CD44 binds to the Shigella IpaB protein and participates in bacterial invasion of epithelial cells

Skoudy, Anouchka; Mounier, Joëlle; Aruffo, Alejandro; Ohayon, Hélène; Gounon, Pierre; Sansonetti, Philippe J.; Nhieu, Guy Tran Van

doi:10.1046/j.1462-5822.2000.00028.x

Cited by 128 publications

(119 citation statements)

References 48 publications

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“…the CD14 receptor for bacterial LPS on monocytes and the CD21 activation regulator on B cells; 16). Bromelain also removes cell surface receptors that can serve as receptors for intestinal bacteria (16,(37)(38)(39)(40)(41), which may decrease exposure of immune cells to bacterial antigens that stimulate detrimental immune responses in IBD. Proteolysis by bromelain may also affect production of pro-inflammatory cytokines and chemokines by altering concentrations of regulatory cytokines such as IL-10 or TGF-β that was not analyzed in the current study.…”

Section: Discussionmentioning

confidence: 99%

Bromelain treatment decreases secretion of pro-inflammatory cytokines and chemokines by colon biopsies in vitro

Onken

Greer

Calingaert

et al. 2008

Clinical Immunology

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Oral bromelain has been anecdotally reported to decrease inflammation in ulcerative colitis (UC). Proteolytically active bromelain is known to decrease expression of mRNAs encoding proinflammatory cytokines by human leukocytes in vitro. To assess the effect of bromelain on mucosal secretion of cytokines in inflammatory bowel disease (IBD), endoscopic colon biopsies from patients with UC, Crohn's disease (CD), and non-IBD controls were treated in vitro with bromelain or media, then cultured. Secretion of pro-inflammatory cytokines and chemokines was measured. Significant increases in granulocyte colony stimulating factor (G-CSF), interferon (IFN)-γ, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF) were detected in the media from actively inflamed areas in UC and CD as compared with non-inflamed IBD tissue and non-IBD controls. In vitro bromelain treatment decreased secretion of G-CSF, granulocyte-macrophage colony stimulating factor (GM-CSF), IFN-γ, CCL4/macrophage inhibitory protein (MIP)-1β, and TNF by inflamed tissue in IBD. Bromelain may be a novel therapy for IBD.

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Section: Discussionmentioning

confidence: 99%

Bromelain treatment decreases secretion of pro-inflammatory cytokines and chemokines by colon biopsies in vitro

Onken

Greer

Calingaert

et al. 2008

Clinical Immunology

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“…Sic also colocalized with ezrin inside human PMNs, strongly suggesting intracellular interaction of the two proteins. Little is known about the role of ERM family members in bacterial internalization by host cells; however, ezrin has been shown to be involved in the uptake of Shigella flexneri by epithelial cells (29). Although the exact molecular mechanism is not yet understood, Sic apparently represents the first GAS antiphagocytic effector molecule to act in the interior of host cells.…”

Section: Discussionmentioning

confidence: 99%

Insight into the molecular basis of pathogen abundance: Group AStreptococcusinhibitor of complement inhibits bacterial adherence and internalization into human cells

Hoe

Ireland

DeLeo

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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Streptococcal inhibitor of complement (Sic) is a secreted protein made predominantly by serotype M1 Group A Streptococcus (GAS), which contributes to persistence in the mammalian upper respiratory tract and epidemics of human disease. Unexpectedly, an isogenic sic-negative mutant adhered to human epithelial cells significantly better than the wild-type parental strain. Purified Sic inhibited the adherence of a sic negative serotype M1 mutant and of non-Sic-producing GAS strains to human epithelial cells. Sic was rapidly internalized by human epithelial cells, inducing cell flattening and loss of microvilli. Ezrin and moesin, human proteins that functionally link the cytoskeleton to the plasma membrane, were identified as Sic-binding proteins by affinity chromatography and matrix-assisted laser desorption͞ionization time-of-flight mass spectrometry analysis. Sic colocalized with ezrin inside epithelial cells and bound to the F-actin-binding site region located in the carboxyl terminus of ezrin and moesin. Synthetic peptides corresponding to two regions of Sic had GAS adherence-inhibitory activity equivalent to mature Sic and inhibited binding of Sic to ezrin. In addition, the sic mutant was phagocytosed and killed by human polymorphonuclear leukocytes significantly better than the wild-type strain, and Sic colocalized with ezrin in discrete regions of polymorphonuclear leukocytes. The data suggest that binding of Sic to ezrin alters cellular processes critical for efficient GAS contact, internalization, and killing. Sic enhances bacterial survival by enabling the pathogen to avoid the intracellular environment. This process contributes to the abundance of M1 GAS in human infections and their ability to cause epidemics. microbiology ͉ Serotype M1 ͉ epidemic waves ͉ ezrin F or most bacterial pathogens, there is relatively little understanding of why certain clonally related isolates cause abundant infections, whereas others do not. Molecular explanation of these phenomena is critical to development of rational methods to limit pathogen emergence, resurgence, and dissemination.Group A Streptococcus (GAS) is an important human pathogen that causes infections ranging from pharyngitis to necrotizing fasciitis and the postinfectious sequelae acute rheumatic fever and acute glomerulonephritis. GAS are genetically highly heterogeneous. For example, more than 150 distinct M-types have been identified on the basis of antigenic differences in the M protein, an antiphagocytic surface molecule that is an important virulence factor (1). However, GAS expressing relatively few M types cause the majority of human invasive infections. In particular, M1 strains are the most common serotype recovered from invasive disease episodes and also have a propensity to cause epidemics (2).Streptococcal inhibitor of complement (Sic) is a secreted protein produced by serotype M1 GAS that inhibits the formation of the membrane attack complex (MAC) of complement in vitro by binding to the C5b-C7 complex (3, 4). Sic production is necessary for per...

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“…En éstos la proteína IpaB, lisa la vacuola en el citoplasma e induce apoptosis vía caspasa 1 para finalmente ser liberada y alcanzar el polo basolateral [107][108][109][110] . secreción tipo VI 92 .…”

Section: Escherichia Coli Enteroagregativaunclassified

Mecanismos de virulencia de Escherichia coli enteropatógena

Farfán-García¹,

Ariza-Rojas²,

Vargas-Cárdenas³

et al. 2016

Rev. chil. infectol.

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CD44 binds to the Shigella IpaB protein and participates in bacterial invasion of epithelial cells

Cited by 128 publications

References 48 publications

Bromelain treatment decreases secretion of pro-inflammatory cytokines and chemokines by colon biopsies in vitro

Bromelain treatment decreases secretion of pro-inflammatory cytokines and chemokines by colon biopsies in vitro

Insight into the molecular basis of pathogen abundance: Group AStreptococcusinhibitor of complement inhibits bacterial adherence and internalization into human cells

Mecanismos de virulencia de Escherichia coli enteropatógena

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