<i>Staphylococcus aureus</i> induces the expression of tumor necrosis factor‐α in primary human keratinocytes

Aufiero, Barbara; Guo, Meng; Young, Chen; Duanmu, Zhengbo; Talwar, H. S.; Lee, Hae Kyung; Murakawa, George J.

doi:10.1111/j.1365-4632.2007.03161.x

Cited by 24 publications

(16 citation statements)

References 36 publications

(37 reference statements)

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“…Central to colonisation and infection is the interaction of S. aureus with keratinocytes, which form an important barrier between the internal organs and external environment. Adhesion of S. aureus to keratinocytes results in inflammatory cytokine release and stimulates secretion of several antimicrobial peptides, of which β-defensin 3 reaches levels sufficient to kill S. aureus [42], [43]. Cellular invasion is apparently not necessary to trigger these responses but internalised bacteria cause necrotic and apoptotic cell death [37].…”

Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus Keratinocyte Invasion Is Dependent upon Multiple High-Affinity Fibronectin-Binding Repeats within FnBPA

et al. 2011

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Staphylococcus aureus is a commensal organism and a frequent cause of skin and soft tissue infections, which can progress to serious invasive disease. This bacterium uses its fibronectin binding proteins (FnBPs) to invade host cells and it has been hypothesised that this provides a protected niche from host antimicrobial defences, allows access to deeper tissues and provides a reservoir for persistent or recurring infections. FnBPs contain multiple tandem fibronectin-binding repeats (FnBRs) which bind fibronectin with varying affinity but it is unclear what selects for this configuration. Since both colonisation and skin infection are dependent upon the interaction of S. aureus with keratinocytes we hypothesised that this might select for FnBP function and thus composition of the FnBR region. Initial experiments revealed that S. aureus attachment to keratinocytes is rapid but does not require FnBRs. By contrast, invasion of keratinocytes was dependent upon the FnBR region and occurred via similar cellular processes to those described for endothelial cells. Despite this, keratinocyte invasion was relatively inefficient and appeared to include a lag phase, most likely due to very weak expression of α5β1 integrins. Molecular dissection of the role of the FnBR region revealed that efficient invasion of keratinocytes was dependent on the presence of at least three high-affinity (but not low-affinity) FnBRs. Over-expression of a single high-affinity or three low-affinity repeats promoted invasion but not to the same levels as S. aureus expressing an FnBPA variant containing three high-affinity repeats. In summary, invasion of keratinocytes by S. aureus requires multiple high-affinity FnBRs within FnBPA, and given the importance of the interaction between these cell types and S. aureus for both colonisation and infection, may have provided the selective pressure for the multiple binding repeats within FnBPA.

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Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus Keratinocyte Invasion Is Dependent upon Multiple High-Affinity Fibronectin-Binding Repeats within FnBPA

et al. 2011

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“…Необходимо отметить, что инфекция, вызванная золотистым стафилококком, приводит к специфи-ческой активации рецептора TNFR1, но не TNFR2 [6]. Продемонстрировано, что TNF-α играет клю-чевую роль в развитии местного воспалительного процесса, но активация его вызывает также небла-гоприятные системные эффекты.…”

Section: Tnf-αunclassified

Розвиток Імунної Відповіді При Стафілококовій Пневмонії (Частина 3)

Абатуров¹,

Никулина²

2021

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У даній статті на підставі літературних даних проаналізовано ключову роль прозапальних і протизапальних цитокінів у розвитку імунної відповіді при пневмонії, викликаної Staphylococcus aureus. Наведено гени, що асоційовані зі схильністю до стафілококової інфекції та/або визначають її. Описано сигнальні шляхи, що індукують продукцію інтерферонів І, ІІ і ІІІ типу, які беруть участь в елімінації Staphylococcus aureus.

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“…S. aureus protein A (SpA) can mimic tumor necrosis factor alpha (TNF-α) and directly activates TNF receptor 1 (TNFR1), which elicits the release of cytokines (14). In kerationocytes, the adherence of S. aureus also causes the induction of TNF-α and TNFR1 expression (3,55). Various virulence factors of staphylococci may stimulate the inflammatory response.…”

Section: Staphylococcus Pseudintermediusmentioning

confidence: 99%

Staphylococcus pseudintermedius, both commensal and pathogen

Chrobak-Chmiel¹,

Golke²,

Dembele³

et al. 2018

Medycyna Weterynaryjna

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Staphylococcus pseudintermedius is considered to be a both commensal and opportunistic canine pathogen. The anal, perineal and nasal locations appear to be the main S. pseudintermedius colonization sites, from which bacteria are transmitted to other body sites, causing secondary infections. When the immune system is compromised because of an underlying condition, the skin becomes susceptible to infection. Thus, the host’s condition seems to play a crucial role in the pathogenesis of S. pseudintermedius infections. There are some predisposing factors, one of which is atopic dermatitis. The pathogenic effects of S. pseudintermedius are mediated by several virulence factors, for instance superantigens, which play an important role by causing dermatitis. The immune system has evolved many different mechanisms to recognize and deal with pathogens, but bacteria have also developed various strategies to evade them. In this review, we focus on early stages of the innate immune response with particular emphasis on the mechanisms of recognition of staphylococci and the action of antimicrobial peptides. .

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Staphylococcus aureus induces the expression of tumor necrosis factor‐α in primary human keratinocytes

Cited by 24 publications

References 36 publications

Staphylococcus aureus Keratinocyte Invasion Is Dependent upon Multiple High-Affinity Fibronectin-Binding Repeats within FnBPA

Staphylococcus aureus Keratinocyte Invasion Is Dependent upon Multiple High-Affinity Fibronectin-Binding Repeats within FnBPA

Розвиток Імунної Відповіді При Стафілококовій Пневмонії (Частина 3)

Staphylococcus pseudintermedius, both commensal and pathogen

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