorferi infected C3H mice develop prominent joint manifestations with joint swelling, periarticular oedema and leukocyte infiltration [2]. Some studies suggest that B. burgdorferi infected and antibiotic treated mice still harbour live but obviously attenuated and non-cultivable bacteria especially in collagen-rich tissues [3?]. Parallel results have been obtained also using dogs and rhesus macaques [6, 7]. We have previously shown that a part of B. burgdorferi infected C3H/He mice treated with ceftriaxone became B. burgdorferi culture positive after immunosuppression by anti-TNF-alpha [8]. In contrast, recent mouse data obtained using intravital microscopy of antibiotic treated mice suggest that persisting B. burgdorferi antigens rather than an on-going infection can be detected in mouse joint after the treatment [9]. Taken together, the above animal data suggest the persistence of some form of B. burgdorferi remnants in animal joints after antibiotic treatment. The molecular mechanisms of this phenomenon are poorly understood. Borrelia burgdorferi sensu lato has several adhesins, which are of critical importance for the virulence [10, 11]. Two such adhesins are decorin binding proteins A and B (DbpA/B) [12?6]. DbpA/B mediate bacterial attachment to decorin, which is a major component at the extracellular matrix, especially in the joint, skin and endothelial tissue [17?9]. The importance of B. burgdorferi adhesion to decorin is further underlined by the partial resistance of decorin deficient mice to LB [20]. Recent mouse data suggest a role for DbpA in the development of joint manifestations in mice [21, 22]. Interestingly, it is suggested that decorin rich tissues, like the joint, might serve as a protective niche for B. burgdorferi where the bacteria can hide from the immune response [23]. The present study was undertaken to test the hypothesis that DbpA and/or B are required for the development of joi.