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Pathogens
Special Issues
Unraveling Chlamydial Pathogenesis
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Unraveling Chlamydial Pathogenesis

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Bacterial Pathogens".

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 11676

Special Issue Editors

Dr. Karthika Rajeeve

E-Mail Website
Guest Editor
1. Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark
2. Rajiv Gandhi Centre for Biotechnology, Kerala 695585, India
Interests: study the pathogenesis of chlamydia infections; as an obligate intracellular parasite, chlamydia metabolically reprograms host cells to deplete the tumor suppressor TP53, predisposing them to a tumor-micro environment; the infection–cancer interface and investigates how the pathogen evades the immune system
Dr. Cindrilla Chumduri

E-Mail Website
Guest Editor
Biocenter, University Wurzburg, 97070 Wurzburg, Germany
Interests: epithelial transition zone; human papillomavirus; HPV; Chlamydia infections; pathogenesis

Special Issue Information

Dear Colleagues,

Chlamydiae are evolutionarily adapted to an obligate intracellular lifestyle with a small genome of 1Mb. They invade the host cell and replicate in the host-derived intracellular vacuole. The phylum Chlamydiae have diverged into different species that have a wide range of hosts from mouse to human and a broad range of tissue tropism from the eyes to the genital tract. As a pathogen, this bacterium contributes to different disease pathologies: trachoma, pneumonia, pelvic inflammatory disease leading to scarring, and infertility. Moreover, the spontaneous development of inflammatory diseases like reactive arthritis (RA) has been observed after chlamydia infection. Chlamydia is also claimed as the etiological agent in the development of coronary artery disease and atherosclerosis. Most recently, persistent infection has also been related to the development of ovarian cancer.

In this Special Issue on chlamydial pathogenesis, we intend to cover a range of topics under the various pathogenicity mechanisms of Chlamydia: How the pathogen drives immunomodulation and remain undetected, how the bacteria contribute to different disease pathologies and how persistent infection might lead to malignancy in the infected tissue.

Dr. Karthika Rajeeve
Dr. Cindrilla Chumduri
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Chlamydial
  • Chlamydia
  • Pathogen
  • Infection
  • Pathogenesis
  • Pathogenicity mechanisms
  • Trachoma
  • Pneumonia
  • Infertility
  • Ovarian cancer
  • Coronary artery disease
  • Atherosclerosis

Published Papers (4 papers)

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Research

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21 pages, 7153 KiB  
Article
Host–Pathogen Interactions of Chlamydia trachomatis in Porcine Oviduct Epithelial Cells
by Amanda F. Amaral, Bryan E. McQueen, Kimberly Bellingham-Johnstun, Taylor B. Poston, Toni Darville, Uma M. Nagarajan, Caroline Laplante and Tobias Käser
Pathogens 2021, 10(10), 1270; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10101270 - 1 Oct 2021
Cited by 1 | Viewed by 2241
Abstract
Chlamydia trachomatis (Ct) causes the most prevalent bacterial sexually transmitted disease leading to ectopic pregnancy and infertility. Swine not only have many similarities to humans, but they are also susceptible to Ct. Despite these benefits and the ease of access [...] Read more.
Chlamydia trachomatis (Ct) causes the most prevalent bacterial sexually transmitted disease leading to ectopic pregnancy and infertility. Swine not only have many similarities to humans, but they are also susceptible to Ct. Despite these benefits and the ease of access to primary tissue from this food animal, in vitro research in swine has been underutilized. This study will provide basic understanding of the Ct host–pathogen interactions in porcine oviduct epithelial cells (pOECs)—the counterparts of human Fallopian tube epithelial cells. Using NanoString technology, flow cytometry, and confocal and transmission-electron microscopy, we studied the Ct developmental cycle in pOECs, the cellular immune response, and the expression and location of the tight junction protein claudin-4. We show that Ct productively completes its developmental cycle in pOECs and induces an immune response to Ct similar to human cells: Ct mainly induced the upregulation of interferon regulated genes and T-cell attracting chemokines. Furthermore, Ct infection induced an accumulation of claudin-4 in the Ct inclusion with a coinciding reduction of membrane-bound claudin-4. Downstream effects of the reduced membrane-bound claudin-4 expression could potentially include a reduction in tight-junction expression, impaired epithelial barrier function as well as increased susceptibility to co-infections. Thereby, this study justifies the investigation of the effect of Ct on tight junctions and the mucosal epithelial barrier function. Taken together, this study demonstrates that primary pOECs represent an excellent in vitro model for research into Ct pathogenesis, cell biology and immunity. Full article
(This article belongs to the Special Issue Unraveling Chlamydial Pathogenesis)
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10 pages, 2346 KiB  
Article
MiR-378b Modulates Chlamydia-Induced Upper Genital Tract Pathology
by Stephanie R. Lundy, Kobe Abney, Debra Ellerson, Joseph U. Igietseme, Darin Carroll, Francis O. Eko and Yusuf O. Omosun
Pathogens 2021, 10(5), 566; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10050566 - 7 May 2021
Cited by 5 | Viewed by 2283
Abstract
Genital Chlamydia trachomatis infection causes severe reproductive pathologies such as salpingitis and pelvic inflammatory disease that can lead to tubal factor infertility. MicroRNAs (miRNAs) are evolutionarily conserved regulators of mammalian gene expression in development, immunity and pathophysiologic processes during inflammation and infection, including [...] Read more.
Genital Chlamydia trachomatis infection causes severe reproductive pathologies such as salpingitis and pelvic inflammatory disease that can lead to tubal factor infertility. MicroRNAs (miRNAs) are evolutionarily conserved regulators of mammalian gene expression in development, immunity and pathophysiologic processes during inflammation and infection, including Chlamydia infection. Among the miRNAs involved in regulating host responses and pathologic outcome of Chlamydia infection, we have shown that miR-378b was significantly differentially expressed during primary infection and reinfection. In this study, we tested the hypothesis that miR-378b is involved in the pathological outcome of Chlamydia infection. We developed miR-378b knockout mice (miR-378b−/−) using Crispr/Cas and infected them along with their wild-type (WT) control with Chlamydia to compare the infectivity and reproductive pathologies. The results showed that miR-378b−/− mice were unable to clear the infection compared to WT mice; also, miR-378b−/− mice exhibited a relatively higher Chlamydia burden throughout the duration of infection. However, gross pathology results showed that miR-378b−/− mice had significantly reduced uterine dilatations and pathologic lesions after two infections compared to WT mice. In addition, the pregnancy and fertility rates for infected miR-378b−/− mice showed protection from Chlamydia-induced infertility with fertility rate that was comparable to uninfected WT mice. These results are intriguing as they suggest that miR-378b is important in regulating host immune responses that control Chlamydial replication and drive the inflammation that causes complications such as infertility. The finding has important implications for biomarkers of Chlamydial complications and targets for prevention of disease. Full article
(This article belongs to the Special Issue Unraveling Chlamydial Pathogenesis)
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Review

