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Scavenger Receptor 1 As a Candidate Gene Response A Quantitative Trait Loci Analysis to Map Genes Involved in Lipopolysaccharide-Induced Inflammatory Response: Identification of Macrophage This information is current as Scavenger Receptor 1 as a Candidate Gene of September 27, 2021. William B. Fulton, Roger H. Reeves, Motohiro Takeya and Antonio De Maio J Immunol 2006; 176:3767-3773; ; doi: 10.4049/jimmunol.176.6.3767 Downloaded from http://www.jimmunol.org/content/176/6/3767 References This article cites 37 articles, 12 of which you can access for free at: http://www.jimmunol.org/ http://www.jimmunol.org/content/176/6/3767.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 27, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology A Quantitative Trait Loci Analysis to Map Genes Involved in Lipopolysaccharide-Induced Inflammatory Response: Identification of Macrophage Scavenger Receptor 1 as a Candidate Gene1 William B. Fulton,* Roger H. Reeves,† Motohiro Takeya,‡ and Antonio De Maio2*† Septic shock, which is a major complication observed after trauma and other human diseases, is likely the product of a prolonged and poorly controlled systemic inflammatory response. Symptoms of sepsis can be partially reproduced by injection of bacterial LPS in mice. Differences in mortality between C57BL/6Jhigh and A/Jlow mice after LPS injection have been previously observed and correlated with differences in the inflammatory response between these two inbred strains. In the present study, we have mapped four loci responsible for differences in levels of LPS-induced IL-10, named modifier of IL-10, between the two strains. A Downloaded from locus within mouse chromosome 8 was confirmed using chromosome 8 consomic mice. This locus was further reduced in size by haplotype analysis and evaluated by the presence of potential candidate genes. The macrophage scavenger receptor 1 (Msr1) within this locus emerged as a candidate gene based on differences at the expression and structural levels between C57BL/6J and A/J mice. In comparison with wild-type (C57BL/6J) mice, Msr1 knockout mice displayed reduced levels of LPS-induced IL-10, but not of TNF-␣ or IL-6, confirming a specific role for this gene in the regulation of IL-10. These results suggest that Msr1 is involved in the regulation of the anti-inflammatory process, thus offering a new perspective on the molecular mechanisms involved in http://www.jimmunol.org/ endotoxemia and sepsis. The Journal of Immunology, 2006, 176: 3767–3773. epsis is a major health problem in the United States, with inflammatory reactants is likely to be responsible for the develop- an occurrence of ϳ750,000 cases per year (1). This con- ment of exaggerated inflammatory response conditions, such as S dition is triggered by an array of insults, including infec- those observed in sepsis. tion, trauma, burn injury, pancreatitis, and even elective surgery. Sepsis is likely modified by multiple factors, including the type The mortality rate for sepsis ranges from 35 to 50%, primarily due and extent of the initiating insult, the environment, and the genetic to the development of multiple organ dysfunction syndrome (1, 2). make-up, sex, and age of the patient (5). Although this assumption Despite tremendous advances in the care of critically ill patients, has been sustained by many clinical observations, it has not been by guest on September 27, 2021 therapy for sepsis remains supportive and extremely costly. A ma- experimentally tested in humans. Studies in experimental animal jor obstacle to the development of treatments for sepsis is the im- models have offered strong support for this hypothesis. For in- mense heterogeneity of the clinical profiles observed in septic pa- stance, a robust inflammatory response can be induced by injection tients. Moreover, there are no reliable predictors for this condition. of LPS. Indeed, mice maintained in identical environmental con- Although the etiology of sepsis is poorly understood, this condition ditions and injected with Escherichia coli LPS displayed an in- has been associated with a prolonged and inadequately controlled flammatory response that differed among the various inbred strains systemic inflammatory response. An important component of the (6, 7). The frequency of mortality was also different among inbred inflammatory process is secretion of cytokines by macrophages, mouse strains following