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Formation and destruction of internal membranes in L cells infected with Chlamydia psittaci
Abstract:
L cells (mouse fibroblasts), uninfected and infected with Chlamydia psittaci (meningopneumonitis strain), were labeled with (14)C-amino acids, and their membranous organelles were separated by isopycnic equilibrium centrifugation of whole cell homogenates on discontinuous sucrose density gradients. Incorporation of labeled amino acids into host and parasitic proteins was differentiated on the basis of susceptibility to cycloheximide. Twenty hours after infection with C. psittaci, incorporation of newly synthesized proteins into the internal membranes of L cells was almost completely inhibited, and internal membranes made prior to infection were altered or destroyed. The unit membrane that at all times surrounds the cytoplasmic vacuole containing the multiplying chlamydiae was made by the host from membranes or membrane precursors present before infection. No proteins synthesized by C. psittaci became associated with host cell membranes. Destruction or modification of the internal membranes of the host cell may be an integral part of the chlamydial developmental cycle.
Insights
Chlamydia psittaci infection inhibits host cell protein synthesis and alters internal membranes. The bacterium forms a protective vacuole using host membrane precursors, without incorporating its own proteins into host membranes.
Area of Science:
- Cell Biology
- Microbiology
- Infectious Diseases
Background:
- Chlamydia psittaci is an obligate intracellular bacterium.
- Understanding host-pathogen interactions is crucial for developing treatments.
Purpose of the Study:
- To investigate the impact of Chlamydia psittaci infection on host cell membrane synthesis and structure.
- To determine if parasitic proteins integrate into host cell membranes.
Main Methods:
- Isopycnic equilibrium centrifugation of L cell homogenates.
- Labeling with 14C-amino acids to track protein synthesis.
- Differentiation of host and parasitic proteins using cycloheximide.
Main Results:
- C. psittaci infection significantly inhibited host internal membrane protein synthesis.
- Pre-existing host internal membranes were altered or destroyed post-infection.
- The membrane surrounding the chlamydial vacuole was host-derived.
- No C. psittaci proteins were found associated with host cell membranes.
Conclusions:
- Host cell membrane modification is likely integral to the Chlamydia psittaci developmental cycle.
- The bacterium utilizes host resources for vacuole formation without direct protein exchange with host membranes.