We investigated whether phagocytosis participates in the protection of insects from viral infection using the natural host–virus interaction between Drosophila melanogaster and Drosophila C virus (DCV). Drosophila S2 cells were induced to undergo apoptotic cell death upon DCV infection. However, UV-inactivated virus was unable to cause apoptosis, indicating the need for productive infection for apoptosis induction. S2 cells became susceptible to phagocytosis by hemocyte-derived l(2)mbn cells after viral infection, and the presence of phagocytes in S2 cell cultures reduced viral proliferation. Phagocytosis depended, in part, on caspase activity in S2 cells, as well as the engulfment receptors Draper and integrin βν in phagocytes. To validate the in vivo situation, adult flies were abdominally infected with DCV, followed by the analysis of fly death and viral growth. DCV infection killed flies in a dose-responding manner, and the activation of effector caspases was evident, as revealed by the cleavage of a target protein ectopically expressed in flies. Furthermore, hemocytes isolated from infected flies contained DCV-infected cells, and preinjection of latex beads to inhibit the phagocytic activity of hemocytes accelerated fly death after viral infection. Likewise, viral virulence was exaggerated in flies lacking the engulfment receptors, and was accompanied by the augmented proliferation of virus. Finally, phagocytosis of DCV-infected cells in vitro was inhibited by phosphatidylserine-containing liposome, and virus-infected flies died early when a phosphatidylserine-binding protein was ectopically expressed. Collectively, our study demonstrates that the apoptosis-dependent, phosphatidylserine-mediated phagocytosis of virus-infected cells plays an important role in innate immune responses against viral infection in Drosophila.

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To determine the source of circulating inhibin and estradiol-17beta during the estrous cycle in mares, the cellular localization of the inhibin alpha, betaA, and betaB subunits and aromatase in the ovary was determined by immunohistochemistry. Concentrations of immunoreactive (ir-) inhibin, estradiol-17beta, progesterone, LH, and FSH in peripheral blood were also measured during the estrous cycle in mares. Immunohistochemically, inhibin alpha subunits were localized in the granulosa cells of small and large follicles and in the theca interna cells of large follicles, whereas inhibin betaA and betaB subunits were localized in the granulosa cells and in the theca interna cells of large follicles. On the other hand, aromatase was restricted to only the granulosa cells of large follicles. Plasma ir-inhibin concentrations began to increase 9 days before ovulation; they remained high until 2 days before ovulation, after which they decreased when the LH surge was initiated. Thereafter, a further sharp rise in circulating ir-inhibin concentrations occurred during the process of ovulation, followed by a second abrupt decline. After the decline, plasma concentrations of ir-inhibin remained low during the luteal phase. Plasma estradiol-17beta concentrations followed a profile similar to that of ir-inhibin, except during ovulation, and these two hormones were positively correlated throughout the estrous cycle. Plasma FSH concentrations were inversely related to ir-inhibin and estradiol-17beta. These findings suggest that the dimeric inhibin is mainly secreted by the granulosa cells and the theca cells of large follicles; granulosa cells of small follicles may secrete inhibin alpha subunit, and estradiol-17beta is secreted by the granulosa cells of only large follicles in mares.

The cellular localization of inhibin alpha, betaA, and betaB subunits, 3beta-hydroxysteroid dehydrogenase (3beta-HSD), and cytochrome P450 aromatase (aromatase) in stallion testes was investigated. In addition, detailed seasonal changes in circulating immunoreactive (ir)-inhibin were investigated in correlation with testosterone, estradiol, LH, and FSH. Inhibin alpha subunit-positive staining was observed in Sertoli cells, and more clearly positive staining was noted in Leydig cells. Inhibin betaA and betaB subunits were also stained in both types of cells. Immunoreactivity of 3beta-HSD and aromatase was confined to the Leydig cells. There was no seasonal effect on the percentage of the areas within seminiferous tubules and interstitial tissues that stained positive for the inhibin alpha subunit. The highest plasma concentrations of ir-inhibin were observed in the breeding season, and the lowest levels were noted during the nonbreeding season. The circulating concentrations of ir-inhibin, steroid hormones, and gonadotropins were positively correlated with each other throughout the 2 years studied. The presence of the inhibin alpha and beta subunits in Leydig cells and Sertoli cells in the equine testis suggests that these cells may secrete dimetric (bioactive) inhibin in circulation of stallions, and that the circulating ir-inhibin may be a useful indicator of the testicular function of stallions.

The platelet counting performance of the PLT-F channel of the XN Series had improved accuracy and precision in the low range and in abnormal samples, avoiding the interference by nonplatelet particles.