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Respiratory viral infections represent the most common cause of allergic asthma exacerbations. Amplification of type 2 immunity is strongly implicated in asthma exacerbation, but how virus infection boosts type 2 responses during exacerbation is poorly understood. We report a significant correlation between release of host double stranded DNA (dsDNA) following rhinovirus infection and exacerbation of type 2 allergic inflammation and disease severity in patients. In a mouse model, we show that rhinovirus infection triggers neutrophil extracellular traps (NETs) formation and host dsDNA release. We further demonstrate that inhibiting NETosis by blocking neutrophil elastase or degrading NETs with DNase protects mice from type 2 allergic asthma exacerbations. Furthermore, injection of host dsDNA alone is sufficient to recapitulate many features of rhinovirus-induced type 2 immune responses and asthma pathology. Thus, NETosis and host dsDNA contribute to exacerbation pathogenesis and may represent potential targets for novel treatments of rhinovirus-induced asthma exacerbations.

Trabajo presentado en la 18th International Conference on Diseases of Fish and Shellfish, celebrada en Belfast, del 4 al 8 de septiembre de 2017, When infected by pathogens, endotherms and ectotherms can both increase their body temperature to limit the infection. Ectotherms do so by moving to warmer places, hence the term ¿behavioral fever¿. We studied the expression of behavioral fever by common carp infected by cyprinid herpesvirus 3 (CyHV-3) using multi-chamber tanks encompassing a 24°C-32°C gradient. We showed that carp maintained at 24°C all died from the infection, whereas those housed in multichamber tanks all survived as a consequence of their transient migration to the warmest compartment. As the expression of behavioral fever occurred only at an advanced stage of the disease, we hypothesized that the virus might delay this phenomenon in order to promote its replication. This hypothesis was proved correct, and the delay mechanism was found to rely on the expression of a soluble viral decoy receptor for Tnf¿ encoded by CyHV-3 ORF12. This conclusion relied on three complementary observations: (i) a CyHV3 ORF12 deleted recombinant induced an early onset of behavioral fever in comparison to wild-type CyHV-3; (ii) ORF12 expression product binds and neutralizes carp Tnf¿; and (iii) injection of anti-Tnf¿ neutralizing antibodies suppressed behavioral fever, and decreased fish survival in response to infection. This study provides a unique example of how viruses have evolved to alter host behavior to increase fitness. It demonstrates that behavioral fever in ectotherms and fever in endotherms are evolutionarily and functionally related through common cytokine mediators that originated more than 400 million years ago. Finally, this study stresses the importance of the environment in the hostpathogen- environment triad.

Myeloperoxidase (MPO) is a specific enzyme of neutrophil azurophilic granules with a strong oxidative activity. Thanks to a radioimmunoassay of equine myeloperoxidase, the authors have observed a significantly higher plasma level of MPO in horses operated for strangulation obstruction of the large intestine (n = 6) than in horses suffering from a non-strangulating displacement of the large intestine (n = 9). For the 2 groups, 3 phases were distinguished: reception (P1), intensive care (P2) and terminal phase (P3). The mean peak values of MPO for these phases were 121.6 ng/mL (P1), 168.6 ng/mL (P2), and 107.0 ng/mL (P3) for the non-strangulating group, and 242.6 ng/mL (P1); 426.0 ng/mL (P2), and 379.5 ng/mL (P3) for the strangulation group. The variations of the mean peak values of plasma MPO were significantly different between the 2 groups and between the different phases. A significant increase of the least square means of MPO was observed between P1 and P2. A significant decrease of the least square means of the number of circulating leukocytes was observed between P1 and P3. Polymorphonuclear neutrophil activation could play a major role in the pathogenesis of acute abdominal disease and endotoxic shock.

During the 1992-1993 133 seabirds found on Belgian beaches were necropsied. Most frequent species were the guillemot (Uria aalge), the oystercatcher (Haematopus ostralegus), the kittiwake (Rissa tridactyla), the razorbill (Alca torda) and the herring gull (Larus argentatus).The three main observations were, in decreasing order, cachexia, acute and hemorrhagic gastroenteritis, and oil contamination of plumage and intestinal tract. The pelagic origin of seabirds was associated with all 3 observations; oil contamination was associated with acute gastro-enteritis and cachexia and, finally, the immature character was associated with cachexia. A hypothetical mechanism of death would be oiled pelagic seabirds that become cachectic and die of acute gastroenteritis.It is unlikely that seabirds act as a reservoir for bacteria, that were only occasionally identified in our material. Therefore, it appears that infectious agents play a minor role in seabirds stranding.