Over the last decades, research regarding innate immune responses has gained increasing importance. A growing body of evidence supports the notion that the innate arm of the immune system could show memory traits. Such traits are thought to be conserved throughout evolution and provide a survival advantage. Several models are available to study these mechanisms. Among them, we find the fruit fly, Drosophila melanogaster. This non-mammalian model has been widely used for innate immune research since it naturally lacks an adaptive response. Here, we aim to review the latest advances in the study of the memory mechanisms of the innate immune response using this animal model.

25 years after the declaration of a Global Emergency by the World Health Organization, tuberculosis (TB) remains a major enemy to the humankind. During this period, much progress has been done to better understand its natural history, revealing its huge complexity, which highlighted the need for implementing systems immunology approaches. Recent advances focused in understanding the role of macrophage subtypes and dendritic cells role, the importance of cytokine balance, and the antigenic repertoire. Identification of early irruption of polymorphonuclear neutrophils and extracellular growth of the bacilli seem to be the most disruptive factors to understand the evolution towards active TB. Their inclusion in future models will provide new tools for the better understanding of the tuberculosis.

Acinetobacter baumannii, a worldwide emerging nosocomial pathogen, acquires antimicrobial resistances in response to DNAdamaging agents, which increase the expression of multiple error-prone DNA polymerase components. Here we show that the aminocoumarin novobiocin, which inhibits the DNA damage response in Gram-positive bacteria, also inhibits the expression of error-prone DNA polymerases in this Gram-negative multidrug-resistant pathogen and, consequently, its potential acquisition of antimicrobial resistance through DNA damage-induced mutagenesis.A cinetobacter baumannii is a highly effective human colonizer in hospital settings worldwide. Its ability to acquire resistance to several extensively used antimicrobials has resulted in its emergence as a problematic nosocomial pathogen (1). As in other bacteria, A. baumannii achieves resistance against certain antimicrobials through single mutations in the corresponding target genes (i.e., point mutations in the rpoB gene can generate resistance to rifampin [2]). In previous works, we demonstrated that this bacterium contains multiple components of error-prone DNA polymerases, whose induction after DNA damage leads to the introduction of point mutations in the bacterial genome, including those conferring antibiotic resistance (3, 4).Topoisomerase enzymes maintain the topological state of DNA and are critical regulators of protein translation and cell replication. Specifically, DNA gyrase (a type II topoisomerase) catalyzes the removal of the torsional stress that accumulates in bacterial chromosomes at sites preceding replication forks and transcriptional complexes by forming double-stranded breaks in the DNA (5). The formation of these double-stranded breaks and, therefore, of single-stranded DNA activates the bacterial SOS response, which results in mutagenic repair through the expression of mutagenic genes, especially those encoding error-prone DNA polymerases. This response guarantees DNA repair and cell survival but also results in some mutations that are able to confer antimicrobial resistance (2, 6). In Escherichia coli and other bacteria, the DNA damage response is regulated by the LexA repressor. However, A. baumannii lacks the LexA repressor, and the errorprone DNA polymerase (UmuDAb) carries out its functional role (3, 4). Thus, the induction of this DNA repair response in A. baumannii also results in the introduction of point mutations, including those conferring antibiotic resistance.DNA gyrase inhibitors such as quinolones take advantage of the potential of topoisomerases to fragment the genome and thereby cause cell death. These drugs bind noncovalently at the enzyme-DNA interface in the cleavage-ligation active site to block ligation (5). Further, because quinolones also cause SOS induction, they ultimately promote antimicrobial resistance. Thus, one approach to combat the increasing prevalence of antimicrobialresistant infections is to prevent SOS activation. Antimicrobials such as novobiocin interfere with the ATPase activity of DNA gyrase, such t...