Bacterial components induce cytokine and intercellular adhesion molecules-1 and activate transcription factors in dermal fibroblasts

Perfetto, Brunella; Donnarumma, Giovanna; Criscuolo, Daniela; Paoletti, Iole; Grimaldi, Elena; Tufano, Maria Antonietta; Baroni, Adone

doi:10.1016/s0923-2508(03)00084-6

Cited by 40 publications

(33 citation statements)

References 34 publications

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“…It is possible that TLR signaling mediated by gonococcal PorB IB may also serve a key regulatory event in the urethral epithelium by modulating the activity of NF-B and subsequent expression of UEC antiapoptotic machinery. Of interest to us was the inability of gonococcal LOS to increase the expression of antiapoptotic genes, despite reports that lipopolysaccharide from gram-negative bacteria is a potent inducer of NF-B activity (7,34). There are several possibilities that may explain this observation.…”

Section: Discussionmentioning

confidence: 99%

“…NF-B activation is required for induced expression of the bfl-1, c-IAP-2, and cox-2 genes and represents a major survival and inflammatory signal in host cells (19,42,43,47). In addition, both gonococcal infection and neisserial porins have been identified to activate NF-B in other cell systems (27,33,34). Therefore, we looked at whether NF-B is activated in UECs that are infected with the gonococcus or treated with PorB IB.…”

Section: Nf-b Is Activated In Gonococcus-infected and Porb Ibtreated mentioning

confidence: 99%

“…Interestingly, infection with N. gonorrhoeae has been demonstrated to activate NF-B in some cell systems (33). Furthermore, bacterial porins have been identified as factors that can influence NF-B activity (34), and neisserial porins, specifically, have been shown to modulate the apoptotic response of host cells (26,28,30).…”

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confidence: 99%

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Gonococcal Porin IB Activates NF-κB in Human Urethral Epithelium and Increases the Expression of Host Antiapoptotic Factors

Binnicker

Williams

Apicella³

2004

Infect Immun

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Infection of human urethral epithelial cells (UECs) with Neisseria gonorrhoeae increases the transcription of several host antiapoptotic genes, including bfl-1, cox-2, and c-IAP-2. In order to identify the bacterial factor(s) responsible for eliciting these changes, the transcriptional status of apoptotic machinery was monitored in UECs challenged with certain gonococcal membrane components. Initially, we observed that infection of UECs with gentamicin-killed gonococci increased the expression of the antiapoptotic Bcl-2 family member, bfl-1. This observation indicated that viable, replicating bacteria are not required for induction of antiapoptotic gene expression. Confirming this observation, treatment of UECs with purified gonococcal membrane increased the expression of bfl-1, cox-2, and c-IAP-2. This finding suggested that a factor or multiple factors present in the outer membrane (OM) are responsible for altering UEC antiapoptotic gene expression. Interestingly, treatment of UECs with gonococcal porin IB (PorB IB), a major constituent of the OM, significantly increased the transcription of bfl-1, cox-2, and c-IAP-2. The upregulation of these genes by PorB IB was determined to be dependent on NF-B activation, as inhibiting NF-B blocked induced expression of these genes. This work demonstrates the altered expression of host apoptotic factors in response to gonococcal PorB IB and supports a model whereby UEC cell death may be modulated as a potential mechanism of bacterial survival and proliferation.

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Section: Discussionmentioning

confidence: 99%

Section: Nf-b Is Activated In Gonococcus-infected and Porb Ibtreated mentioning

confidence: 99%

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Gonococcal Porin IB Activates NF-κB in Human Urethral Epithelium and Increases the Expression of Host Antiapoptotic Factors

Binnicker

Williams

Apicella³

2004

Infect Immun

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“…Protein A, which is a major surface protein of S. aureus strains, is covalently anchored to the peptidoglycan and belongs to the cell wall-associated virulence factors of S. aureus. Purified protein A elicits release of IL-1␤, IL-4, IL-6, IL-8, and IFN-␥ and weak release of TNF-␣ from monocytes and fibroblasts (149,193). This virulence factor has also been shown to contribute to staphylococcal sepsis.…”

