Macrophages are endowed with a variety of receptors for lineage-determining growth factors, T helper (Th) cell cytokines, and B cell, host, and microbial products. In tissues, macrophages mature and are activated in a dynamic response to combinations of these stimuli to acquire specialized functional phenotypes. As for the lymphocyte system, a dichotomy has been proposed for macrophage activation: classic vs. alternative, also M1 and M2, respectively. In view of recent research about macrophage functions and the increasing number of immune-relevant ligands, a revision of the model is needed. Here, we assess how cytokines and pathogen signals influence their functional phenotypes and the evidence for M1 and M2 functions and revisit a paradigm initially based on the role of a restricted set of selected ligands in the immune response.

/pdf/the-m1-and-m2-paradigm-of-macrophage-activation-time-for-2dluegudcr.pdf

The M1 and M2 paradigm of macrophage activation: time for reassessment.

The precise function of eosinophils in parasitic infection in vivo remains poorly understood despite eosinophils having been shown to be potent effectors in killing parasites in vitro. Although it has long been held that the primary function of the eosinophil is protection against helminth parasites, there are little data to prove this unequivocally. Moreover, eosinophils are responsible for a considerable amount of inflammatory pathology accompanying helminth infections. This article will provide an overview of our current knowledge about eosinophils and their role, both protective and pathogenetic, in parasitic helminth infections.

The role of eosinophils in host defense against helminth parasites

▪ Abstract Immune responses can cause severe disease, despite the role immunity plays in defending against parasitism. Indeed, immunopathology is a remarkably common cause of disease and has strong impacts upon both host and parasite fitness. Why has immune-mediated disease not been eliminated by natural selection? What constraints might immunopathology impose upon the evolution of resistance? In this review, we explore two major mechanistic causes of immunopathology in mammals and consider how such disease may have influenced immune system design. We then propose hypotheses that could explain the failure of natural selection to eliminate immunopathology. Finally, we suggest how the evolution of strategies for parasite virulence and host resistance may be shaped by this “double-edged sword” of immunity. Future work may reveal whether immunopathology constrains the evolution of resistance in all host taxa.

Evolutionary Causes and Consequences of Immunopathology

Wolbachia Bacteria of Filarial Nematodes

Resistance of filarial nematode parasites to oxidative stress.

The susceptibility of Brugia malayi microfilariae and adults to injury by the murine macrophage cell line J774 activated with gamma interferon and bacterial lipopolysaccharide has been examined in vitro. Parasites of both stages showed a decline in viability over 48 h of coculture with activated macrophages, assessed by their capacity to reduce the tetrazolium salt 3-[4,5-diethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT), although adult parasites were more resistant than microfilariae. Removal of parasites to cell-free medium following exposure to activated macrophages for up to 48 h resulted in partial recovery of their capacity to reduce MTT, suggesting that the effects were primarily cytostatic. However, prolonged exposure to activated J774 cells for 72 h resulted in parasite death. Addition of the nitric oxide synthase inhibitor L-NMMA (N(G)-monomethyl-L-arginine monoacetate) indicated that nitric oxide derivatives were responsible for cytostasis and ultimate toxicity. The toxicity of nitric oxide derivatives was confirmed by coincubation of parasites with chemical donors, although far higher concentrations were required than those generated by activated J774 cells, implying additional complexity in macrophage-mediated cytotoxicity. These experiments further suggested that peroxynitrite or its by-products were more potently damaging to filariae than nitric oxide per se. Examination of ultrastructural changes on exposure of parasites to activated macrophages or donors of nitric oxide indicated that hypodermal mitochondria were highly vacuolated, with less prominent cristae. The data are discussed with reference to immunity to lymphatic filariae and their mechanisms of energy generation.

https://iai.asm.org/content/iai/65/7/2732.full.pdf

Cytostatic and cytotoxic effects of activated macrophages and nitric oxide donors on Brugia malayi.

Brugia malayi: differential susceptibility to and metabolism of hydrogen peroxide in adults and microfilariae.

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Cytostatic and cytotoxic effects of activated macrophages and nitric oxide donors on Brugia malayi.

Brugia malayi: differential susceptibility to and metabolism of hydrogen peroxide in adults and microfilariae.