Publications by authors named "Karina K Sanchez"

Infections cause catabolism of fat and muscle stores. Traditionally, studies have focused on understanding how the innate immune system contributes to energy stores wasting, while the role of the adaptive immune system remains elusive. In the present study, we examine the role of the adaptive immune response in adipose tissue wasting and cachexia using a murine model of the chronic parasitic infection Trypanosoma brucei, the causative agent of sleeping sickness.

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Article Synopsis
  • - Disease tolerance is a vital survival strategy that minimizes physical damage from infections without directly killing the pathogens, and this tolerance shifts as an organism ages.
  • - Research using a polymicrobial sepsis model revealed distinct health responses in young and old mice after infection, highlighting different disease courses related to their age.
  • - Young mice utilized a protective mechanism involving FoxO1 that helped them survive, while the same mechanism contributed to heart issues and death in older mice, underscoring the need for age-specific therapy in infections.
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Article Synopsis
  • Hosts utilize both aggressive and cooperative strategies to defend against infections, with Leptin playing a key role in resistance mechanisms but its impact on cooperation with pathogens not fully understood.
  • In a study on mice infected with Yersinia pseudotuberculosis, a lack of Leptin signaling resulted in increased cooperation between the host and pathogen, leading to protection against infection, though it wasn't due to resistance or changes in energy metabolism.
  • The findings suggest that in certain situations, it may be more advantageous for hosts to tolerate organ damage caused by infection rather than solely focusing on preventing damage or killing the pathogen.
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Pathogen virulence exists on a continuum. The strategies that drive symptomatic or asymptomatic infections remain largely unknown. We took advantage of the concept of lethal dose 50 (LD50) to ask which component of individual non-genetic variation between hosts defines whether they survive or succumb to infection.

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