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Category: Microbial Genetics and Molecular Biology; Bacterial Pathogenesis
Macrophages in Helminth Infection: Effectors, Regulators, and Wound Healers, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555816650/9781555814014_Chap31-1.gif /docserver/preview/fulltext/10.1128/9781555816650/9781555814014_Chap31-2.gifAbstract:
Parasitic worms that infect people and animals cover an enormous phylogenetic spectrum within the animal kingdom. The infective larvae migrate into the nearby lymphatics and take up residence, where they mature, mate, and produce microfilaria that circulate in the bloodstream. Eggs that lodge in the tissues, particularly the liver, gut, and bladder wall, are the main cause of pathology. In the context of helminth infection, macrophages will be exposed to many signals beyond IL-4 and IL-13 that may modulate or enhance the alternatively activated phenotype. The role of macrophages in granuloma formation and control not only is important in the consideration of parasite containment, but also is one of the most important processes associated with the pathology of helminth infection. The study of macrophages in wound healing has implications far beyond helminth infection, including tissue remodeling associated with asthma and pulmonary fibrosis. Thus, although macrophages during helminth infection are actively recruited in an inflammatory context, the nature of this inflammation differs from that seen during classical macrophage activation by microbial products and IFN-γ. The induction of arginase by IL-4/IL-13 will reduce NO levels, thus acting to reduce one of the main mediators of "classical inflammation". Consistent with their roles as immune regulators, macrophages recruited to helminth infection produce high levels of the downregulatory cytokines IL-10 and TGF-β. More radically, the authors have begun to appreciate that macrophages in helminth infection have major roles in wound healing, with implications for the understanding of the evolution of Th2 immunity.
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