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Vol. 46. Issue 3.
Pages 135-142 (March 2010)
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Vol. 46. Issue 3.
Pages 135-142 (March 2010)
Review Article
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Role of toll-like receptors in respiratory diseases
Papel de los receptores toll-like en las enfermedades respiratorias
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Astrid Crespo-Lessmanna, Cándido Juárez-Rubiob, Vicente Plaza-Morala,
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vplaza@santpau.cat

Corresponding author.
a Pneumology department, Santa Creu i Sant Pau Hospital. Barcelona, Spain
b Inmunology department, Santa Creu i Sant Pau Hospital. Barcelona, Spain
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Abstract

There has been growing interest in the last 10 years in the study of innate immunity, in particular because of the possible role that toll-like receptors (TLR) may play in the pathogenesis of some respiratory diseases including, asthma, chronic obstructive pulmonary disease, and infections. TLR are a family of type 1 transmembrane proteins, responsible for recognising molecular patterns associated with pathogens (PAMP, pathogen-associated molecular patterns), and expressed by a broad spectrum of infectious agents. This recognition leads to a quick production of cytokines and chemokines which provides a long-lasting adaptive response to the pathogen. At present, it is considered //It is currently considered that the administration of drugs which modulate the activity of these receptors upwards or downwards may represent major therapeutic progress for handling these diseases.

The aim of this review is to describe the different TLS, define their possible role in the pathogenesis of the main respiratory diseases and finally, speculate over the therapeutic possibilities which their modulation, agonist or antagonist, offers as possible therapeutic targets.

Keywords:
Innate immunity
Acquired immunity
Toll-like receptors
Asthma
COPD
Resumen

En los últimos 10 años se ha constatado un creciente interés por el estudio de la inmunidad innata, particularmente por el posible papel que los denominados “receptores toll-like” (TLR) pueden desempeñar en la patogenia de algunas enfermedades respiratorias, como, por ejemplo, el asma, la enfermedad pulmonar obstructiva crónica y las infecciones. Los TLR son una familia de proteínas transmembranarias de tipo I, responsables del reconocimiento de patrones moleculares asociados a patógenos (PAMP, de pathogen-associated molecular patterns), y expresados por un amplio espectro de agentes infecciosos. Este reconocimiento lleva a una rápida producción de citocinas y quimiocinas, lo que proporciona una respuesta adaptativa duradera contra el patógeno. En la actualidad se considera que la administración de fármacos que modulen, al alza o a la baja, la actividad de estos receptores puede suponer un gran avance terapéutico en el manejo de dichas enfermedades.

El propósito de la presente revisión es describir los diferentes TLR, definir su posible papel en la patogenia de las principales enfermedades respiratorias y, finalmente, conjeturar las posibilidades terapéuticas que su modulación, agonista o antagonista, ofrece como posibles dianas terapéuticas.

