![]() ![]() Taken together, these results suggest that loss of circadian oscillation of a specific immune function (phagocytosis) can have significant effects on long-term survival of infection.Ĭircadian rhythms, or daily oscillations in physiological functions, are nearly ubiquitous among animals. Interestingly, inhibition of phagocytosis in wild type flies results in survival kinetics similar to Tim mutants after infection with S. Tim appears to regulate an upstream event in phagocytosis, such as bacterial recognition or activation of phagocytic hemocytes. Wild-type flies exhibit up-regulated phagocytic activity at night Tim mutants have normal phagocytic activity during the day but lack this night-time peak. ![]() We then show that phagocytosis is circadian-regulated. We further found that basal levels of AMP gene expression exhibit time-of-day oscillations but that these are Tim-independent moreover, infection-induced AMP gene expression is not circadian-regulated. We found that melanization is not circadian-regulated. Drosophila have at least three main resistance mechanisms to kill high levels of bacteria in their hemolymph: melanization, antimicrobial peptides, and phagocytosis. ![]() pneumoniae, we found that resistance oscillates daily in adult wild-type flies and that these oscillations are absent in Tim mutants. We set out to characterize and identify the underlying mechanism of resistance that is circadian-regulated. Here we show that Tim regulates resistance against both S. Sensitivity to infection can be mediated either by changes in resistance (control of microbial load) or tolerance (endurance of the pathogenic effects of infection). ![]() Previously, we demonstrated that Drosophila mutants lacking the circadian regulatory proteins Timeless (Tim) and Period (Per) are sensitive to infection by S. An often-overlooked aspect of these interactions is the circadian state of the host. Survival of bacterial infection is the result of complex host-pathogen interactions. ![]()
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