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Pneumophila Legionella Intracellular Infection with Modulated After The Neuronal Apoptosis Inhibitory Protein (Naip) Is Expressed in Macrophages and Is Modulated After Phagocytosis and During Intracellular Infection with Legionella This information is current as pneumophila of September 24, 2021. Eduardo Diez, Zahra Yaraghi, Alex MacKenzie and Philippe Gros J Immunol 2000; 164:1470-1477; ; doi: 10.4049/jimmunol.164.3.1470 Downloaded from http://www.jimmunol.org/content/164/3/1470 References This article cites 35 articles, 12 of which you can access for free at: http://www.jimmunol.org/ http://www.jimmunol.org/content/164/3/1470.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 24, 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 © 2000 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Neuronal Apoptosis Inhibitory Protein (Naip) Is Expressed in Macrophages and Is Modulated After Phagocytosis and During Intracellular Infection with Legionella pneumophila1 Eduardo Diez,* Zahra Yaraghi,† Alex MacKenzie,†‡ and Philippe Gros2* Legionella pneumophila is an intracellular pathogen that causes Legionnaires’ disease in humans. Inbred mouse strains are uniformly resistant to L. pneumophila infection with the notable exception of A/J, where the chromosome 13 locus Lgn1 renders A/J macrophages permissive to L. pneumophila replication. The mouse Lgn1 region is syntenic with the spinal muscular atrophy (SMA) locus on human chromosome 5 and includes several copies of the neuronal apoptosis inhibitory protein (Naip) gene. We have analyzed a possible link among Lgn1, Naip, and macrophage function. RNA expression studies show that Naip (mostly copy 2) mRNA transcripts are expressed in macrophage-rich tissues, such as spleen, lung, and liver and are abundant in primary Downloaded from macrophages. Immunoblotting and immunoprecipitation analyses identify Naip protein expression in mouse macrophages and in macrophage cell lines RAW 264.7 and J774A. Interestingly, macrophages from permissive A/J mice express significantly less Naip protein than their nonpermissive C57BL/6J counterpart. Naip protein expression is increased after phagocytic events. Naip protein levels during infection with either virulent or avirulent strains of L. pneumophila increase during the first 6 h postinfection and remain elevated during the 48-h observation period. This enhanced expression is also observed in macrophages infected with Salmonella typhimurium. Likewise, an increase in Naip protein levels in macrophages is observed 24 h after phagocytosis of Latex http://www.jimmunol.org/ beads. The cosegregation of Lgn1 and Naip together with the detected Naip protein expression in host macrophages as well as its modulation after phagocytic events and during intracellular infection make it an attractive candidate for the Lgn1 locus. The Journal of Immunology, 2000, 164: 1470–1477. egionella pneumophila is a facultative intracellular parasite is an exception, however, as A/J inflammatory peritoneal macro- that in humans can cause an acute form of pneumonia called phages are highly permissive to L. pneumophila replication in L Legionnaires’ disease (1). L. pneumophila enters macro- vitro, resulting in a 1000-fold increase in viable bacteria during a phages through a unique coiling phagocytosis mechanism (2) and 72-h infection, compared with macrophages from nonpermissive replicates within maturation-defective phagosomes (3), which do mouse strains such as C57BL/6J, C3H, and DBA/2J (10, 11). The by guest on September 24, 2021 not fuse to endosomes or lysosomes (4). These replicative phago- permissiveness of A/J macrophages to L. pneumophila replication somes are morphologically distinct and are associated with endo- provides a unique experimental system to study the parallel human plasmic reticulum membranes and dotted with ribosomes (5). Al- disease (9, 12). Linkage studies have indicated that a single auto- though certain Legionella proteins (dot/icm) have recently been somal, recessive gene, designated Lgn1 (11), determines macro- shown to play an important role in the inhibition of phagosome- phage permissiveness to intracellular replication of L. pneumo- lysosome fusion (6–8), the molecular mechanisms underlying suc- phila. Lgn1 maps to the distal mouse chromosome 13 (13–17), cessful intracellular survival and replication of L. pneumophila,in within a genetic interval of 0.32 centiMorgan (95% confidence particular the host