Maternally inherited intracellular bacteria Wolbachia cause both parasitic and mutualistic effects on their numerous insect hosts, including manipulating the host reproductive system in order to increase the bacteria spreading in a host population, and increasing the host fitness. Here, we demonstrate that the type of Wolbachia infection determines the effect on Drosophila melanogaster egg production as a proxy for fecundity, and metabolism of juvenile hormone (JH), which acts as gonadotropin in adult insects. For this study, we used six D. melanogaster lineages carrying the nuclear background of interbred Bi90 lineage and cytoplasmic backgrounds with or without Wolbachia of different genotype variants. The wMelCS genotype of Wolbachia decreases egg production in infected D. melanogaster females in the beginning of oviposition and increases it later (from the sixth day after eclosion), whereas the wMelPop Wolbachia strain causes the opposite effect, and the wMel, wMel2 and wMel4 genotypes of Wolbachia do not show any effect on these traits compared with uninfected Bi90 D. melanogaster females. The intensity of JH catabolism negatively correlates with the fecundity level in the flies carrying both wMelCS and wMelPop Wolbachia The JH catabolism in females infected with genotypes of the wMel group does not differ from that in uninfected females. The effects of wMelCS and wMelPop infection on egg production can be levelled by the modulation of JH titre (via precocene/JH treatment of the flies). Thus, at least one of the mechanisms promoting the effect of Wolbachia on D. melanogaster female fecundity is mediated by JH.