The mitochondrial heat shock protein 60 (HSP60) is up-regulated inOnchocerca volvulusafter the depletion ofWolbachia

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Abstract
SUMMARY: Wolbachia, a genus of endosymbiotic bacteria of filarial worms, represent novel targets for anti-filarial therapy. The efficacy of compounds againstWolbachiahas been evaluated using antiserum raised against the 60 kDa heat shock protein (HSP60) which binds specifically to this protein in bothWolbachiaand mitochondria. It has been shown thatWolbachiastains (using such specific probes) stronger than the mitochondria in untreatedOnchocerca volvulus, whereas after the depletion ofWolbachia(with drugs) staining of the mitochondria is increased. Herein, immunogold electron microscopy showed that specific anti-HSP60 serum specifically labelledWolbachiaand filarial mitochondria, and that both have distinct localization patterns, thus allowing them to be differentiated. Immunohistochemistry ofO. volvulusshowed that HSP60 staining is increased in the mitochondria afterWolbachiadepletion in the hypodermis, epithelia, muscles, oocytes, embryos, and developing spermatozoa. This could have been the result of the antiserum preferentially binding to theWolbachiawhen they are present or due to increased expression of the protein in the absence of the bacteria. To address this, mRNA levels of filarialhsp60inO. volvuluswere measured. After the depletion ofWolbachia, the transcription ofhsp60was significantly greater (7·7 fold) compared with untreated worms. We hypothesize that the increased expression of HSP60 in the absence ofWolbachiais due to a disruption of the homeostasis of the endosymbiosis.