Role of M cells in initial antigen uptake and in ulcer formation in the rabbit intestinal loop model of shigellosis

Wassef, J S; Keren, David F.; Mailloux, J L

doi:10.1128/iai.57.3.858-863.1989

Cited by 251 publications

(99 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Shigella cause bacillary dysentery in humans by infecting the colonic mucosal barrier via M cell entry (Wassef et al ., 1989;Sansonetti et al ., 1996). After crossing the M cells, the pathogen infects the resident macrophages and induces cell death (Zychlinsky et al ., 1992).…”

Section: Introductionmentioning

confidence: 99%

IcsB, secreted via the type III secretion system, is chaperoned by IpgA and required at the post‐invasion stage of Shigella pathogenicity

Ogawa

Suzuki

Tatsuno

et al. 2003

Molecular Microbiology

View full text Add to dashboard Cite

SummaryShigella deliver a subset of effector proteins such as IpaA, IpaB and IpaC via the type III secretion system (TTSS) into host cells during the infection of colonic epithelial cells. Many bacterial effectors including some from Shigella require specific chaperones for protection from degradation and targeting to the TTSS. In this study, we have investigated the role of the icsB gene located upstream of the ipaBCDA operon in Shigella infection because the role of IcsB as a virulence factor remains unknown. Here, we found that the IcsB protein is secreted via the TTSS of Shigella in vitro and in vivo . We show that IpgA protein encoded by ipgA , the gene immediately downstream of icsB , serves as the chaperone required for the stabilization and secretion of IcsB. We have shown that IcsB binds to IpgA in bacterial cytosol and the binding site is in the middle of the IcsB protein. Intriguingly, although its significance in Shigella pathogenicity is as yet unclear, the icsB gene can be read-through into the ipgA gene to create a translational fusion protein. Furthermore, the contribution of IcsB to the pathogenicity of Shigella was demonstrated by plaque-forming assay and the Sereny test. The ability of the icsB mutant to form plaques was greatly reduced compared with that of the wild type in MDCK cell monolayers. Furthermore, when guinea pig eyes were infected with a non-polar icsB mutant, the bacteria failed to provoke keratoconjunctivitis. These results suggest that IcsB is secreted via the TTSS, chaperoned by IpgA, and required at the postinvasion stage of Shigella pathogenicity

show abstract

Section: Introductionmentioning

confidence: 99%

IcsB, secreted via the type III secretion system, is chaperoned by IpgA and required at the post‐invasion stage of Shigella pathogenicity

Ogawa

Suzuki

Tatsuno

et al. 2003

Molecular Microbiology

View full text Add to dashboard Cite

show abstract

“…Shigella traverse the intestinal wall through specialized M cells (Philpott et al, 2000;Wassef et al, 1989). Transmigrated bacteria then enter epithelial layer through the basolateral side (Philpott et al, 2000).…”

Section: Shigella Flexnerimentioning

confidence: 99%

The route less taken: pulmonary models of enteric Gram-negative infection

2013

View full text Add to dashboard Cite

Many pathogens are capable of causing a fulminant infection in pulmonary tissues of mammals. Animal models have provided an extensive understanding of the genetic and molecular mechanisms of bacterial pathogenesis as well as host immune response in the lungs. Many clinically relevant Gram-negative bacteria are host restricted. Thus, the powerfully informative tools of mouse models are not available for study with these organisms. However, over the past 30 years, enterprising work has demonstrated the utility of pulmonary infection with enteric pathogens. Such infection models have increased our understanding host-pathogen interactions in these organisms. Here we provide a review and comparison of lung models of infection with enteric Gram-negative bacteria relative to naturally occurring lung pathogens.

show abstract

“…The transcytotic properties of M cells are exploited as a route for invasion of the impermeable epithelial lining by a number of pathogens, including S. flexneri ( Fig. 1) [15].…”

Section: Crossing the Colonic Epithelial Layermentioning

confidence: 99%

Shigella flexneriinfection: pathogenesis and vaccine development

2004

View full text Add to dashboard Cite

Shigella flexneri is a gram-negative bacterium which causes the most communicable of bacterial dysenteries, shigellosis. Shigellosis causes 1.1 million deaths and over 164 million cases each year, with the majority of cases occurring in the children of developing nations. The pathogenesis of S. flexneri is based on the bacteria's ability to invade and replicate within the colonic epithelium, which results in severe inflammation and epithelial destruction. The molecular mechanisms used by S. flexneri to cross the epithelial barrier, evade the host's immune response and enter epithelial cells have been studied extensively in both in vitro and in vivo models. Consequently, numerous virulence factors essential to bacterial invasion, intercellular spread and the induction of inflammation have been identified in S. flexneri. The inflammation produced by the host has been implicated in both the destruction of the colonic epithelium and in controlling and containing the Shigella infection. The host's humoral response to S. flexneri also appears to be important in protecting the host, whilst the role of the cellular immune response remains unclear. The host's immune response to shigellosis is serotype-specific and protective against reinfection by the same serotype, making vaccination a possibility. Since the 1940s vaccines for S. flexneri have been developed with little success, however, the growing understanding of S. flexneri's pathogenesis and the host's immune response is assisting in the generation of more refined vaccine strategies. Current research encompasses a variety of vaccine types, which despite disparity in their efficacy and safety in humans represent promising progress in S. flexneri vaccine development.

show abstract

Role of M cells in initial antigen uptake and in ulcer formation in the rabbit intestinal loop model of shigellosis

Cited by 251 publications

References 22 publications

IcsB, secreted via the type III secretion system, is chaperoned by IpgA and required at the post‐invasion stage of Shigella pathogenicity

IcsB, secreted via the type III secretion system, is chaperoned by IpgA and required at the post‐invasion stage of Shigella pathogenicity

The route less taken: pulmonary models of enteric Gram-negative infection

Shigella flexneriinfection: pathogenesis and vaccine development

Contact Info

Product

Resources

About