Neutrophil-derived S100A12 in acute lung injury and respiratory distress syndrome

Wittkowski, Helmut; Sturrock, Anne; Zoelen, Marieke A. D. van; Viemann, Dorothee; Poll, Tom van der; Hoidal, John R.; Roth, Johannes; Foell, Dirk

doi:10.1097/01.ccm.0000262386.32287.29

Cited by 109 publications

(128 citation statements)

References 36 publications

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“…In blacks, there was a heightened neutrophil response to dental plaque accumulation; neutrophil hyperactivity has been shown to play a role in endothelial injury (Lentsch and Ward, 2000) and subsequent tissue damage in several disease processes (Di Filippo et al, 2007;Wittkowski et al, 2007). It was also suggested that long-term, low-grade infectious challenges may be of greater systemic importance than isolated, clinically obvious events (Roberts, 1999).…”

Section: Discussionmentioning

confidence: 99%

Neutrophil Response to Dental Plaque by Gender and Race

et al. 2009

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The inflammatory response, which has both genetic and environmental components, is a central mechanism linking oral and systemic diseases. We hypothesized that dental plaque accumulation over 21 days in the experimental gingivitis model would elicit systemic inflammatory responses [change in white blood cell (WBC) count and neutrophil activity], and that these responses would differ by gender/race. We recruited 156 healthy young adults, including black and white males and females. Plaque Index (PI), Gingival Index (GI), systemic WBC counts, and peripheral neutrophil oxidative activity were recorded. Overall, 128 participants completed the study. During the experimental phase, the correlation between PI and GI was 0.79. Total WBC and neutrophil counts did not change. Neutrophil activity increased in blacks but not whites, suggesting that there may be racial differences in the inflammatory response to dental plaque accumulation.

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Section: Discussionmentioning

confidence: 99%

Neutrophil Response to Dental Plaque by Gender and Race

et al. 2009

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“…Morbini et al observed increased RAGE expression in patients with interstitial and postobstructive pneumonia [32]; this report left unanswered whether patients with bacterial pneumonia were included in the analysis. Notably, two other studies showed that constitutively present RAGE was not upregulated during pulmonary infl ammation associated with ALI or acute respiratory distress syndrome (ARDS): First, rats with ALI induced by intratracheally administered LPS displayed no change in the distribution of RAGEexpressing cells [29]; and second, patients with ARDS did not have increased pulmonary expression of RAGE [26].…”

Section: Rage Expression During Pneumoniamentioning

confidence: 99%

“…Furthermore, S100A12 -also known as EN-RAGE (extracellular newly identifi ed ligand of RAGE) or myeloid-related protein (MRP)-6 -is found in monocytes and lymphocytes and provokes pro-infl ammatory responses in endothelial cells [26]. Although many RAGE ligands are promiscuous with regard to receptor use, S100A12 has only been shown to bind to RAGE.…”

Section: S100a12mentioning

confidence: 99%

“…S100A12 expression is high in infl ammatory diseases such as atherosclerosis, rheumatoid arthritis, Crohn's disease, Kawaski disease, and cystic fi brosis. Within the lungs, S100A12 and RAGE are increased during acute lung injury (ALI) [26]. S100A12 expression may refl ect activation of neutrophils during pulmonary infl ammation and may contribute to endothelial activation via binding to RAGE [26].…”

Section: S100a12mentioning

confidence: 99%

“…Physiologically, RAGE is expressed at high basal levels in the lungs relative to other tissues [26,[29][30][31][32][33][34], suggesting that RAGE may have lung-specifi c functions distinct from the role of RAGE in other adult tissues. In particular, although the kidney is dramatically aff ected by microangiopathy and fi brosiswhich is substantially attributed to RAGE -in patients with diabetes, the lungs, with a signifi cantly higher baseline RAGE expression than the kidney, remain unaff ected.…”

Section: Rage During Pneumonia Localization and Role Of Rage In The Lmentioning

confidence: 99%

See 2 more Smart Citations

The Role of Receptor for Advanced Glycation Endproducts (RAGE) in Infection

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Immunological Danger Signals

Jong

Wiersinga

2016

Encyclopedia of Life Sciences

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The conventional role of the immune system has been viewed as the first line of defence discriminating self from nonself. However, in the past decade, the innate immune response has proven to be more advanced sensing signals of danger, such as pathogen‐specific molecules ( PAMPs , pathogen‐associated molecular patterns) or endogenous host‐derived signals released during cellular damage, while remaining unresponsive to normal host molecules, dietary antigens or commensal bacteria. The host response to invading microbial pathogens relies on both the innate and adaptive immune response. The danger theory of Matzinger (1994) proposed a similar model for the adaptive immune response in discriminating self from nonself. This theory proposed that the immune system does not react to foreign substances but instead responds to situations that are potentially harmful. These danger signals, or damage‐associated molecular patterns ( DAMPs ), released by damaged cells, can provide for a second signal which is necessary to activate the immune response while avoiding collateral damage in situations in which harmless nonself is present. Key Concepts According to the danger theory of Matzinger, the immune system does not merely distinguish whether an entity is foreign or not, it mainly determines whether it will cause damage to the body. Damage‐associated molecular patterns (DAMP) are danger signals released during inflammatory stress such as burns, trauma and infection. Each pathogen is recognised by its specific molecular signature or pathogen‐associated molecular pattern (PAMP). Activation of the innate immune system relies on both pathogen‐specific molecules and endogenous danger signals. DAMPs can be recognised by pattern‐recognition receptors on antigen‐presenting cells or by distinct receptors such as the receptor for advanced glycation end products (RAGE). Key DAMPs that are recognised by Toll‐like receptors (TLRs) include heat shock proteins (HSPs), high‐mobility group box 1 (HMGB)‐1 and the S100 proteins.

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Neutrophil-derived S100A12 in acute lung injury and respiratory distress syndrome

Cited by 109 publications

References 36 publications

Neutrophil Response to Dental Plaque by Gender and Race

Neutrophil Response to Dental Plaque by Gender and Race

The Role of Receptor for Advanced Glycation Endproducts (RAGE) in Infection

Immunological Danger Signals

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