injection of LPS (6). The genetic contri- monocytes, and polymorphic nuclear leukocytes. Proinflammatory bution to sepsis has been further supported by studies using a cytokines, such as TNF-␣ and IL-6, modulate gene expression in model of polymicrobial sepsis (8, 9). A direct correlation between a variety of organs (e.g., acute phase genes in the liver). Anti- extremely elevated anti-inflammatory (IL-10) cytokine levels and inflammatory cytokines, such as IL-10, are necessary to control the increased mortality has been observed after peritonitis (8, 9). Such inflammatory process. Specifically, IL-10 is involved in the down- studies, conducted on animals housed in identical environments regulation of TNF-␣ (3, 4). The imbalance between pro- and anti- and subjected to the same initiating insult, clearly illustrate that the genetic background is an important modifier of the inflammatory response and outcome. The question that emerges is whether these *Division of Pediatric Surgery, Department of Surgery, and †Department of Physi- genetic differences can be exploited to identify genes that modulate ology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205; and the inflammatory response. The identification of such genes would ‡Second Department of Pathology, Kumamoto University School of Medicine, Ku- mamoto, Japan shed light on the possible pathways activated in response to sepsis. Received for publication October 5, 2005. Accepted for publication December In addition, this knowledge could result in the detection of genetic 23, 2005. markers to be used as predictors for the development of sepsis. 3 The costs of publication of this article were defrayed in part by the payment of page Mapping quantitative trait loci (QTL) is a direct approach to the charges. This article must therefore be hereby marked advertisement in accordance identification of genes that modify the inflammatory response (5). with 18 U.S.C. Section 1734 solely to indicate this fact. 1 This study was supported by grants from the National Institutes of Health (GM50878 and GM62599). 3 Abbreviations used in this paper: QTL, quantitative trait loci; Chr, chromosome; 2 Address correspondence and reprint requests to the current address of Dr. Antonio Msr1, macrophage scavenger receptor 1; PM␾, peritoneal macrophage; LRS, likeli- De Maio, Department of Surgery, University of California, San Diego, 9500 Gilman hood ratio statistic; LOD, logarithm of the odds; RI, recombinant inbred; Milt, mod- Drive, #0739, La Jolla, CA 92093-0739. Email address: [email protected] ifier of IL-10; PVDF, polyvinylidene difluoride. Copyright © 2006 by The American Association of Immunologists, Inc. 0022-1767/06/$02.00 3768 ROLE OF Msr1 IN INFLAMMATION Using an intercross strategy, we previously identified loci on Immunostaining mouse chromosomes (Chr) 13 and 5 showing an epistatic relation- PM␾ were fixed with 4% paraformaldehyde for 10 min, then washed twice ship for the infiltration of polymorphonuclear leukocytes in the with PBS. Nonspecific binding was blocked by incubation with 10% FCS liver after LPS challenge (7). In the present study, we mapped in PBS for 30 min at 25°C. Fixed cells were incubated with anti-mouse several loci for plasma levels of IL-10 as part of the inflammatory MSR1 (1/200) in PBS-5% FCS for1hat25°C. Cells were washed three times with PBS and incubated with anti-rabbit IgG Cy3 Conjugate F(abЈ) response induced by LPS. A candidate gene associated with LPS- 2 (1/1000; Sigma-Aldrich) in PBS-5% FCS for 40 min at 25°C. Cells were induced IL-10 plasma levels was identified using a combination of washed three times with PBS, then mounted and visualized with a fluo- genetic mapping and informatics. rescent microscope. FACS analysis Materials and Methods PM␾ were isolated as described above, washed twice with PBS, and re- Experimental animal model of endotoxemia suspended in PBS containing 5% FCS and 1 mm NaN3. Cells were incu- bated at 25°C with anti-mouse MSR1 (1 ␮g/1 ϫ 106 cells) for1hand Male mice (A/J, AKR/J, BALB/cJ, B6, DBA/2J, B6AF1/J (BXA), AXB/ washed twice with PBS. Cells were resuspended in PBS containing 5% BXA recombinant inbred, B6-Chr 8A/NaJ, and B6-Chr 9A/NaJ) were ob- FCS and 1 mm NaN3 and incubated with anti-rabbit IgG FITC Conjugate tained from The Jackson Laboratory. AB6F1/J (AXB) mice were bred in Ј F(ab )2 (1/1000; Sigma-Aldrich) for 40 min at 25°C. Cells were then our animal
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