Serum amyloid A induction of cytokines in monocytes/macrophages and lymphocytes

Song, Chongmin; Hsu, Kang; Yamen, Eric; Yan, Wei; Fock, Jianyi; Witting, Paul K.; Geczy, Carolyn L.; Freedman, Ben

doi:10.1016/j.atherosclerosis.2009.05.007

Cited by 116 publications

(83 citation statements)

References 32 publications

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“…The infrequently expressed SAA, unlike the most abundant SAA1, significantly induced HMGB1 release in TLR4/RAGE-and PKR-dependent mechanisms. These novel findings were consistent with several studies that echoed their dramatic differences in stimulating other cytokines/chemokines (22)(23)(24)(25). Although SAA contained minute amount of endotoxins, this trivial contamination was not likely the underlying cause for SAAmediated HMGB1 release, because (a) Ultrapure LPS (free from bacterial proteins and nucleic acids; catalog # tlrl-pelps, InvivoGen) fails to trigger HMGB1 release even when given up to 10 μg/mL (29,30); (b) the similarly prepared SAA1 that contained comparable amounts of endotoxin still failed to induce HMGB1 release; (c) endotoxin-neutralizing agent (for example, polymyxin B) effectively abrogated LPS-induced (0.5 μg/mL), but not SAAinduced (0.5 μg/mL), HMGB1 release; and (d) the disruption of TLR4 receptor impaired crude LPS-, but not SAAinduced, HMGB1 release.…”

Section: Discussionsupporting

confidence: 77%

“…SAA signals via a family of receptors (for example, TLR2, TLR4 and/or RAGE) to activate NLRP3 inflammasome (21,44) and to induce various cytokines/ chemokines and NO (22)(23)(24)(25). However, the signaling pathways leading to different proinflammatory mediators appear to be distinguishable.…”

Section: Discussionmentioning

confidence: 99%

“…Clinically, SAAs have been implicated as biomarkers in cardiovascular disorders (14), ulcerative colitis (15) and sepsis (16). Extracellular SAA signals via a family of receptors including the receptor for advanced glycation end products (RAGE) (17), TLR2 (18,19) and TLR4 (20) to activate NLRP3 inflammasome (21) and to induce various cytokines and chemokines (22)(23)(24)(25).…”

mentioning

confidence: 99%

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Serum Amyloid A Stimulates PKR Expression and HMGB1 Release Possibly through TLR4/RAGE Receptors

Zhu

et al. 2015

Mol Med

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Serum Amyloid A Stimulates PKR Expression and HMGB1 Release Possibly through TLR4/RAGE Receptors

Zhu

et al. 2015

Mol Med

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“…SAA has been identified to interact with a growing family of diverse receptors, including TLR2, RAGE, CD36, and FPRL1 [146]. Through these receptors, SAA can exert diverse immunological effects, including the induction of TNF, IL6, IL8, and IL1β in peripheral blood mononuclear cells, cytokines that are upregulated in sarcoidosis [147]. SAA has also been shown capable of promoting Th17 responses [148].…”

Section: Role Of Serum Amyloid a Aggregation In Sarcoidosismentioning

confidence: 98%

Etiologies of Sarcoidosis

Chen

Möller

2015

Clinic Rev Allerg Immunol

125

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Since sarcoidosis was first described more than a century ago, the etiologic determinants causing this disease remain uncertain. Studies suggest that genetic, host immunologic, and environmental factors interact together to cause sarcoidosis. Immunologic characteristics of sarcoidosis include non-caseating granulomas, enhanced local expression of T helper-1 (and often Th17) cytokines and chemokines, dysfunctional regulatory T-cell responses, dysregulated Toll-like receptor signaling, and oligoclonal expansion of CD4+ T cells consistent with chronic antigenic stimulation. Multiple environmental agents have been suggested to cause sarcoidosis. Studies from several groups implicate mycobacterial or propionibacterial organisms in the etiology of sarcoidosis based on tissue analyses and immunologic responses in sarcoidosis patients. Despite these studies, there is no consensus on the nature of a microbial pathogenesis of sarcoidosis. Some groups postulate sarcoidosis is caused by an active viable replicating infection while other groups contend there is no clinical, pathologic, or microbiologic evidence for such a pathogenic mechanism. The authors posit a novel hypothesis that proposes that sarcoidosis is triggered by a hyperimmune Th1 response to pathogenic microbial and tissue antigens associated with the aberrant aggregation of serum amyloid A within granulomas, which promotes progressive chronic granulomatous inflammation in the absence of ongoing infection.

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“…A-SAA stimulates the hydrolytic activity of secretory group IIA phospholipase A2 (sPLA2), which is responsible for the production of atherogenic oxygenated and nonoxygenated fatty acids [14]. Other evidence includes its ability to induce secretion of extracellular matrix degrading enzymes such as collagenase, matrix metalloproteinases 2 and 3 from synovial fibroblasts [15,16], and inflammatory cytokines from monocytes and macrophages [17].…”

Section: Introductionmentioning

confidence: 99%