Recent advances in crystal-induced acute inflammation

Current Opinion in Rheumatology

Volumn 19, Issue 2, 2007, Pages 146-150

  Akahoshi, Tohru ^a,c   Murakami, Yousuke ^b   Kitasato, Hidero ^a  

^a KITASATO UNIVERSITY   (Japan)

^b Institute of Physical and Chemical Research   (Japan)

^c KITASATO UNIVERSITY SCHOOL OF MEDICINE   (Japan)

Author keywords

Inflammasome; Innate immunity; Nuclear hormone receptors; Toll like receptors; TREM 1

Indexed keywords

HORMONE RECEPTOR; LIVER X RECEPTOR ALPHA; MYELOID DIFFERENTIATION FACTOR 88; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR GAMMA; TOLL LIKE RECEPTOR; URATE;

CELL STIMULATION; CRYSTAL; GOUT; IMMUNOLOGY; INFLAMMATION; INNATE IMMUNITY; LABORATORY; PATHOLOGY; PHAGOCYTE; PRIORITY JOURNAL; PROTEIN EXPRESSION; REVIEW; UPREGULATION;

ACUTE DISEASE; CARRIER PROTEINS; GOUT; HUMANS; IMMUNITY, NATURAL; INFLAMMATION; INTERLEUKIN-1BETA; MEMBRANE GLYCOPROTEINS; RECEPTORS, IMMUNOLOGIC; TOLL-LIKE RECEPTORS; URIC ACID;

EID: 33846798047     PISSN: 10408711     EISSN: None     Source Type: Journal    
DOI: 10.1097/BOR.0b013e328014529a     Document Type: Review

References (17)

1. Terkeltaub R. Pathogenesis and treatment of crystal-induced inflammation. In: Koopman WJ, editor. Arthritis and allied conditions, 15th ed. Philadelphia: Lippincott Williams & Wilkins; 2005. pp. 2357-2372.
2. Lioté F, Ea H-K. Gout: Update on some pathogenic and clinical aspects. Rheum Dis Clin N Am 2006; 32:295-311.
3. Shin Y, Evans JE, Rock KL. Molecular identification of a danger signal that alerts the immune system to dying cells. Nature 2003; 425:516-521.
4. Medzhitov R, Janeway C Jr. Innate immune recognition: mechanisms and pathways. Immunol Rev 2000; 173:89-97.
5. Liu-Bryan R, Pritzker K, Firestein GS, Terkeltaub R. TLR2 signaling in chondrocytes derives calcium pyrophosphate dehydrate and monosodium urate crystal-induced nitric oxide generation. J Immunol 2005; 174:5016-5023. This paper demonstrated that CPPD and MSU crystals critically use TLR2-mediated signaling in chondrocytes to trigger nitric oxide generation. These findings indicate the potential for innate immunity at the level of the articular chondrocyte to directly contribute to inflammatory and degenerative tissue reactions associated with both gout and pseudogout.
6. Liu-Bryan R, Scott P, Sydlaske A, et al. Innate immunity conferred by toll-like receptor 2 and 4 and myeloid differentiation factor 88 expression is pivotal to monosodium urate monohydrate crystal-induced inflammation. Arthritis Rheum 2005; 52:2936-2946. This paper showed the requirement of TLR-2, TLR-4, and MyD88 for macrophage activation and development of MSU crystal-induced acute inflammation. These findings indicate innate immune cellular recognition of naked MSU crystals by specific TLRs as a major factor in determining the inflammatory potential of MSU crystal deposits and the course of gouty arthritis.
7. Kawai T, Akira S. TLR signaling. Cell Death Differ 2006; 13:816-825.
8. Chen C-J, Shi Y, Hearn A, et al. MyD88-dependent IL-1 receptor signaling is essential for gouty inflammation stimulated by monosodium urate crystals. J Clin Invest 2006; 116:2262-2271. This paper documented that the Toll/IL-1R (TIR) signal transduction adaptor MyD88, but not other TIR adaptor molecules, is required for acute gouty inflammation. The MyD88-dependent TLR1, 2, 4, 6, 7, 9, and 11 and IL-18 receptor (IL-18R) are not essential for MSU-induced inflammation. These findings indicate that IL-1 is essential for the MSU-induced inflammatory response and that the requirement of MyD88 in this process is primarily through its function as an adaptor molecule in the IL-1R signaling pathway.
9. Martinon F, Pétrilli V, Mayor A, et al. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature 2006; 440:237-241. This paper demonstrated that MSU and CPPD engage the caspase-1-activating NALP3 inflammasome, resulting in the production of active IL-1β and IL-18. Macrophages from mice deficient in various components of the inflammasome are defective in crystal-induced IL-1β activation. Moreover, an impaired neutrophil influx is found in an in-vivo model of crystal-induced peritonitis in inflammasome-deficient mice or mice deficient in the IL-1R. These findings provide insight into the molecular processes underlying the inflammatory conditions of gout and pseudogout.
10. Ogura Y, Sutterwala FS, Flavell RA. The inflammasome: first line of the immune response to cell stress. Cell 2006; 126:659-662. The NALP3-inflammasome is a protein complex that stimulates caspase-1 activation to promote the processing and secretion of proinflammatory cytokines. This paper reviewed the NALP3-inflammasome and discussed new insights into the regulation of caspase-1 activity in the inflammatory response.
11. Martinon F, Tschopp J. NLRs join TLRs as innate sensors of pathogens. Trends in Immunol 2005; 26:447-454.
12. Murakami Y, Akahoshi T, Hayashi I, et al. Induction of triggering receptor expressed on myeloid cells in murine resident peritoneal macrophages by monosodium urate monohydrate crystals. Arthritis Rheum 2006; 54:455-462. This paper demonstrated that TREM-1 expression by resident peritoneal macrophages was significantly induced by MSU crystals, and costimulation of resident peritoneal macrophages with MSU crystals and an anti-TREM-1 agonist antibody synergistically increased the production of both IL-1β and MCP-1. These findings suggest that rapid induction of TREM-1 expression on resident peritoneal macrophages and neutrophils by MSU crystals may contribute to the development of acute gout through enhancement of inflammatory responses.
13. Colonna M. TREMs in the immune system and beyond. Nat Rev Immunol 2003; 3:445-453.
14. Bouchon A, Dietrich J, Colonna M. Cutting edge: inflammatory responses can be triggered by TREM-1, a novel receptor expressed on neutrophils and monocytes. J Immunol 2000; 164:1991-1995.
15. Akahoshi T, Namai R, Murakami Y, et al. Rapid induction of peroxisome proliferators-activated receptor γ expression in human monocytes by monosodium urate monohydrate crystals. Arthritis Rheum 2003; 48:231-239.
16. Zelcer N, Tontonoz P. Liver X receptors as integrators of metabolic and inflammatory signaling. J Clin Invest 2006; 116:607-614.
17. Castrillo A, Joseph SB, Vaidya SA, et al. Crosstalk between LXR and toll-like receptor signaling mediates bacterial and viral antagonism of cholesterol metabolism. Mol Cell 2003; 12:805-816.