An article published this year in “Frontiers
in Cellular and Infection Microbiology” using our “Apoptosis Detection Kit FITC”, by our customers from France, Czechia, Spain,
Brazil and US, in the analysis of how Ixodes scapularis Tick Cells Control Anaplasma
phagocytophilum Infection by Increasing the Synthesis of
Phosphoenolpyruvate from Tyrosine. Congrats and Thanks.
Summay:
The obligate intracellular pathogen, Anaplasma
phagocytophilum, is the causative
agent of life-threatening diseases in humans and animals. A.
phagocytophilum is an
emerging tick-borne pathogen in the United States, Europe, Africa and Asia,
with increasing numbers of infected people and animals every year. It is
increasingly recognized that intracellular pathogens modify host cell metabolic
pathways to increase infection and transmission in both vertebrate and
invertebrate hosts. Recent reports have shown that amino acids are central to
the host–pathogen metabolic interaction. In this study, a genome-wide search
for components of amino acid metabolic pathways was performed in Ixodes
scapularis, the main tick
vector of A. phagocytophilum in the United States, for which the genome was recently
published. The enzymes involved in the synthesis and degradation pathways of
the twenty amino acids were identified. Then, the available transcriptomics and
proteomics data was used to characterize the mRNA and protein levels of I.
scapularis amino acid
metabolic pathway components in response to A. phagocytophilum infection of
tick tissues and ISE6 tick cells. Our analysis was focused on the interplay
between carbohydrate and amino acid metabolism during A.
phagocytophilum infection in
ISE6 cells. The results showed that tick cells increase the synthesis of
phosphoenolpyruvate (PEP) from tyrosine to control A.
phagocytophiluminfection.
Metabolic pathway analysis suggested that this is achieved by (i) increasing
the transcript and protein levels of mitochondrial phosphoenolpyruvate
carboxykinase (PEPCK-M), (ii) shunting tyrosine into the tricarboxylic acid
(TCA) cycle to increase fumarate and oxaloacetate which will be converted into
PEP by PEPCK-M, and (iii) blocking all the pathways that use PEP downstream
gluconeogenesis (i.e., de novo serine synthesis pathway (SSP), glyceroneogenesis and
gluconeogenesis). While sequestering host PEP may be critical for this
bacterium because it cannot actively carry out glycolysis to produce PEP,
excess of this metabolite may be toxic for A. phagocytophilum. The present work
provides a more comprehensive view of the major amino acid metabolic pathways
involved in the response to pathogen infection in ticks, and provides the basis
for further studies to develop novel strategies for the control of granulocytic
anaplasmosis.
Reference:
Product link:
Apoptosis Detection Kit FITC
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