Call off the dog(ma): M1/M2 polarization is concurrent following traumatic brain injury

Josh M. Morganti, Lara Kirstie Riparip, Susanna Rosi

Research output: Contribution to journalArticlepeer-review

180 Scopus citations


Following the primary mechanical impact, traumatic brain injury (TBI) induces the simultaneous production of a variety of pro- and anti-inflammatory molecular mediators. Given the variety of cell types and their requisite expression of cognate receptors this creates a highly complex inflammatorymilieu. Increasingly in neurotrauma research there has been an effort to define injury-induced inflammatory responses within the context of in vitro defined macrophage polarization phenotypes, known as "M1" and "M2". Herein, we expand upon our previous work in a rodent model of TBI to show that the categorization of inflammatory response cannot be so easily delineated using this nomenclature. Specifically, we show that TBI elicited a wide spectrum of concurrent expression responses within both pro- and anti-inflammatory arms. Moreover, we show that the cells principally responsible for the production of these inflammatory mediators, microglia/macrophages, simultaneously express both "M1" and "M2" phenotypic markers. Overall, these data align with recent reports suggesting thatmicroglia/macrophages cannot adequately switch to a polarized "M1-only" or "M2-only" phenotype, but display a mixed phenotype due to the complex signaling events surrounding them.

Original languageEnglish
Article numbere0148001
JournalPLoS ONE
Issue number1
StatePublished - Jan 1 2016

Bibliographical note

Publisher Copyright:
© 2016 Morganti et al.This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

ASJC Scopus subject areas

  • General


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