Macrophage diversity in cardiac inflammation: a review

Abstract

Cardiac inflammatory disease represents a significant public health burden, and interesting questions of immunopathologic science and clinical inquiry. Novel insights into the diverse programming and functions within the macrophage lineages in recent years have yielded a view of these cells as dynamic effectors and regulators of immunity, host defense, and inflammatory disease. In this review, we examine and discuss recent investigations into the complex participation of mononuclear phagocytic cells in the pathology of animal models of myocarditis.

Figure 1

Monocyte and macrophage infiltration into cardiac tissue in EAM. A)Time course of absolute enumeration of total CD45⁺ leukocytes. B) Representative gating of monocytes and macrophages from heart-infiltrating CD45⁺ leukocytes. C) Absolute enumeration of CD11b⁺F4/80^–CD45⁺ monocytes and CD11b⁺F4/80⁺CD45⁺ macrophages. Individual data points represent individual wild type female BALB/c mice immunized on days 0 and 7 with 100 μg/mL MyHCα_614-629 in supplemented CFA, as previously described (91). Heart-infiltrating leukocytes were isolated as previously described (67). Bars indicate mean of each group. Asterisks denote significant t-test statistics, compared to day 0 (*, p < 0.05; **, p < 0.005).

Figure 2

Cardiac infiltration by macrophage subpopulations in EAM. A) Time course of absolute enumeration of Ly6C^hiCD11b⁺F4/80⁺CD45⁺ “inflammatory” macrophages and Ly6C^loCD11b⁺F4/80⁺CD45⁺ “resident” macrophages. B) Expression of markers of classical and alternative activation on intracardiac CD11b⁺F4/80⁺CD45⁺-gated macrophages during EAM. Individual data points represent individual wild type female BALB/c mice. Bars indicate mean of each group. Asterisks denote significant t-test statistics, compared to day 0 (*, p < 0.05; **, p < 0.005).