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Lung Infections Aeruginosa Pseudomonas Hypersusceptibility TLRs 2 and 4 Are Not Involved in Hypersusceptibility to Acute Pseudomonas aeruginosa Lung Infections This information is current as Reuben Ramphal, Viviane Balloy, Michel Huerre, Mustapha of September 29, 2021. Si-Tahar and Michel Chignard J Immunol 2005; 175:3927-3934; ; doi: 10.4049/jimmunol.175.6.3927 http://www.jimmunol.org/content/175/6/3927 Downloaded from References This article cites 51 articles, 24 of which you can access for free at: http://www.jimmunol.org/content/175/6/3927.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 29, 2021 *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 © 2005 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology TLRs 2 and 4 Are Not Involved in Hypersusceptibility to Acute Pseudomonas aeruginosa Lung Infections1 Reuben Ramphal,* Viviane Balloy,† Michel Huerre,‡ Mustapha Si-Tahar,† and Michel Chignard2† TLRs are implicated in defense against microorganisms. Animal models have demonstrated that the susceptibility to a number of Gram-negative pathogens is linked to TLR4, and thus LPS of many Gram-negative bacteria have been implicated as virulence factors. To assess the role of this pathogen-associated molecular pattern as it is exposed on intact Pseudomonas aeruginosa, the susceptibility of mice lacking TLR4 or both TLR2 and TLR4 was examined in a model of acute Pseudomonas pneumonia. These mutant mice were not hypersusceptible to the Pseudomonas challenge and mounted an effective innate response that cleared the organism despite low levels of TNF-␣ and KC in the airways. Bacterial and neutrophil counts in the lung were similar in control ؊ ؊ and TLR-deficient mice at 6 and 24 h after infection. MyD88 / mice were, however, hypersusceptible, with 100% of mice dying Downloaded from within 48 h with a lower dose of P. aeruginosa. Of note there were normal levels of IL-6 and G-CSF in the airways of TLR mutant mice that were absent from the MyD88؊/؊ mice. Thus, the susceptibility of mice to P. aeruginosa acute lung infection does not go through TLR2 or TLR4, implying that Pseudomonas LPS is not the most important virulence factor in acute pneumonia caused ,by this organism. Furthermore, G-CSF treatment of infected MyD88؊/؊ mice results in improved clearance and survival. Thus the resistance to infection in TLR2/TLR4؊/؊ mice may be linked to G-CSF and possibly IL-6 production. The Journal of Immunology, 2005, 175: 3927–3934. http://www.jimmunol.org/ seudomonas aeruginosa is the major cause of morbidity The role of LPS as a virulence factor in lung disease has been in cystic fibrosis (CF),3 where there is a state of chronic under considerable investigation for a number of organisms (8, 12, P colonization, punctuated by recurrent exacerbations. This 13). Although the inhalation of P. aeruginosa LPS has been re- organism is also a major cause of acute nosocomial pneumonias in ported to result in severe lung inflammation (9), a critical role for patients who are ventilated (1). Besides the very high frequency of LPS expressed by the whole organism has only been occasionally infection in this patient population, P. aeruginosa is notable for the demonstrated to be responsible for susceptibility. Indeed, there are very high rate of attributable mortality in acute pulmonary infec- studies with C3H/HeJ mice, which have a loss-of-function muta- by guest on September 29, 2021 tions (1) that occurs even in the face of appropriate effective an- tion in the TLR4 gene, that do not support the idea that the LPS of tibiotics (2). Given our current state of knowledge concerning bac- this organism is the primary virulence factor (14, 15). It is believed terial virulence, inflammation, and disease, it may be deduced that that the proinflammatory action of LPS is mediated through TLR4 this susceptibility is due either to intoxication by a virulence factor in cooperation with CD14 and MD-2 molecules making up the or to the innate immune response, with severe inflammation re- TLR4 receptor complex (16), although studies by Pier et al. in sulting from the response to a virulence factor(s). In humans, there 1981 (17) indicated that C3H/HeJ mice do respond to Pseudomo- is an association between the production of the type III secreted nas LPS. However, the LPS of P. aeruginosa has been reported to toxins (TTSTs) of P. aeruginosa and the severity of the lung dis- be recognized by both TLR4 and TLR2, depending on the origin ease and mortality caused by this organism (3). Animal studies of the strain of P. aeruginosa