Response to lipopolysaccharide in Octodon degus pups produces age-related sickness behavior but does not have effects in juveniles

During vertebrate development,the immune function is inefficient and is mainly controlled by innate defense.While there have been detailed studies of various aspects of innate immune function,the effects of this func­tion in the growth of vertebrates is still not well known.Similarly,there is little information regarding how ear­ly endotoxin exposure would affect juvenile phenotypes,specifically in a non-model mammal like a precocial rodent.We evaluated the response to an antigen and its cost in offspring of the rodent Octodon degus.We in­oculated pups at 4 different ages(8,15,22 and 30 days after birth)with an antigen to determine the ontogeny and costs of the response to an endotoxin.We assessed changes in body mass,body temperature,sickness be­havior and the levels of a key mediator of the inflammatory response,the cytokine interleukin-1β.We also de­termined the effects of early endotoxin exposure on the resting metabolic rate of juvenile animals(i.e.90 days after birth).The cytokine levels,body mass and body temperature were unaffected by time of inoculation and treatment.However,pups subjected to inoculation at 22 days after birth with the antigen showed reduced loco­motion.Juvenile resting metabolic rate was not affected by early endotoxin exposure.These results suggest that the magnitude of O.degus responses would not change with age.We discuss whether the lack of effect of the response on body mass or body condition is caused by environmental variables or by the precocial characteris­tics of O.degus.

Insights on the crosstalk between dendritic cells and helper T cells in novel genetic etiology for mendelian susceptible mycobacterial disease

Mendelian susceptibility to mycobacterial disease(MSMD)is an inherited predisposition to infections by Bacille-Calmette Guérin(BCG)vaccine or by environmental mycobacteria.The etiology of MSMD has been associated with up to nineteen different genetic mutations in interferon(IFN)-γ-related genes.1 Although mycobacteria susceptibility-associated genetic mutations are rare in the population,their diagnosis is crucial for an efficient and timely treatment.Kong et al.2 have recently described an autosomal recessive deficiency in the signal peptidase-like 2 A(SPPL2-a)as a new genetic etiology for MSMD in three patients that had suffered BCG dissemination disease.