Given the threat presented by parasites and pathogens, insects employ various defences to protect themselves against infection, including chemical secretions. The red flour beetle Tribolium castaneum releases a secretion containing the benzoquinones methyl-1,4-benzoquinone (MBQ) and ethyl-1,4-benzoquinone (EBQ) into the environment. These compounds have known antimicrobial effects; however, their role in defence against macroparasites is not known. Entomopathogenic nematodes, such as Steinernema carpocapsae, present a serious threat to insects, with successful infection leading to death. Thus, quinone-containing secretions may also aid in host defence. We tested how exposure to the individual components of this quinone secretion, as well as a mix at naturally-occurring proportions, affected the survival and thrashing behaviour of S. carpocapsae, as well as their virulence to a model host (Galleria mellonella). Exposure to high concentrations of MBQ and EBQ, as well as the quinone mix, significantly increased nematode death but did not consistently reduce thrashing, which would otherwise be expected given their toxicity. Rather, quinones may act as a host cue to S. carpocapsae by triggering increased activity. We found that exposure to quinones for 24 or 72 hours did not reduce nematode virulence, and surviving nematodes remained infective after non-lethal exposure. Our results indicate that quinone secretions likely serve as a defence against multiple infection threats by reducing S. carpocapsae survival, but further research is required to contextualize their roles by testing against other nematodes, as well as other helminths using insects as hosts.

Ectoparasitic copepods have been reported in a wide range of aquatic animals, including crustacean shellfish. However, with the exception of the salmon louse, Lepeophtheirus salmonis, our knowledge of such parasites in commercial species is rudimentary. The current study examines the morphology and pathology of the parasitic copepod, Nicothoë astaci (the ‘lobster louse’) in its host, the European lobster, Homarus gammarus. Lobsters were sampled from waters surrounding Lundy Island (Bristol Channel, UK) and all individuals collected were found to harbour female adult N. astaci in their gills, with a mean of 47·3 parasites/lobster. The majority of N. astaci were found in the basal region of pleurobranch gills. The parasite was found to attach to gill filaments via its oral sucker, maxillae and maxillipeds, and to feed on host haemolymph (blood) through a funnel-like feeding channel. It caused varying degrees of damage to the host gill, including occlusion of gill filaments and disruption to the vascular system in the central axis. Although there was evidence of extensive host response (haemocytic infiltration) to the parasite, it was displaced from the parasite attachment site and thus was observed in the central gill axis below. The region of gill filament immediately underlying the parasite feeding channel was devoid of such activity suggesting that the parasite interferes with the cellular defence and haemostatic mechanisms of the lobster in order to maintain invasion of the host.

French oyster farming has been subject to severe mortalities during the summer months.Results from the research program “Morest”, which ran from 2000 to 2006 and examined thepossible causes of these mortalities, led to the construction of a model to explain theinteraction between environmental factors, oyster physiology and different opportunisticpathogens underlying oyster summer mortality. Temperature, food, reproduction and stresswere the main factors required for oyster mortality. Genetically-based resistance (“R”oysters) or susceptibility (“S” oysters) to summer mortality was revealed by divergentselection. Building on these results, a literature search was made in 2007 on themolecular origin of genetic resistance to such a complex mortality risk. The objectiveswere to lay a foundation for the preparation and orientation of future research directionsand to improve understanding of the underlying physiological mechanism leading to summermortality. Three years later, the resulting conceptual analysis reported here waspresented as an introductory lecture to Physiomar 2010, a conference where many newresults contributing to this research field were also reported. The literature reviewhighlighted two major review articles: the first dealing with nutrition and reproduction(Schneider 2004), the second with reproduction,temperature, oxidative stress and mortality (Heineinger 2002). The effect of nutrition level on energy orientation to growth orreproduction is controlled by endocrine factors. Among these, neuropeptide Y (NPY),ghrelin and leptin neuropeptides appeared to be potential candidates involved in germ-somaorientation in relation to trophic conditions. Depending on reproductive effort andtemperature, a metabolic stress resulting from the germ-soma conflict can appear,characterized by mitochondrial reactive oxygen species (ROS) production. Such an excess ofROS induces perturbations in mitochondrial activity leading to cell death. Many organisms,such as annual plants or the Pacific salmon, do not survive their first reproduction. Incontrast, others increase stress resistance by selection of antioxidant processes(superoxide dismutase SOD, catalase, etc.) through evolution, and survive firstreproduction. A similar difference was observed in the comparison made between R and Soysters, which differed in ROS production, SOD and catalase levels. Such factorscontrolling reproduction and ROS detoxification processes could therefore provide newmarkers for selection of oysters with better resistance to non-specific pathogens,complementing other classic selection approaches against specific pathogens or forimproved immunity. This antioxidant defence mechanism is found in many organisms includingvertebrates and in some invertebrates, including oysters. Its role needs to be consideredin pathology events involving other aquaculture species and it may also contribute toexplaining the increase in marine pathologies under anthropogenic environmental changes.

