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Differences in Macrophage Polarization Between More Healthy and Less Healthy Elders

Macrophages of the innate immune system take on different states known as polarizations depending on their duties. M1 macrophages are aggressive and inflammatory, involved in the destruction of pathogens and harmful cells. M2 macrophages aid in the processes of regeneration. The immune system becomes more inflammatory with advancing age. This chronic inflammation drives progression of most of the common age-related diseases, and an excess of M1 macrophages appears as a feature of many of those conditions. The research community is looking into ways to force more macrophages into the M2 polarization, as a possible approach to override a fraction of age-related immune dysfunction. In this context, researchers here report on their evaluation of differences in the macrophage population between more and less healthy older individuals.

The low-grade, chronic inflammatory state affecting aging organisms - inflammaging - is among the major risk factors for the development of the most common human age-related diseases (ARDs). Increasing evidence suggests that inflammaging is underpinned by monocytes/macrophages, while the acquisition of a senescent phenotype - a phenomenon that has been defined as macroph-aging - impairs the ability of immune cells to cope with stressors, thus contributing to immunosenescence. In this framework, the role of macrophage polarization in the modulation of inflammatory and repair processes is attracting growing interest.

The two main, and opposite activities of macrophages have led them to be classified into pro-inflammatory classically activated macrophages (M1) and anti-inflammatory and immunoregulatory alternatively activated macrophages (M2). Despite its value, this classification is however insufficient to describe the diverse phenotypes and functions of monocytes/macrophages in vivo. Intense research is being devoted to associate the polarization profiles, seen in vitro in relation to specific stimuli, with circulating and/or tissue macrophage polarization in health and disease conditions. Clearly, in vitro models are unable to mimic the complex environment that influences the M1/M2 balance in vivo, and since macrophages can develop mixed M1/M2 phenotypes, novel in vivo detection strategies are required. Several biomarkers have been associated with M1/M2 profiles. CD163, the high-affinity scavenger receptor for the haemoglobin-haptoglobin complex, is selectively expressed on M2 macrophages and monocytes, whereas CD80, a costimulatory signal for T cell activation and survival, is preferentially expressed on M1 macrophages.

Since data on the M1/M2 phenotype of circulating monocytes in healthy aging are not available, this study was undertaken to analyse monocyte profiles in healthy subjects of different ages using flow cytometry. To establish whether an M1/M2 imbalance could be disease-associated, the M1/M2 phenotype of elderly healthy subjects was compared with the one of elderly patients with acute myocardial infarction (AMI). The AMI patients showed a significantly decreased proportion of CD163+CD80+ and an increased proportion of CD163+ and CD163-CD80- cells among classical monocytes, opposite trends to those observed in healthy aging. Moreover, a significantly greater proportion of intermediate and non-classical CD80+ monocytes suggested a shift to a pro-inflammatory phenotype. Overall, CD163/CD80 characterization of circulating monocytes provides additional information about their polarization and could be an innovative tool to monitor aging.

Link: https://doi.org/10.18632/aging.101465

Comments

https://www.sciencedaily.com/releases/2018/04/180425093745.htm

"In the spleen, as well as the blood and kidneys, they found after drinking water with baking soda for two weeks, the population of immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. Macrophages, perhaps best known for their ability to consume garbage in the body like debris from injured or dead cells, are early arrivers to a call for an immune response."

Posted by: Jim at July 5th, 2018 6:01 AM

I wonder if the elevated inflammation is an indication of some other underlying process...

Posted by: cuberat at July 5th, 2018 9:36 AM

what strikes me most is the sheer...hostility, I suppose.

Posted by: TJ at July 5th, 2018 11:57 AM

@TJ - god that Slate article is annoying. The whole thing is a straw man argument. Rather than disagreeing with the proposal that damage repair could lead to negligible senescence, with the same chance of death from ill health per year as for someone in their twenties, the author constructs the straw man that longevity research proponents are arguing that as chance of death per year levels off at 50% people could live indefinitely (just keep flipping heads).

This is such an obviously stupid straw man that it shows the power of the pro aging trance. Someone writing for Slate will be tertiary educated and intelligent, yet even with these advantages over the average Joe are unable to overcome their coping mechanisms which prevent them dwelling on ideas of the suffering of aging and then death.

Posted by: Jim at July 6th, 2018 4:21 AM

The Slate article gave me cancer from reading it! Such a smug little asshole about it all too.

Posted by: Steve Hill at July 6th, 2018 8:09 AM

@Steve Hill: I always like reading your comments on these pages and that one perfectly sums up my thoughts about that quite pointless article.

Posted by: Steven B at July 6th, 2018 8:43 AM

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