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Changes in macrophage phenotype as the immune response evolves.

ABSTRACT: Mononuclear phagocytic cells (MPCs), including macrophages and dendritic cells (DCs), are widely distributed throughout our organs where they perform important homeostatic, surveillance and regenerative tasks. In response to infection or injury, the composition and number of MPCs change remarkably, in part due to the recruitment of inflammatory monocytes from bone marrow. In infection or injury, macrophages and DCs perform important innate and adaptive immune roles from the initial insult through repair and regeneration of the tissue and resolution of inflammation. Evidence from mouse models of disease has shown increasing complexity and subtlety to the mononuclear phagocytic system, which will be reviewed here. New studies show that in addition to monocytes, the resident populations of mononuclear phagocytes expand in disease states and play distinct but important roles in the immune response. Finally, new insights into these functionally diverse cells are now translating into therapeutics to treat human disease.

SUBMITTER: Lichtnekert J

PROVIDER: S-EPMC3732570 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature

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Changes in macrophage phenotype as the immune response evolves.

Lichtnekert Julia J Kawakami Takahisa T Parks William C WC Duffield Jeremy S JS

Current opinion in pharmacology 20130607 4

Mononuclear phagocytic cells (MPCs), including macrophages and dendritic cells (DCs), are widely distributed throughout our organs where they perform important homeostatic, surveillance and regenerative tasks. In response to infection or injury, the composition and number of MPCs change remarkably, in part due to the recruitment of inflammatory monocytes from bone marrow. In infection or injury, macrophages and DCs perform important innate and adaptive immune roles from the initial insult throug ...[more]

PMID: 23747023

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Project description:The evolution of hypermutators in response to antibiotic treatment in both clinical and laboratory settings provides a unique context for the study of adaptive evolution. With increased mutation rates, the number of hitchhiker mutations within an evolving hypermutator population is remarkably high and presents substantial challenges in determining which mutations are adaptive. Intriguingly however, hypermutators also provide an opportunity to explore deeply the accessible evolutionary trajectories that lead to increased organism fitness, in this case the evolution of antibiotic resistance to the clinically relevant antibiotic tigecycline by the hospital pathogen Acinetobacter baumannii. Using a continuous culture system, AB210M, a clinically derived strain of A. baumannii, was evolved to tigecycline resistance. Analysis of the adapted populations showed that nearly all the successful lineages became hypermutators via movement of a mobile element to inactivate mutS. In addition, metagenomic analysis of population samples revealed another 896 mutations that occurred at a frequency greater than 5% in the population, while 38 phenotypically distinct individual colonies harbored a total of 1712 mutations. These mutations were scattered throughout the genome and affected ~40% of the coding sequences. The most highly mutated gene was adeS, a known tigecycline-resistance gene; however, adeS was not solely responsible for the high level of TGC resistance. Sixteen other genes stood out as potentially relevant to increased resistance. The five most prominent candidate genes (adeS, rpsJ, rrf, msbA, and gna) consistently re-emerged in subsequent replicate population studies suggesting they are likely to play a role in adaptation to tigecycline. Interestingly, the repeated evolution of a hypermutator phenotype in response to antibiotic stress illustrates not only a highly adaptive strategy to resistance, but also a remarkably efficient survey of successful evolutionary trajectories.

Dataset Information

Changes in macrophage phenotype as the immune response evolves.

Publications

Changes in macrophage phenotype as the immune response evolves.

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