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19 pages, 2634 KiB  
Review
Bacteria–Cancer Interface: Awaiting the Perfect Storm
by Jonathan Pommer Hansen, Waled Mohammed Ali, Rajeeve Sivadasan and Karthika Rajeeve
Pathogens 2021, 10(10), 1321; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10101321 - 14 Oct 2021
Cited by 5 | Viewed by 2899
Abstract
Epidemiological evidence reveal a very close association of malignancies with chronic inflammation as a result of persistent bacterial infection. Recently, more studies have provided experimental evidence for an etiological role of bacterial factors disposing infected tissue towards carcinoma. When healthy cells accumulate genomic [...] Read more.
Epidemiological evidence reveal a very close association of malignancies with chronic inflammation as a result of persistent bacterial infection. Recently, more studies have provided experimental evidence for an etiological role of bacterial factors disposing infected tissue towards carcinoma. When healthy cells accumulate genomic insults resulting in DNA damage, they may sustain proliferative signalling, resist apoptotic signals, evade growth suppressors, enable replicative immortality, and induce angiogenesis, thus boosting active invasion and metastasis. Moreover, these cells must be able to deregulate cellular energetics and have the ability to evade immune destruction. How bacterial infection leads to mutations and enriches a tumour-promoting inflammatory response or micro-environment is still not clear. In this review we showcase well-studied bacteria and their virulence factors that are tightly associated with carcinoma and the various mechanisms and pathways that could have carcinogenic properties. Full article
(This article belongs to the Special Issue Unraveling Chlamydial Pathogenesis)
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13 pages, 793 KiB  
Review
Hijacking and Use of Host Kinases by Chlamydiae
by Prakash Sah and Erika I. Lutter
Pathogens 2020, 9(12), 1034; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens9121034 - 10 Dec 2020
Cited by 5 | Viewed by 3157
Abstract
Chlamydia species are causative agents of sexually transmitted infections, blinding trachoma, and animal infections with zoonotic potential. Being an obligate intracellular pathogen, Chlamydia relies on the host cell for its survival and development, subverting various host cell processes throughout the infection cycle. A [...] Read more.
Chlamydia species are causative agents of sexually transmitted infections, blinding trachoma, and animal infections with zoonotic potential. Being an obligate intracellular pathogen, Chlamydia relies on the host cell for its survival and development, subverting various host cell processes throughout the infection cycle. A key subset of host proteins utilized by Chlamydia include an assortment of host kinase signaling networks which are vital for many chlamydial processes including entry, nutrient acquisition, and suppression of host cell apoptosis. In this review, we summarize the recent advancements in our understanding of host kinase subversion by Chlamydia. Full article
(This article belongs to the Special Issue Unraveling Chlamydial Pathogenesis)
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