An insight into the ligand–receptor interactions involved in the translocation of pathogens across blood–brain barrier

Bencúrová, Elena; Mlynárčik, Patrik; Bhide, Mangesh

doi:10.1111/j.1574-695x.2011.00867.x

Cited by 27 publications

(18 citation statements)

References 206 publications

(217 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Pathogens utilising the paracellular mechanism break the TJ and AJ complexes and cross the epithelial barrier by passage between neighboring epithelial cells [12]. In contrast, some other pathogens specialised on the transcellular mechanism and invade epithelial or specialised M cells at the apical surface followed by intracellular trafficking and exit these cells at the basolateral membrane [81,82]. Studies on the translocation capabilities of C .…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Transmigration route of Campylobacter jejuni across polarized intestinal epithelial cells: paracellular, transcellular or both?

Backert

Boehm

Weßler

et al. 2013

Cell Communication and Signaling

108

100

View full text Add to dashboard Cite

Intact intercellular junctions and cellular matrix contacts are crucial structural components for the formation and maintenance of epithelial barrier functions in humans to control the commensal flora and protect against intruding microbes. Campylobacter jejuni is one of the most important zoonotic pathogens causing food-borne gastroenteritis and potentially more severe diseases such as reactive arthritis or Guillain–Barré syndrome. Crossing the intestinal epithelial barrier and host cell invasion by C. jejuni are considered to represent the primary reasons of gut tissue damage in humans and various animal model systems including monkeys, piglets, rabbits, hamsters and ferrets. C. jejuni is also able to invade underlying tissues such as the lamina propria, can enter the bloodstream, and possibly reach distinct organs such as spleen, liver or mesenteric lymph nodes. However, the molecular mechanisms as well as major bacterial and host cell factors involved in these activities are poorly understood. Various models exist by which the pathogen can trigger its own transmigration across polarized intestinal epithelial cells in vitro, the paracellular and/or transcellular mechanism. Recent studies suggest that bacterial factors such as flagellum, serine protease HtrA and lipooligosaccharide LOS may play an active role in bacterial transmigration. Here we review our knowledge on transmigration of C. jejuni as well as some other Campylobacter species, and discuss the pros and cons for the route(s) taken to travel across polarized epithelial cell monolayers. These studies provide fresh insights into the infection strategies employed by this important pathogen.

show abstract

Section: Introductionmentioning

confidence: 99%

“…Different mechanisms are used by various enteropathogens to transmigrate across the host intestinal epithelium, including transcytosis through specialized M cells, phagocytosis by interepithelial leukocytes or transcytosis of enterocytes [35,81,82]. C .…”

Section: Introductionmentioning

confidence: 99%

Transmigration route of Campylobacter jejuni across polarized intestinal epithelial cells: paracellular, transcellular or both?

Backert

Boehm

Weßler

et al. 2013

Cell Communication and Signaling

108

100

View full text Add to dashboard Cite

show abstract

“…Recent reviews have been focused on bacterial invasion across the BBB, but also covered broader aspects by which various microbes spread to the nervous system 2 - 4 . In this review we will describe the mechanisms by which one extracellular parasite, Trypanosoma brucei ( T. b. )…”

Section: Introductionmentioning

confidence: 99%

Passage of parasites across the blood-brain barrier

Masocha

Kristensson

2012

Virulence

View full text Add to dashboard Cite

The blood-brain barrier (BBB) is a structural and functional barrier that protects the central nervous system (CNS) from invasion by blood-borne pathogens including parasites. However, some intracellular and extracellular parasites can traverse the BBB during the course of infection and cause neurological disturbances and/or damage which are at times fatal. The means by which parasites cross the BBB and how the immune system controls the parasites within the brain are still unclear. In this review we present the current understanding of the processes utilized by two human neuropathogenic parasites, Trypanosoma brucei spp and Toxoplasma gondii, to go across the BBB and consequences of CNS invasion. We also describe briefly other parasites that can invade the brain and how they interact with or circumvent the BBB. The roles played by parasite-derived and host-derived molecules during parasitic and white blood cell invasion of the brain are discussed.

show abstract

“…The most commonly utilised route is transcellular migration. This receptor-mediated process results in endocytosis of the pathogen by endothelial cells that line the blood vessels and is used by Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis (Bencurova, Mlynarcik, & Bhide, 2011;Kim, 2008;Orihuela et al, 2009;van Sorge & Doran, 2013). A second route is paracellular migration, which usually occurs when BBB integrity is disrupted by direct contact with the pathogen or as a result of secreted bacterial toxins.…”

mentioning

confidence: 99%

Mycobacteria employ two different mechanisms to cross the blood-brain barrier

Leeuwen

Boot

Kuijl

et al. 2018

Cellular Microbiology

View full text Add to dashboard Cite

Central nervous system (CNS) infection by Mycobacterium tuberculosis is one of the most devastating complications of tuberculosis, in particular in early childhood. In order to induce CNS infection, M. tuberculosis needs to cross specialised barriers protecting the brain. How M. tuberculosis crosses the blood–brain barrier (BBB) and enters the CNS is not well understood. Here, we use transparent zebrafish larvae and the closely related pathogen Mycobacterium marinum to answer this question. We show that in the early stages of development, mycobacteria rapidly infect brain tissue, either as free mycobacteria or within circulating macrophages. After the formation of a functionally intact BBB, the infiltration of brain tissue by infected macrophages is delayed, but not blocked, suggesting that crossing the BBB via phagocytic cells is one of the mechanisms used by mycobacteria to invade the CNS. Interestingly, depletion of phagocytic cells did not prevent M. marinum from infecting the brain tissue, indicating that free mycobacteria can independently cause brain infection. Detailed analysis showed that mycobacteria are able to cause vasculitis by extracellular outgrowth in the smaller blood vessels and by infecting endothelial cells. Importantly, we could show that this second mechanism is an active process that depends on an intact ESX‐1 secretion system, which extends the role of ESX‐1 secretion beyond the macrophage infection cycle.

show abstract

An insight into the ligand–receptor interactions involved in the translocation of pathogens across blood–brain barrier

Cited by 27 publications

References 206 publications

Transmigration route of Campylobacter jejuni across polarized intestinal epithelial cells: paracellular, transcellular or both?

Transmigration route of Campylobacter jejuni across polarized intestinal epithelial cells: paracellular, transcellular or both?

Passage of parasites across the blood-brain barrier

Mycobacteria employ two different mechanisms to cross the blood-brain barrier

Contact Info

Product

Resources

About