Publications by authors named "J McCarville"

Colorectal cancer (CRC) is driven by genomic alterations in concert with dietary influences, with the gut microbiome implicated as an effector in disease development and progression. While meta-analyses have provided mechanistic insight into patients with CRC, study heterogeneity has limited causal associations. Using multi-omics studies on genetically controlled cohorts of mice, we identify diet as the major driver of microbial and metabolomic differences, with reductions in α diversity and widespread changes in cecal metabolites seen in high-fat diet (HFD)-fed mice.

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  • - 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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  • 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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  • The link between infectious diseases and allergies is still not well understood.
  • Agaronyan et al. (2022) research reveals that the bacteria Pseudomonas aeruginosa can alter the immune system, leading to an increase in type 2 immune responses.
  • This immune shift may change how the body reacts to harmless substances, triggering allergic reactions.
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