TLR4 Endogenous Ligand S100A8/A9 Levels in Adult-Onset Still’s Disease and Their Association with Disease Activity and Clinical Manifestations

Kim, Hyoun‐Ah; Han, Jae Ho; Kim, Woo-Jung; Noh, Han-Jin; An, Jie; Yim, Hyunee; Jung, Ju‐Yang; Kim, You‐Sun; Suh, Chang‐Hee

doi:10.3390/ijms17081342

Cited by 33 publications

(30 citation statements)

References 35 publications

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“…Hypothetically, S100A8/A9 is expressed by tonsil epithelial cells due to disruption of barrier function. A positive feedback mechanism with amplification of inflammation, induction of proinflammatory cytokine production, and simultaneous proliferation of keratinocytes as described in patients with systemic lupus erythematosus or psoriasis is assumable in tonsils and tonsillitis [ 36 ]. Thus, associated with leukocyte recruitment, pathogens could be eliminated and invasion could be averted [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Increased Levels of S100A8/A9 in Patients with Peritonsillar Abscess: A New Promising Diagnostic Marker to Differentiate between Peritonsillar Abscess and Peritonsillitis

et al. 2017

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Peritonsillar abscess (PTA) is a very frequent reason for urgent outpatient consultation and otolaryngological hospital admission. Early, correct diagnosis and therapy of peritonsillar abscess are important to prevent possible life-threatening complications. Based on physical examinations, a reliable differentiation between peritonsillar cellulitis and peritonsillar abscess is restricted. A heterodimeric complex called calprotectin consists of the S100 proteins A8 and A9 (S100A8/A9) and is predominantly expressed not only in monocytes and neutrophils but also in epithelial cells. Due to its release by activated phagocytes at local sites of inflammation, we assumed S100A8/A9 to be a potential biomarker for peritonsillar abscess. We examined serum and saliva of patients with peritonsillitis, acute tonsillitis, peritonsillar abscess, and healthy controls and found significantly increased levels of S100A8/A9 in patients with PTA. Furthermore, we could identify halitosis, trismus, uvula edema, and unilateral swelling of the arched palate to be characteristic symptoms for PTA. Using a combination of these characteristic symptoms and S100A8/A9 levels, we developed a PTA score as an objective and appropriate tool to differentiate between peritonsillitis and peritonsillar abscess with a sensitivity of 92% and specificity of 93%.

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Section: Discussionmentioning

confidence: 99%

Increased Levels of S100A8/A9 in Patients with Peritonsillar Abscess: A New Promising Diagnostic Marker to Differentiate between Peritonsillar Abscess and Peritonsillitis

et al. 2017

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“…The levels of S100A8/A9 proteins correlate with disease activity and severity (38,47,48). A positive correlation was found with leukocyte count, ESR, CRP, ferritin, TNF-, IL-1 and systemic disease scores (38,47,48). The calprotectin levels also showed a decrease in treated patents, after disease activity status resolution (47).…”

Section: Proteins S100 A8/a9 and A12mentioning

confidence: 96%

“…AOSD patients exhibit higher serum levels of calprotectin when compared to RA patients or healthy controls (38,47,48). The levels of S100A8/A9 proteins correlate with disease activity and severity (38,47,48). A positive correlation was found with leukocyte count, ESR, CRP, ferritin, TNF-, IL-1 and systemic disease scores (38,47,48).…”

Section: Proteins S100 A8/a9 and A12mentioning

confidence: 99%

“…In these conditions, a dysregulation of alternative secretory pathways leading to hypersecretion of calgranulins may be involved in disease pathogenesis (12,46). AOSD patients exhibit higher serum levels of calprotectin when compared to RA patients or healthy controls (38,47,48). The levels of S100A8/A9 proteins correlate with disease activity and severity (38,47,48).…”

Section: Proteins S100 A8/a9 and A12mentioning

confidence: 99%

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New Markers for Adult-Onset Still's Disease

Mitrovic

Fautrel

2018

Joint Bone Spine

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Adult-onset Still's disease (AOSD) is a rare systemic auto-inflammatory disorder (SAID). Although the pathogenesis of the disease is complex and far from being fully understood, recent progresses in pathophysiological knowledge have paved the way to new diagnostic approaches. Indeed, AOSD diagnosis can be a real challenge, owing to its infrequency, and to the lack of specificity of the principal clinical features (high fever, arthralgia or arthritis, skin rash) and laboratory findings (elevated acute phase reactants, hyperleukocytosis≥10,000 cells/mm with neutrophils≥80%). None of these manifestations is disease-specific, so clinicians must first rule out neoplastic, infectious or inflammatory conditions. Besides these diagnostic difficulties, several other challenges remain. AOSD is very heterogeneous in terms of clinical presentation, evolution and severity. Thus, new biomarkers are required to assess: (i) disease activity; (ii) disease severity (through the identification of patients at risk of severe organ failure, and eventually of life-threatening complications, such as reactive haemophagocytic lymphohistiocytosis); (iii) disease evolution (which can be monophasic, relapsing, or progressive, with either systemic inflammation or chronic erosive arthritis); (iv) and treatment efficacy. The identification of new markers can only be done through a better understanding of the pathogenesis of the disease. After a short focus on the current AOSD pathophysiological knowledge, this article reviews the main biomarkers that have been proposed in the literature over the last few years.

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“…Serum level of calprotectin (i.e., S100A8/S100A9 protein) could be an additional disease activity biomarker because alarmins seem to play a key role in AoSD pathogenesis. However, it is not specific to AoSD and may be elevated in many other inflammatory conditions [42,44,111,112]. Finally, serum amyloid A protein (SAA) is an inflammatory biomarker found predictive of amyloidosis [42].…”

Section: Biomarkers For Routine Clinical Settingmentioning

confidence: 99%