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Keywords:

  • cytokines;
  • fitness;
  • infectious disease;
  • nematode infection;
  • toll-like receptors;
  • trichostrongylid

It's a wormy world. All natural vertebrate populations are subject to infection and re-infection with helminth parasites (Stoll 1947). Even in humans, around one billion people in developing nations are infected by one or several of a range of helminth parasites (Lustigman et al. 2012). Infection by worms is therefore the norm and is reflected in vertebrate immune responses. Thus, there is probably little point in generating an inflammatory response to clear every last worm, with ensuing collateral damage to our own tissue, when rapid re-infection from the environment by another worm is pretty much assured. Instead, the vertebrate immune system modifies its response to worms, controlling (but not always clearing) these infections and at the same time limiting damage to host tissue caused by inflammatory immune responses (Jackson et al. 2009). The immune system, however, has to fight battles on several fronts and, while fighting a prolonged war of attrition against helminth parasites, it also has to protect against periodic invasion by bacteria, where a rapid response to kill invading microbes before they spread is essential (Fig. 1). In this issue of Molecular Ecology, Friberg et al. (2013) ask what effect worm infections have on a host's ability to mount antimicrobial responses.

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Figure 1. Helminths generally produce chronic infections that elicit immune responses characterized by both the activation of T helper type 2 (Th2) cells and the production of regulatory responses, such as the cytokines transforming growth factor beta (TGF-β) and interleukin-10 (IL-10) and regulatory T helper cells (TREG). In combination, this immunological phenotype is often called a ‘modified’ Th2 response. Bacterial infections are recognized by pattern recognition receptors such as the Toll-like receptors (TLRs) that are able to detect bacterial molecules such as lipopolysaccharides (by TLR-4), flagellins (by TLR-5) and unmethylated CpG (by TLR-9) and generate a rapid inflammatory response [characterized by tumour necrosis factor (TNF)-α production], particularly at the site of infection. As indicated by the dashed line, these contrasting responses have the potential to interact, especially in animals that spend much of their life harbouring chronic helminth infections that may have systemic anti-inflammatory effects.

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