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Attachment defect in mouse fibroblasts (L cells) persistently infected with Chlamydia psittaci
Abstract:
Almost all the cells in populations of mouse fibroblasts (L cells) persistently infected with the 6BC strain of Chlamydia psittaci were immune to superinfection with high multiplicities of C. psittaci, whether or not the L cells contained visible chlamydial inclusions. As ascertained by experiments with 14C-labeled C. psittaci, immunity to superinfection resulted from the failure of added chlamydiae to attach to persistently infected host cells. However, when exogenous C. psittaci was introduced into persistently infected L cells by centrifuging the inoculum onto host cell monolayers or by pretreating the monolayers with diethylaminoethyl-dextran, these chlamydiae produced expected numbers of infectious progeny. Persistently infected L cells were associated in an unknown way with a C. psittaci population that entered the host cells only with the aid of centrifugation or pretreatment with diethylaminoethyl-dextran. Inclusion-free, persistently infected L cells appeared to present at least two separate hindrances to chlamydial activity: blockage of the attachment of exogenous elementary bodies to persistently infected host cells and prevention of the initiation of chlamydial multiplication by means of a normal developmental cycle in the absence of added C. psittaci.
Insights
Persistently infected mouse fibroblasts resist Chlamydia psittaci superinfection due to attachment blockage. However, forced entry allows normal Chlamydia psittaci replication, indicating complex host-pathogen interactions.
Area of Science:
- Microbiology
- Cell Biology
- Infectious Diseases
Background:
- * Persistent infections with Chlamydia psittaci in mouse fibroblasts (L cells) establish a unique cellular environment.
- * Understanding host-pathogen interactions is crucial for developing effective antimicrobial strategies.
Purpose of the Study:
- * To investigate the mechanisms underlying resistance to superinfection in Chlamydia psittaci-infected L cells.
- * To determine if inclusion-free infected cells exhibit altered susceptibility to secondary Chlamydia psittaci challenge.
Main Methods:
- * Utilized 14C-labeled Chlamydia psittaci to track infection and attachment in persistently infected L cells.
- * Employed centrifugation and diethylaminoethyl-dextran treatment to facilitate exogenous Chlamydia psittaci entry.
- * Assessed Chlamydia psittaci replication and inclusion formation in treated and untreated infected cells.
Main Results:
- * Persistently infected L cells, regardless of visible inclusions, demonstrated immunity to superinfection by blocking Chlamydia psittaci attachment.
- * Forced entry via centrifugation or diethylaminoethyl-dextran enabled normal Chlamydia psittaci replication, yielding infectious progeny.
- * Inclusion-free infected cells presented two barriers: inhibited attachment and prevention of normal developmental cycle initiation.
Conclusions:
- * Persistent Chlamydia psittaci infection induces resistance to superinfection primarily by preventing pathogen attachment.
- * Alternative entry methods can overcome this resistance, leading to successful Chlamydia psittaci replication.
- * Inclusion-free infected cells exhibit multifaceted defense mechanisms against secondary Chlamydial infections.