Oral supplementation with bovine colostrum (COL) has been shown to enhance immunity in human subjects. However, there is limited research on the use of bovine COL supplementation to counter exercise-induced immunodepression, as a model of stress-induced immunodepression, and previous research has focused primarily on salivary IgA. The aim of the present study was to determine the effects of bovine COL supplementation on exercise-induced changes in innate immunity (neutrophil function and salivary lysozyme) in addition to salivary IgA. Twenty healthy, active men cycled for 2 h at approximately 64 % maximal oxygen uptake after 4 weeks of daily bovine COL (n 10) or placebo (PLA, n 10) supplementation. Blood and saliva samples were obtained before and after supplementation, before and after exercise. Exercise induced significant increases in markers of physiological stress and stress to the immune system (circulating neutrophils, neutrophil:lymphocyte ratio, immature granulocytes, atypical lymphocytes and plasma cortisol), but there were no differences between the COL and PLA groups. Significant group × time interactions (two-way mixed model ANOVA) were observed for neutrophil function (stimulated degranulation) and salivary lysozyme concentration and release (P < 0·05). Significant exercise-induced decreases were observed in these parameters, and bovine COL supplementation either speeded the recovery (neutrophil function) or prevented the decrease (salivary lysozyme) in these measures of innate immunity. These results suggest that 4 weeks of bovine COL supplementation limits the immunodepressive effects induced by an acute prolonged physical stressor, such as exercise, which may confer some benefits to host defence.

Toll-like receptors (TLRs) play a principle role in distinct pathogen recognition and in the initiation of innate immune responses of the intestinal mucosa. Activated innate immunity interconnects downstream with adaptive immunity in complex feedback regulatory loops. Intestinal disease might result from inappropriate activation of the mucosal immune system driven by TLRs in response to normal luminal flora.

Sepsis stimulates an increase in the number and activity of mononuclear phagocytes in systemic host-defence organs. The present study was conducted to define the ultrastructural and cytochemical characteristics of the mononuclear phagocytes that sequester in the lung microvasculature of septic rats. Fourteen rats were challenged with a single intraperitoneal injection of saline (0.5 ml/100 g), E. coli (2×107/100 g) or glucan (4 mg/100 g), and euthanased 2, 4, or 7 d later. The lungs were inflation fixed and processed for transmission electron microscopy. Cellular morphology was used to identify the intravascular mononuclear phagocytes and acid phosphatase (AcPase) expression was monitored as an index of cellular differentiation and activation. Control rats contained a limited number of monocytes in the pulmonary vasculature. In contrast, large numbers of activated mononuclear phagocytes were seen in the microvasculature within 48 h of treatment with either microbial product. The recruited pulmonary intravascular mononuclear phagocytes (PIMP) exhibited AcPase-reactive Golgi complexes, accumulation of secretory vesicles and other features of cell activation consistent with enhanced biosynthetic activity. Subsequent electron microscopy, conducted 4 and 7 d posttreatment, suggested that a progressive decline in the number and activity of PIMPs then occurred. In order to quantify the sepsis-induced accumulation of AcPase-positive PIMP, the experimental challenges were repeated in 11 rats and, 48 h later, tissue samples were evaluated by light microscopy for tartrate-insensitive acid phosphatase. Control rats exhibited 0.148±0.107 AcPase-positive PIMP/alveoli. E. coli and glucan challenged animals exhibited significant (P<0.01) increases in AcPase-positive mononuclear phagocytes, with 0.782±0.073 and 0.636±0.170 PIMP/alveoli respectively. The results demonstrate that focal sepsis stimulates a significant, but transient, recruitment of activated mononuclear phagocytes into the rat pulmonary microvasculature.