and the cell types used to examine with certain, but not all, strains of this organism also suggest the the TLR4-LPS interaction (18). Thus, there may be other pathways involvement of these toxins (4–6), but other virulence factors, by which cells respond to LPS. LPS from a strain adapted to the such as LPS (7–10), phospholipase C (10), and flagellin (11), have CF respiratory tract was recognized by human TLR4, whereas LPS also been suggested to play roles. from an environmental strain was not recognized (18). This dif- ferential recognition occurred with human cells, but not with *Department of Medicine, University of Florida, Gainesville, FL 32610; †Institut mouse cells, i.e., mouse TLR4 recognizes LPS from the environ- Pasteur, De´fense Inne´e et Inflammation, Paris, France; Institut National de la Sante´et de la Recherche Me´dicale, E336, Paris, France; and ‡Institut Pasteur, Recherche et mental strain (18). In contrast, LPS from a nonadapted or envi- Expertise Histotechnologie et Pathologie, Paris, France ronmental strain of P. aeruginosa is recognized by human TLR2 Received for publication December 9, 2004. Accepted for publication July 8, 2005. (19). Such strains, coming from the environment, are likely to be The costs of publication of this article were defrayed in part by the payment of page found in acute lung disease. Thus, any analysis of the role of charges. This article must therefore be hereby marked advertisement in accordance Pseudomonas LPS in animal models of disease needs to consider with 18 U.S.C. Section 1734 solely to indicate this fact. these variations in recognition of LPS by TLRs. To dissect the 1 This work was supported by National Institutes of Health Grants AI45014 and AI47852 (to R.R.). relevant virulence factors in acute lung disease due to P. aerugi- nosa, we have begun by examining the responses of mice that have 2 Address correspondence and reprint requests to Dr. Michel Chignard, Institut Pas- teur, De´fense Inne´e et Inflammation, Institut National de la Sante´et de la Recherche deletions in the genes encoding either TLR4 or both TLR2 and Me´dicale E336, 25 rue du Dr. Roux, Paris 75015, France. E-mail address: TLR4. We find that neither mutation confers increased suscepti- [email protected] bility to acute lung infections produced by the intratracheal injec- 3 Abbreviations used in this paper: CF, cystic fibrosis; BAL, bronchoalveolar lavage; LB, Luria Bertoni; PAMP, pathogen-associated molecular pattern; PMN, polymor- tion of a reasonably well-characterized laboratory strain of P. phonuclear neutrophil; TTST, type III secreted toxin; WT, wild type. aeruginosa. However, we note that LPS-independent susceptibility Copyright © 2005 by The American Association of Immunologists, Inc. 0022-1767/05/$02.00 3928 TLRs AND P. aeruginosa to the lung infection in this animal model goes through the MyD88 LD50 doses for the normal control mice. Similar survival experiments were Ϫ Ϫ pathway, thus implicating another TLR or another receptor sharing performed with the MyD88 / mice using one-tenth of the wild-type (WT) LD to ascertain that susceptibility was mediated through a MyD88-depen- a similar signaling pathway. We observed that this MyD88 path- 50 dent pathway and to verify that the clone of strain PAK used in these exper- way is essential for IL-6 and G-CSF production, and that G-CSF iments was capable of causing rapid death in a susceptible mouse strain. treatment was partially protective of P. aeruginosa-infected A last series of animal experiments was performed to ascertain the ef- MyD88Ϫ/Ϫ mice. fects of the TLR and MyD88 mutations in defense against this strain of P. aeruginosa. Groups of eight mice were infected by the intratracheal route using approximately one-tenth of the LD50 for the control mice. Bron- Materials and Methods choalveolar lavages (BAL) were performed on these mice 6 and 24 h after Bacterial strain and growth conditions used infection, after pentobarbital euthanasia. The lavage fluids were diluted or used undiluted and plated on LB agar plates to obtain viable bacterial P. aeruginosa P. aeruginosa The strain PAK, a widely studied strain of counts in the lavage fluid. Total and differential cell counts were performed originally obtained from S. Lory (Harvard University, Boston, MA) was on the lavage fluid. Total cell counts were measured in the BAL fluids with grown overnight in Luria Bertoni (LB) broth, then transferred to fresh a Coulter counter (Coulter Electronics), and cell differential counts were medium and grown for 4–5 h to midlog phase.
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