Degradation of<i>Chlamydia pneumoniae</i>by Peripheral Blood Monocytic Cells

Wolf, Katerina; Fischer, Elizabeth R.; Hackstadt, Ted

doi:10.1128/iai.73.8.4560-4570.2005

Cited by 34 publications

(35 citation statements)

References 55 publications

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“…For instance, C. pneumoniae was recovered in HEp-2 cells from CD14 ϩ cells from patients with coronary artery disease who had been treated with azithromycin (16). On the other hand, C. pneumoniae was eradicated from human alveolar Ms shortly after in vitro infection (46). Lastly, Ms allow the survival and modest replication of lymphogranuloma venereum strains of C. trachomatis (26,48).…”

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confidence: 99%

Survival ofChlamydia muridarumwithin Dendritic Cells

et al. 2007

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Immune responses to Chlamydia trachomatis underlay both immunity and immunopathology. Immunopathology in turn has been attributed to chronic persistent infection with persistence being defined as the presence of organisms in the absence of replication. We hypothesized that dendritic cells (DCs) play a central role in Chlamydia immunity and immunopathology by favoring the long-term survival of C. muridarum. This hypothesis was examined based on (i) direct staining of Chlamydia in infected DCs to evaluate the development of inclusions, (ii) titration of infected DCs on HeLa cells to determine cultivability, and (iii) transfer of Chlamydia-infected DCs to naive mice to evaluate infectivity. The results show that Chlamydia survived within DCs and developed both typical and atypical inclusions that persisted in a subpopulation of DCs for more than 9 days after infection. Since the cultivability of Chlamydia from DCs onto HeLa was lower than that estimated by the number of inclusions in DCs, this suggests that the organisms may be in state of persistence. Intranasal transfer of long-term infected DCs or DCs purified from the lungs of infected mice caused mouse lung infection, suggesting that in addition to persistent forms, infective Chlamydia organisms also developed within chronically infected DCs. Interestingly, after in vitro infection with Chlamydia, most DCs died. However, Chlamydia appeared to survive in a subpopulation of DCs that resisted infection-induced cell death. Surviving DCs efficiently presented Chlamydia antigens to Chlamydia-specific CD4 ؉ T cells, suggesting that the bacteria are able to both direct their own survival and still allow DC antigen-presenting function. Together, these results raise the possibility that Chlamydia-infected DCs may be central to the maintenance of T-cell memory that underlies both immunity and immunopathology.

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Survival ofChlamydia muridarumwithin Dendritic Cells

et al. 2007

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“…Multiple reports have documented the ability of professional phagocytes to directly kill intracellular chlamydiae (12,14,18). Given the constitutive expression of Mpeg1/perforin-2 in macrophages (15) and the role of perforin-2 in limiting intracellular bacterial replication (17), we questioned whether perforin-2 might contribute to the limitation of chlamydial growth in macrophages.…”

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Perforin-2 Restricts Growth of Chlamydia trachomatis in Macrophages

et al. 2013

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Chlamydia trachomatis is a Gram-negative obligate intracellular bacterium that preferentially infects epithelial cells. Professional phagocytes provide C. trachomatis only a limited ability to survive and are proficient killers of chlamydiae. We present evidence herein that identifies a novel host defense protein, perforin-2, that plays a significant role in the eradication of C. trachomatis during the infection of macrophages. Knockdown of perforin-2 in macrophages did not alter the invasion of host cells but did result in chlamydial growth that closely mirrored that detected in HeLa cells. C trachomatis L2, serovar B, and serovar D and C. muridarum were all equally susceptible to perforin-2-mediated killing. Interestingly, induction of perforin-2 expression in epithelial cells is blocked during productive chlamydial growth, thereby protecting chlamydiae from bactericidal attack. Ectopic expression of perforin-2 in HeLa cells, however, does result in killing. Overall, our data implicate a new innate resistance protein in the control of chlamydial infection and may help explain why the macrophage environment is hostile to chlamydial growth.

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“…It is commonly accepted, based on studies first with Chlamydia psittaci (17,18), an avian pathogen that accidentally infects humans, and later with other species, including human pathogens C. trachomatis (26,38,39,42) and C. pneumoniae (3), that in epithelial cells, the primary target of chlamydiae, and also in fibroblasts, the chlamydial inclusion does not fuse with the lysosome, although invading EBs are degraded mostly in the lysosomes of blood monocytes and in neutrophils (44)(45)(46). In contrast to chlamydiae, a large number of other pathogens are taken into the lysosome and readily degraded by lysosomal enzymes in both phagocytes and nonprofessional phagocytes, including epithelial cells (29).…”

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Regulation of Chlamydial Infection by Host Autophagy and Vacuolar ATPase-Bearing Organelles

Yasir¹,

Pachikara

Bao³

et al. 2011

Infect Immun

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As arguably the most successful parasite, Chlamydia is an obligate intracellular bacterium replicating inside a vacuole of eukaryotic host cells. The chlamydial vacuole does not fuse with the defense cell organelle lysosome. We previously showed that chlamydial infection increases markers of autophagy, an innate antimicrobial activity requiring lysosomal function. However, the work presented here demonstrates that p62, an autophagy protein that is degraded in lysosomes, either remained unchanged or increased in chlamydiainfected human epithelial, mouse fibroblast, and mouse macrophage cell lines. In addition, the activities of three lysosomal enzymes analyzed were diminished in chlamydia-infected macrophages. Bafilomycin A1 (BafA), a specific inhibitor of vacuolar ATPase (vATPase) required for lysosomal function, increased the growth of the human pathogen Chlamydia trachomatis (L2) in wild-type murine fibroblasts and macrophages but inhibited growth in the autophagy-deficient ATG5 ؊/؊ fibroblasts. BafA exhibited only slight inhibition or no effect on L2 growth in multiple human genital epithelial cell lines. In contrast to L2, the mouse pathogen Chlamydia muridarum (MoPn) was consistently inhibited by BafA in all cell lines examined, regardless of species origin and autophagy status. Finally, L2 but not MoPn grew more efficiently in the ATG5؊/؊ cells than in wild-type cells. These results suggest that there are two types of vATPase-bearing organelles that regulate chlamydial infection: one supports chlamydial infection, while the other plays a defensive role through autophagy when cells are artificially infected with certain chlamydiae that have not been adapted to the host species.

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Degradation ofChlamydia pneumoniaeby Peripheral Blood Monocytic Cells

Cited by 34 publications

References 55 publications

Survival ofChlamydia muridarumwithin Dendritic Cells

Survival ofChlamydia muridarumwithin Dendritic Cells

Perforin-2 Restricts Growth of Chlamydia trachomatis in Macrophages

Regulation of Chlamydial Infection by Host Autophagy and Vacuolar ATPase-Bearing Organelles

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