Association between Staphylococcus aureus nasal carriage and disease phenotype in patients affected by systemic lupus erythematosus

Conti, Fabrizio; Ceccarelli, Fulvia; Iaiani, Giancarlo; Perricone, Carlo; Giordano, Alessandra; Amori, Luigino; Miranda, F.; Massaro, Laura; Pacucci, Viviana Antonella; Truglia, S.; Girelli, Gabriella; Fakeri, Azis; Taliani, Gloria; Temperoni, Chiara; Alessandri, Cristiano; Valesini, Guido

doi:10.1186/s13075-016-1079-x

Cited by 30 publications

(16 citation statements)

References 34 publications

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“…Although more than 30% of healthy individuals are colonized asymptomatically by S. aureus 75,76 , it can cause a wide spectrum of infections: some are limited to a single hair follicle (furuncle), others involve subcutaneous tissues (cellulitis), and the most serious feature potentially fatal penetration into any organ in the body, including bone (osteomyelitis), bloodstream (bacterial sepsis), and heart valves (bacterial endocarditis). S. aureus has also been implicated in the pathogenesis of chronic diseases such as atopic dermatitis 22,77–79 , and more recently in systemic lupus erythematosus with renal and skin involvement 80 .…”

Section: Host–pathogen Interactionsmentioning

confidence: 99%

Skin microbiota–host interactions

Chen

Fischbach

Belkaid

2018

Nature

513

396

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The skin is a complex and dynamic ecosystem that is inhabited by bacteria, archaea, fungi and viruses. These microbes—collectively referred to as the skin microbiota—are fundamental to skin physiology and immunity. Interactions between skin microbes and the host can fall anywhere along the continuum between mutualism and pathogenicity. In this Review, we highlight how host–microbe interactions depend heavily on context, including the state of immune activation, host genetic predisposition, barrier status, microbe localization, and microbe–microbe interactions. We focus on how context shapes the complex dialogue between skin microbes and the host, and the consequences of this dialogue for health and disease.

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Section: Host–pathogen Interactionsmentioning

confidence: 99%

Skin microbiota–host interactions

Chen

Fischbach

Belkaid

2018

Nature

513

396

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“…It has been suggested that the microbial persistence is a factor contributing to chronicity in inflammatory arthritides [38]. In particular, P. gingivalis DNA seems to be able to induce the production of proinflammatory cytokines such as interleukin (IL)-6, IL-1 and tumour necrosis factor (TNF), playing a central role in RA pathogenesis [39][40][41]. This production seems to occur through the signalling pathway of Toll-like receptor (TLR)-9, expressed highly in pathological periodontal tissue in comparison with healthy tissue [39,42,43].…”

Section: Discussionmentioning

confidence: 99%

Porphyromonas gingivalis in the tongue biofilm is associated with clinical outcome in rheumatoid arthritis patients

Ceccarelli

Orrù

Pilloni

et al. 2018

Clinical and Experimental Immunology

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Several studies have suggested a link between human microbiome and rheumatoid arthritis (RA) development. Porphyromonas gingivalis seems involved in RA initiation and progression, as supported by the high occurrence of periodontitis. In this case-control study, we analysed tongue P. gingivalis presence and quantification in a large healthy and RA cohort. We enrolled 143 RA patients [male/female (M/F) 32/111, mean ± standard deviation (s.d.), age 57·5 ± 19·8 years, mean ± s.d. disease duration 155·9 ± 114·7 months); 36 periodontitis patients (M/F 11/25, mean ± s.d., age 56 ± 9·9 years, mean ± s.d. disease duration 25·5 ± 20·9 months); and 57 patients (M/F 12/45, mean ± s.d., age 61·4 ± 10·9 years, mean ± s.d. disease duration 62·3 ± 66·9 months) with knee osteoarthritis or fibromyalgia. All subjects underwent a standard cytological swab to identify the rate of P. gingivalis/total bacteria by using quantitative real-time polymerase chain reaction. The prevalence of P. gingivalis resulted similarly in RA and periodontitis patients (48·9 versus 52·7%, P = not significant). Moreover, the prevalence of this pathogen was significantly higher in RA and periodontitis patients in comparison with control subjects (P = 0·01 and P = 0·003, respectively). We found a significant correlation between P. gingivalis rate in total bacteria genomes and disease activity score in 28 joints (DAS28) (erythrocyte sedimentation rate) (r = 0·4, P = 0·01). RA patients in remission showed a significantly lower prevalence of P. gingivalis in comparison with non-remission (P = 0·02). We demonstrated a significant association between the percentage of P. gingivalis on the total tongue biofilm and RA disease activity (DAS28), suggesting that the oral cavity microbiological status could play a role in the pathogenic mechanisms of inflammation, leading to more active disease.

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“…In addition, disruption of the epithelial barrier, which is important in promotion of S. aureus colonization (Wanke et al, 2013), is able to drive lupus disease activity (Clark et al, 2015). Moreover, S. aureus is the leading cause of bacteremia in patients with lupus, and its carriage may be associated with disease flares and development of lupus nephritis (Chen et al, 2008;Conti et al, 2016;Hajialilo et al, 2015). Reflecting the importance of S. aureusedriven immune activation, repeated injections of S. aureus superantigen in wild type mice results in the development of a disease that mimics lupus (Chowdhary et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Staphylococcus aureus Colonization Is Increased on Lupus Skin Lesions and Is Promoted by IFN-Mediated Barrier Disruption

Sirobhushanam

Parsa

Reed

et al. 2020

Journal of Investigative Dermatology

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Cutaneous inflammation is recurrent in systemic lupus erythematosus (SLE), yet mechanisms that drive cutaneous inflammation in SLE are not well defined. Type I IFNs are elevated in nonlesional SLE skin and promote inflammatory responses. Staphylococcus aureus, known to induce IFN production, could play a role in cutaneous inflammation in SLE. We show here that active cutaneous lupus erythematosus lesions are highly colonized (w50%) by S. aureus. To define the impact of IFNs on S. aureus colonization, we examined the effects of type I and type II IFNs on S. aureus adherence and invasion. An increase in adherent S. aureus was observed after exposure to both IFN-a and-g, whereas IFN-g appeared to inhibit invasion of S. aureus. Cutaneous lupus erythematosus lesional skin microarray data and RNA sequencing data from SLE keratinocytes identified repression of barrier gene expression, such as filaggrin and loricrin, and SLE keratinocytes exhibited increased S. aureusebinding integrins. These SLE-associated changes could be replicated by IFN treatment of keratinocytes. Further, SLE keratinocytes exhibited increased binding to S. aureus. Together, these data suggest that chronic exposure to IFNs induces barrier disruption that allows for higher S. aureus colonization in SLE skin.

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Association between Staphylococcus aureus nasal carriage and disease phenotype in patients affected by systemic lupus erythematosus

Cited by 30 publications

References 34 publications

Skin microbiota–host interactions

Skin microbiota–host interactions

Porphyromonas gingivalis in the tongue biofilm is associated with clinical outcome in rheumatoid arthritis patients

Staphylococcus aureus Colonization Is Increased on Lupus Skin Lesions and Is Promoted by IFN-Mediated Barrier Disruption

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