proteins targeted for inhibition, remain largely interval), defined distally by the genetic marker D13Die3 and unknown. proximally by D13Die6/D13Die26. Physical mapping studies and In contrast to their human and guinea pig counterparts, mouse assembly of a cloned contig of BAC and YAC clones for the macrophages are not permissive to L. pneumophila replication region suggest a minimal physical interval for Lgn1 of ϳ350 kb even though the bacteria still rapidly inhibit phagosome-lysosome (15–18). fusion soon after phagocytosis (reviewed in Ref. 9). The A/J strain The murine chromosome 13 Lgn1 region is syntenic with the spinal muscular atrophy (SMA)3 locus on human chromosome 5, which includes the survival motor neuron SMN gene and the neu- *Department of Biochemistry, McGill University, Montreal, Canada; †Department of ronal apoptosis inhibitory protein NAIP gene (19, 20). There is one Biochemistry and Pediatrics, University of Ottawa, Ottawa, Canada; and ‡Apoptogen, Inc., Ottawa, Ontario, Canada functional copy of NAIP in the human genome and approximately Received for publication August 13, 1999. Accepted for publication November two-thirds of type I SMA cases are associated with its homozygous 16, 1999. deletion (21). Although it was later shown that the closely linked The costs of publication of this article were defrayed in part by the payment of page SMN gene is the SMA-determining gene (22), NAIP remains a charges. This article must therefore be hereby marked advertisement in accordance strong candidate as a phenotypic modifier of SMN mutations. The with 18 U.S.C. Section 1734 solely to indicate this fact. NAIP protein has been shown to inhibit apoptosis of neurons and 1 This work was supported by grants (to P.G.) from the Network of Centers of Ex- cellence (Canadian Genetic Diseases Network). P.G. is supported by a Senior Scien- tist award, and E.D. is supported by a studentship from the Medical Research Council of Canada. P.G. is an International Research Scholar of the Howard Hughes Medical 3 Abbreviations used in this paper: SMA, spinal muscular atrophy; BAC, bacterial Institute. artificial chromosome; BIR, baculovirus inhibition of apoptosis protein repeat; IOD, 2 Address correspondence and reprint requests to Dr. Philippe Gros, Department of indexed optical density; MOI, multiplicity of infection; NAIP, neuronal apoptosis Biochemistry, McGill University, Montreal, Canada H3G 1Y6. E-mail address: inhibitory protein; SMN, survival motor neuron; TGC, thioglycolate; YAC, yeast [email protected] artificial chromosome. Copyright © 2000 by The American Association of Immunologists 0022-1767/00/$02.00 The Journal of Immunology 1471 FIGURE 1. Schematic representation of the Lgn1 region on distal mouse chromosome 13. Genetic mapping has defined a 0.32-centiMorgan minimal interval for Lgn1 delineated proximally by Dl3Die6 (Die6) and distally by D13Die3 (Die3; 2/1270 recombinations each). Physical mapping has suggested that the size of the Lgn1 locus is between 125–350 kb and contains six copies of the Naip gene (mNaip, shown as squares). Copy 2 is the most closely linked to Smn, followed distally by copy 5 (25). Although a preliminary order has been proposed for five of the Naip copies by Scharf et al. in 1996 (16), the order of the remaining four Naip copies has not been established with certainty. Smn and M4f5 have recently been segregated from Lgn1 (17). The asterisk identifies the Naip2 copy most abundantly expressed in macrophages. The data shown were obtained from maps in the reports by Scharf et al. (16), Diez et al. (18), Yaraghi et al. (25), and Endrizzi et al. (17). other cell types both in vitro and in vivo (23, 24). In addition, conditions were as recommended by the supplier. In other experiments NAIP has been shown to inhibit the proapoptotic cysteine pro- total cellular RNA was extracted from normal mouse tissues and cultured Downloaded from teases known as caspases; in particular, caspases 3 and 7 have been cells using 6 M guanidium hydrochloride, and purified by sequential eth- anol precipitations and phenol-chloroform extractions. Equal amounts of shown to interact with NAIP (A. MacKenzie, unpublished obser- RNA (10 ␮g/lane) were separated on a 1% agarose gel containing 0.66 M vations). The mouse Lgn1 locus includes the Smn gene as well as formaldehyde in MOPS buffer (40 mM morpholinopropanesulfonic acid, six copies of the Naip gene (Fig. 1). Analysis of mouse brain RNA 10 mM
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