Section: Tnfr1mentioning

confidence: 99%

Recognition ofStaphylococcus aureusby the Innate Immune System

2005

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The gram-positive bacterium Staphylococcus aureus is a major pathogen responsible for a variety of diseases ranging from minor skin infections to life-threatening conditions such as sepsis. Cell wall-associated and secreted proteins (e.g., protein A, hemolysins, and phenol-soluble modulin) and cell wall components (e.g., peptidoglycan and alanylated lipoteichoic acid) have been shown to be inflammatory, and these staphylococcal components may contribute to sepsis. On the host side, many host factors have been implicated in the innate detection of staphylococcal components. One class of pattern recognition molecules, Toll-like receptor 2, has been shown to function as the transmembrane component involved in the detection of staphylococcal lipoteichoic acid and phenol-soluble modulin and is involved in the synthesis of inflammatory cytokines by monocytes/macrophages in response to these components. Nod2 (nucleotide-binding oligomerization domain 2) is the intracellular sensor for muramyl dipeptide, the minimal bioactive structure of peptidoglycan, and it may contribute to the innate immune defense against S. aureus. The staphylococcal virulence factor protein A was recently shown to interact directly with tumor necrosis factor receptor 1 in airway epithelium and to reproduce the effects of tumor necrosis factor alpha. Finally, peptidoglycan recognition protein L is an amidase that inactivates the proinflammatory activities of peptidoglycan. However, peptidoglycan recognition protein L probably plays a minor role in the innate immune response to S. aureus. Thus, several innate immunity receptors may be implicated in host defense against S. aureus

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“…The promoter region of the ICAM-1 gene contains binding sites for both NF-kB and AP-1. Thus, the induction of ICAM-1 by cytokines, Gram-negative bacteria, or bacterial products requires the activation of NF-kB and/or AP-1 and their binding to the promoter region (15,35,(46)(47)(48). We demonstrated that treatment of ECs with BFT strongly activated NF-kB and AP-1.…”

Section: Discussionmentioning

confidence: 72%

Bacteroides fragilis Enterotoxin Upregulates Intercellular Adhesion Molecule-1 in Endothelial Cells via an Aldose Reductase-, MAPK-, and NF-κB–Dependent Pathway, Leading to Monocyte Adhesion to Endothelial Cells

Roh

Yoo

et al. 2011

The Journal of Immunology

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Enterotoxigenic Bacteroides fragilis (ETBF) produces a ∼20-kDa heat-labile enterotoxin (BFT) that plays an essential role in mucosal inflammation. Although a variety of inflammatory cells is found at ETBF-infected sites, little is known about leukocyte adhesion in response to BFT stimulation. We investigated whether BFT affected the expression of ICAM-1 and monocytic adhesion to endothelial cells (ECs). Stimulation of HUVECs and rat aortic ECs with BFT resulted in the induction of ICAM-1 expression. Upregulation of ICAM-1 was dependent on the activation of IκB kinase (IKK) and NF-κB signaling. In contrast, suppression of AP-1 did not affect ICAM-1 expression in BFT-stimulated cells. Suppression of NF-κB activity in HUVECs significantly reduced monocytic adhesion, indicating that ICAM-1 expression is indispensable for BFT-induced adhesion of monocytes to the endothelium. Inhibition of JNK resulted in a significant attenuation of BFT-induced ICAM-1 expression in ECs. Moreover, inhibition of aldose reductase significantly reduced JNK-dependent IKK/NF-κB activation, ICAM-1 expression, and adhesion of monocytes to HUVECs. These results suggest that a signaling pathway involving aldose reductase, JNK, IKK, and NF-κB is required for ICAM-1 induction in ECs exposed to BFT, and may be involved in the leukocyte–adhesion cascade following infection with ETBF.

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Bacterial components induce cytokine and intercellular adhesion molecules-1 and activate transcription factors in dermal fibroblasts

Cited by 40 publications

References 34 publications

Gonococcal Porin IB Activates NF-κB in Human Urethral Epithelium and Increases the Expression of Host Antiapoptotic Factors

Gonococcal Porin IB Activates NF-κB in Human Urethral Epithelium and Increases the Expression of Host Antiapoptotic Factors

Recognition ofStaphylococcus aureusby the Innate Immune System

Bacteroides fragilis Enterotoxin Upregulates Intercellular Adhesion Molecule-1 in Endothelial Cells via an Aldose Reductase-, MAPK-, and NF-κB–Dependent Pathway, Leading to Monocyte Adhesion to Endothelial Cells

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