Bacterial modulins: a novel class of virulence factors which cause host tissue pathology by inducing cytokine synthesis.

Henderson, Brian E.; Poole, Stephen; Wilson, Michael

doi:10.1128/mmbr.60.2.316-341.1996

Cited by 281 publications

(155 citation statements)

References 172 publications

(204 reference statements)

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“…Oral or dental lesions are probably the portal of entry of these bacteria, but the mechanisms by which these streptococci disseminate and contribute to these diseases are not yet fully elucidated. Recent data have demonstrated that the binding of various bacterial adhesins to their cell receptors leads to the release of cytokines that play important roles in in£ammatory disorders [10], and we have shown that protein I/II, an adhesin from oral viridans streptococci, exerts immunomodulatory e¡ects on human cells. After binding to its cell receptors via lectin interactions, protein I/II promotes the release of TNF-K, IL-1L, IL-6 and IL-8 from monocytes, IL-6 and IL-8 from endothelial cells, and IL-8 from epithelial cells [11,12].…”

Section: Introductionmentioning

confidence: 83%

Pro-inflammatory cytokine production by synoviocytes following exposure to protein I/II, a modulin from oral streptococci

Gourieux

Al-Okla

Schöller-Guinard

et al. 2001

FEMS Immunology &Amp; Medical Microbiology

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We have tested the ability of protein I/II, an adhesin from oral streptococci, to stimulate the production of pro-inflammatory cytokines by synovial cells isolated from both rheumatoid arthritis and control patients. Protein I/II triggers synovial fluid cells to produce interleukin (IL)-6 and IL-8 while secretion of tumor necrosis factor-alpha (TNF-alpha) was less enhanced. Using fibroblast-like synoviocytes, we found that protein I/II also exerts an immunomodulatory effect (IL-6 and IL-8 release) on these cells. These findings indicate that, if it gains access to the joint cavity, protein I/II could participate in the initiation and/or perpetuation of rheumatic diseases, by stimulating pro-inflammatory cytokine release from various synovial cells.

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Section: Introductionmentioning

confidence: 83%

Pro-inflammatory cytokine production by synoviocytes following exposure to protein I/II, a modulin from oral streptococci

Gourieux

Al-Okla

Schöller-Guinard

et al. 2001

FEMS Immunology &Amp; Medical Microbiology

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“…Proinflammatory cytokines such as interleukin-1b (IL-1b) and tumor necrosis factor a (TNF-a) serve to promote inflammation by promoting a diverse range of activities including the induction of adhesion molecules required for the transmigration of leukocytes to infection sites (Dinarello, 2000). The release of proinflammatory cytokines can be triggered by various bacterial products including LPS of Gram-negative bacteria, peptidoglycan of Gram-positive bacteria or specific molecules from diverse microorganisms (Henderson et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Role of pneumococcal pneumolysin in the induction of an inflammatory response in human epithelial cells

Yoo

Shin

Kim

et al. 2010

FEMS Immunology &Amp; Medical Microbiology

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Epithelial cells act as the first line of host defense against microorganisms by producing a range of molecules for clearance. Proinflammatory cytokines facilitate the clearance of invaders by the recruitment and activation of leukocytes. Upregulation of cytokine expression thus represents an important host innate defense response against invading microorganisms such as Streptococcus pneumoniae. Histological analysis of the airway revealed less leukocyte infiltration during the early stage of pneumococcal infection, when compared with nontypable Haemophilus influenzae (NTHi) infection. Here, we report that S. pneumoniae is less potent in inducing proinflammatory cytokine expression compared with NTHi. Among numerous virulence factors, pneumococcal pneumolysin was found to be the major factor responsible for the induction of inflammation. Interestingly, pneumolysin induces cytokine expression to a lesser extent at the early stage of infection, but becomes more potent in inducing inflammation at the late stage. Thus, this study reveals that pneumolysin induces the proinflammatory cytokine expression in a time-dependent manner.

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“…Apart from the bacterial compounds capable of eliciting a virucidal response reviewed, there are also a variety of bacterial virulence factors that can cause host tissue pathology, stimulating the mammalian cells to produce a diverse array of cytokines (that can result in the production of an antiviral state). These factors were classified by Henderson and co-workers in 1996 [234] into four families: adhesins, aggressins, impedins, and invasins; these substances are not included here because their antiviral action has not been confirmed.…”

Section: Antivirals From Bacteriamentioning

confidence: 99%

Antivirals against animal viruses

Villa

Feijoo-Siota

Rama

et al. 2017

Biochemical Pharmacology

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Antivirals are compounds used since the 1960s that can interfere with viral development. Some of these antivirals can be isolated from a variety of sources, such as animals, plants, bacteria or fungi, while others must be obtained by chemical synthesis, either designed or random. Antivirals display a variety of mechanisms of action, and while some of them enhance the animal immune system, others block a specific enzyme or a particular step in the viral replication cycle. As viruses are mandatory intracellular parasites that use the host's cellular machinery to survive and multiply, it is essential that antivirals do not harm the host. In addition, viruses are continually developing new antiviral resistant strains, due to their high mutation rate, which makes it mandatory to continually search for, or develop, new antiviral compounds. This review describes natural and synthetic antivirals in chronological order, with an emphasis on natural compounds, even when their mechanisms of action are not completely understood, that could serve as the basis for future development of novel and/or complementary antiviral treatments.

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Bacterial modulins: a novel class of virulence factors which cause host tissue pathology by inducing cytokine synthesis.

Cited by 281 publications

References 172 publications

Pro-inflammatory cytokine production by synoviocytes following exposure to protein I/II, a modulin from oral streptococci

Pro-inflammatory cytokine production by synoviocytes following exposure to protein I/II, a modulin from oral streptococci

Role of pneumococcal pneumolysin in the induction of an inflammatory response in human epithelial cells

Antivirals against animal viruses

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