Early induction of antibacterial activities distinguishes response of mice to infection with non-permissive from response to permissive Salmonella release_bsaxqq64snahdlx62mu3dpl7lm

by Jitender Yadav, Ayub Qadri

Released as a post by Cold Spring Harbor Laboratory.



<jats:italic>Salmonella enterica</jats:italic> serovar Typhi (<jats:italic>S</jats:italic>. Typhi), the causative agent of typhoid in humans, shares very high homology with closely related serovar, <jats:italic>S</jats:italic>. Typhimurium. Yet, unlike <jats:italic>S</jats:italic>. Typhimurium, <jats:italic>S</jats:italic>. Typhi does not establish infection in mice. We show that intraperitoneal infection of mice with <jats:italic>S</jats:italic>. Typhi is associated with induction of antibacterial activities. Cell-free peritoneal fluids from <jats:italic>S</jats:italic>. Typhi but not <jats:italic>S</jats:italic>. Typhimurium-infected mice inhibited replication of <jats:italic>Salmonella ex vivo</jats:italic>. Administration of serine protease inhibitor, phenylmethylsulfonly fluoride (PMSF), during <jats:italic>S</jats:italic>. Typhi infection reduced production of this activity. <jats:italic>In vitro</jats:italic>, generation of this antibacterial activity from peritoneal macrophages infected with <jats:italic>S</jats:italic>. Typhi was inhibited with PMSF, and its release was dependent on cell death. Peritoneal cells infected with <jats:italic>S</jats:italic>. Typhi in vivo or in vitro showed increased mRNA levels of ferroportin and lipocalin. Our findings implicate early induction of antibacterial molecules in the failure of <jats:italic>S</jats:italic>. Typhi to establish infection in mice.
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