Six costs of immunity to gastrointestinal nematode infections

Abstract

The strength of the immune response and the outcome of the interaction of a host with a parasite are influenced by genetic and phenotypic characteristics of both parties, and by environmental variables. Allocation of host resources to immune defence reduces resources available for other life-history traits. This review identifies six potential costs to the host from immune activation. The costs are likely to be broadly applicable to other immune responses in vertebrate species. Five phenotypic costs arise from: (i) increased metabolic activity; (ii) reduced nutrient availability due to anorexia; (iii) altered priorities for nutrient utilization; (iv) change in size and turnover of pools of immune cells and proteins; and (v) immunopathology from inappropriate or excessive immune activation. Subsumed by these costs is the cost of altered efficiency of nutrient use. A sixth cost is the genetic cost which arises from a change in the capacity of offspring to express production and life-history traits following selection for parasite resistance. The sensitivity of immune responses to the phenotypic status of the host, and the role the immune system shares with the neuroendocrine system in controlling use of resources underpin the importance of immunocompetence to the life-history of the host.

Maize supplementation of Pelibuey sheep in a silvopastoral system: fodder selection, nutrient intake and resilience against gastrointestinal nematodes

“…In the supplemented lambs, the cost of parasitism was lower than that found in nonsupplemented lambs (ME: 0.70 and MP: 9.2 v. ME: 1.46 and MP: 12.71, respectively). This difference could be the result of the differences in the worm burden (higher in the I-NS group than in the I-S group), which might have altered the nutrient partition during infection (Adams and Liu, 2003;Colditz, 2008). In this way, non-supplemented animals used more nutrients to repair the injuries caused by the larger worm burdens and eventually counteract the infection through an immune response, using less nutrients for growth (Coop and Kyriazakis, 1999).…”

“…The role of strategic supplementation as an alternative tool in the control of GIN in small ruminants under semi-intensive systems has been studied in recent years (Knox et al, 2006;Hoste et al, 2008;Torres-Acosta and Hoste, 2008). Infections with GIN can alter the host's feed intake, the nutrient partition (Adams and Liu, 2003;Colditz, 2008) and possibly the metabolism of the host. The extra nutrients provided in the supplement fulfill the daily requirements for maintenance (including repair of damaged tissues due to GIN infection and possibly the development of an immune response; Coop and Holmes, 1996;Van Houtert and Sykes, 1996).…”

A rat model of mild intestinal inflammation induced byStaphylococcus aureusenterotoxin B

“…However, if the immune system is stimulated and the response is not controlled, the tissue may be damaged; there may be extracellular matrix destruction due to metalloproteinase release and increased pass of neutrophils and other immune cells across the epithelium due to increased epithelial permeability (3) . In addition, stimulation of the immune system diverts energy and nutrients from growth and other productive functions (4) . Gut-associated lymphoid tissue (GALT) accounts for up to 80 % of the mucosal immune system and is distributed along the intestine in two forms: as organized GALT, which includes Peyer's patches (PP), isolated follicles and mesenteric lymph nodes, and as diffuse GALT, consisting of lymphocytes scattered in the epithelium and the lamina propria (5) .…”

Immune and other factors modulating host resistance against gastrointestinal nematode parasites in sheep

“…Nutrients are required for the repair of the damaged gut mucosa and the enhancement of immune response against these infections. The boosting of immunity is due to extensive replication of lymphocytes and other immune cells as well as the synthesis of acute phase proteins (Colditz, 2008). Nutrient management can enhance host resistance against GIN infection and improve clinical signs (Wagland et al, 1984).…”