The<i>Chlamydia trachomatis</i>Ctad1 invasin exploits the human integrin β1 receptor for host cell entry

Stallmann, Sonja; Hegemann, Johannes H.

doi:10.1111/cmi.12549

Cited by 48 publications

(48 citation statements)

References 58 publications

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“…The level and position of sulfation in HSPGs have important roles in the binding of C. muridarum and C. trachomatis L2 (REFS 17,28,29) and may contribute to tissue tropism. Other adhesins include lipopolysaccharide (LPS) in C. trachomatis , which is proposed to bind to the cystic fibrosis transmembrane conductance regulator 17,30 , major outer membrane protein (MOMP; also known as CT681), which binds to the mannose receptor and the mannose 6-phosphate receptor 18 , and CT017 (also known as Ctad1) in C. trachomatis , which binds to β1 integrin 31 . The polymorphic membrane protein (Pmp) family in C. trachomatis and C. pneumoniae also mediates adhesion 32 .…”

Section: Binding and Invasionmentioning

confidence: 99%

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Chlamydia cell biology and pathogenesis

2016

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Chlamydia spp. are important causes of human disease for which no effective vaccine exists. These obligate intracellular pathogens replicate in a specialized membrane compartment and use a large arsenal of secreted effectors to survive in the hostile intracellular environment of the host. In this Review, we summarize the progress in decoding the interactions between Chlamydia spp. and their hosts that has been made possible by recent technological advances in chlamydial proteomics and genetics. The field is now poised to decipher the molecular mechanisms that underlie the intimate interactions between Chlamydia spp. and their hosts, which will open up many exciting avenues of research for these medically important pathogens.

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Section: Binding and Invasionmentioning

confidence: 99%

“…In addition to the β1 integrin subunit 31 and EGFR 33 , receptor tyrosine kinases (RTKs) contribute to binding, invasion and signalling during entry. C. trachomatis and C. muridarum interact with the fibroblast growth factor receptor (FGFR) and its ligand FGF as well as platelet derived growth factor receptor (PDGFR) 34,35 .…”

Section: Binding and Invasionmentioning

confidence: 99%

Chlamydia cell biology and pathogenesis

2016

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“…Much of our current understanding of the roles that specific chlamydial effectors and their interactive host partners play in these processes is derived from cell systems 58596061 and animal models 6263. Candidate receptors that promote chlamydial attachment to susceptible cells have been identified 646566. Not unsurprisingly for a microorganism that interacts with its host cell across the plasma membrane at attachment and entry and with the inclusion membrane during the remainder of the developmental cycle, secretion systems represent a significant portion of the chlamydial genome.…”

Section: Chlamydia Trachomatis - Genital Tract Pathogenmentioning

confidence: 99%

Chlamydia trachomatis Genital Infections

O’Connell¹,

Ferone²

2016

MIC

174

153

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Etiology, transmission and protection: Chlamydia trachomatis is the leading cause of bacterial sexually transmitted infection (STI) globally. However, C. trachomatis also causes trachoma in endemic areas, mostly Africa and the Middle East, and is a leading cause of preventable blindness worldwide. Epidemiology, incidence and prevalence: The World Health Organization estimates 131 million new cases of C. trachomatis genital infection occur annually. Globally, infection is most prevalent in young women and men (14-25 years), likely driven by asymptomatic infection, inadequate partner treatment and delayed development of protective immunity. Pathology/Symptomatology: C. trachomatis infects susceptible squamocolumnar or transitional epithelial cells, leading to cervicitis in women and urethritis in men. Symptoms are often mild or absent but ascending infection in some women may lead to Pelvic Inflammatory Disease (PID), resulting in reproductive sequelae such as ectopic pregnancy, infertility and chronic pelvic pain. Complications of infection in men include epididymitis and reactive arthritis. Molecular mechanisms of infection: Chlamydiae manipulate an array of host processes to support their obligate intracellular developmental cycle. This leads to activation of signaling pathways resulting in disproportionate influx of innate cells and the release of tissue damaging proteins and pro-inflammatory cytokines. Treatment and curability: Uncomplicated urogenital infection is treated with azithromycin (1 g, single dose) or doxycycline (100 mg twice daily x 7 days). However, antimicrobial treatment does not ameliorate established disease. Drug resistance is rare but treatment failures have been described. Development of an effective vaccine that protects against upper tract disease or that limits transmission remains an important goal.

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“…Recent studies have shown that two C. pneumoniae proteins, adhesin CPn0473 and invasin Pmp21, bind to host epidermal growth factor receptor (EGFR) and trigger lipid raft-mediated uptake (Mölleken et al, 2013; Fechtner et al, 2016). C. trachomatis also adhered to the lipid raft protein EphrinA2 receptor (EphA2) (Chakraborty et al, 2012; Subbarayal et al, 2015), and the C. trachomatis invasin protein Ctad1 bound to β1 integrin in lipid rafts during internalization (Stallmann and Hegemann, 2016). Targeting multiple host cell lipid raft receptors may broaden host cell tropism and increase the potential for successful host cell colonization.…”

Section: Role Of Cholesterol In Bacterial Entry and Exitmentioning

confidence: 99%

Manipulation of Host Cholesterol by Obligate Intracellular Bacteria

Samanta

Mulye

Clemente

et al. 2017

Front. Cell. Infect. Microbiol.

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Cholesterol is a multifunctional lipid that plays important metabolic and structural roles in the eukaryotic cell. Despite having diverse lifestyles, the obligate intracellular bacterial pathogens Chlamydia, Coxiella, Anaplasma, Ehrlichia, and Rickettsia all target cholesterol during host cell colonization as a potential source of membrane, as well as a means to manipulate host cell signaling and trafficking. To promote host cell entry, these pathogens utilize cholesterol-rich microdomains known as lipid rafts, which serve as organizational and functional platforms for host signaling pathways involved in phagocytosis. Once a pathogen gains entrance to the intracellular space, it can manipulate host cholesterol trafficking pathways to access nutrient-rich vesicles or acquire membrane components for the bacteria or bacteria-containing vacuole. To acquire cholesterol, these pathogens specifically target host cholesterol metabolism, uptake, efflux, and storage. In this review, we examine the strategies obligate intracellular bacterial pathogens employ to manipulate cholesterol during host cell colonization. Understanding how obligate intracellular pathogens target and use host cholesterol provides critical insight into the host-pathogen relationship.

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TheChlamydia trachomatisCtad1 invasin exploits the human integrin β1 receptor for host cell entry

Cited by 48 publications

References 58 publications

Chlamydia cell biology and pathogenesis

Chlamydia cell biology and pathogenesis

Chlamydia trachomatis Genital Infections

Manipulation of Host Cholesterol by Obligate Intracellular Bacteria

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