Palabras clave:
Inmunidad innata
Inmunidad adquirida
Receptores toll-like
Asma
EPOC
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References
[1.]
S. Arancibia, C. Beltrán, I. Aguirre, P. Silva, A. Peralta, F. Malinarich, et al.
Toll-like receptor are key participants in innate immune responses [revision].
Biol Res, 40 (2007), pp. 97-112
[2.]
D. Xu, H. Liu, M. Komai-Koma.
Direct and indirect role of toll-like receptor in T cell mediated immunity [revisión].
Cell Mol Inmunol, 1 (2004), pp. 239-246
[3.]
V. Redecke, H. Häcker, S. Datta, A. Fermin, P. Pitha, D. Broide, et al.
Cutting edge: activation of toll-like receptor 2 induces a Th2 immune respose and promote experimental asthma.
J Immunol, 172 (2004), pp. 2739-2743
[4.]
C. Duez, P. Gosset, A. Tonnel.
Dendritic cells and toll-like receptors in allergy and asthma [revisión].
Eur J Dermatol, 16 (2006), pp. 12-16
[5.]
Y. Gon.
Toll-Like receptors and airway inflammation [revision].
Allergol Int, 57 (2008), pp. 33-37
[6.]
B. Lemaitre, E. Nicolas, L. Michaut, J.M. Reichhart, J.A. Hoffmann.
The dorsoventral regulatory gene cassette spatzle/toll/cactus controls the potent antifungal response in Drosophila adults.
Cell, 86 (1996), pp. 973-983
[7.]
R. Medzhitov, P. Preston-Hurlburt, C.A. Janeway.
A human homologue of the Drosophila toll protein signals activation of adaptative immunity.
Nature, 388 (1997), pp. 394-397
[8.]
S. Akira, S. Uematsu, O. Takeuchi.
Pathogen recognition and innate immunity.
[9.]
E.M. Creagh, L.A. O’Neill.
TLRs, NLRs and RLRs: a trinity of pathogen sensors that co-operate in innate immunity.
Trends Immunol, 27 (2006), pp. 352-357
[10.]
S. Akira.
Mammalian. Toll-like receptors.
Curr Opin Immunol, 15 (2003), pp. 5-11
[11.]
M. Yamamoto, K. Takeda, S. Akira.
TIR domain-containing adaptors define the specificity of TLR signaling.
Mol Immunol, 40 (2004), pp. 861-868
[12.]
E.B. Kopp, R. Medzhitov.
The toll-receptor family and control of innate immunity.
Curr Opin Immunol, 11 (1999), pp. 13-18
[13.]
N.J. Gay, F.J. Keith.
Drosophila toll and IL-1 receptor.
Nature, 351 (1991), pp. 355-356
[14.]
J.H. Fritz, D.E. Girardon.
How toll-like receptors and Nod-like receptors contribute to innate immunity in mammals.
J Endotoxin Res, 11 (2005), pp. 390-394
[15.]
K. Takeda, T. Kaisho, S. Akira.
Toll-like receptors.
Annu Rev Immunol, 27 (2006), pp. 352-357
[16.]
C.W. Eiland, S. Knapp, S. Florquin, A.F. De Vos, K. Takeda, S. Akira, et al.
Non-mannose-capped lipoarabinomannan induces ling inflammation via toll-like receptor 2.
Am J Respir Crit Care Med, 170 (2004), pp. 1367-1374
[17.]
J. Sa Silva, K. Soldau, U. Cristen, P.S. Tobias, R.J. Ulevith.
Lipopolysaccharide is in close proximity to each of the proteins in its membrane receptor complex, transfer from CD14 to TLR4 and MD-2.
J Biol Chem, 276 (2001), pp. 21129-21135
[18.]
K.D. Smith, E. Andersen, F. Hayashi, B.T. Cookson, A. Aderem.
Toll-like receptor 5 recognizes a conserved site on flagellin required for protofilament formation and bacterial motility.
Nat Immunol, 4 (2003), pp. 1247-1253
[19.]
C.A. Jefferies, K.A. Fitzgerald.
Interferon gene regulation:not all roads lead to Tolls.
Trends Mol Med, 11 (2005), pp. 403-411
[20.]
A.G. Bowie, I.R. Haga.
The role of toll-like receptors in the host response to viruses.
Mol Immunol, 42 (2005), pp. 859-867
[21.]
K.W. Boehme, T. Compton.
Innate sensing of viruses by toll-like receptors.
[22.]
T. Kawai, S. Sato, K.J. Ishii, C. Coban, H. Hemmi, M. Yamamoto, et al.
Interferon-alpha induction through toll-like receptors involves a direct interaction of IRF7 with MyD88 and TRAF6.
Nat Immunol, 5 (2004), pp. 1061-1068
[23.]
P.N. Moynagh.
TLR signalling and activation of IRFs: revisiting old friends from the NF-kappaB pathway.
Trends Immunol, 26 (2005), pp. 469-476
[24.]
X. Du, A. Poltorak, Y. Wei, B. Beutler.
Three novel mammalian toll-like receptors: gene structure, expression, and evolution.
Eur Cytokine Netw, 11 (2000), pp. 362-371
[25.]
T.H. Chuang, R.J. Ulevitch.
Cloning and characterization of a sub-family of human toll-like receptors: hTLR7, hTLR8 and hTLR9.
Eur Cytokine Netw, 11 (2000), pp. 372-378
[26.]
F.L. Rock, G. Hardiman, J.C. Timans, R.A. Kastelein, J.F. Bazan.
A family of human receptors structurally related to Drosophila toll.
Proc Natl Acad Sci U S A, 95 (1998), pp. 588-593
[27.]
K.A. Zarember, P.J. Godowski.
Tissue expression of human toll-like receptors and differential regulation of toll-like receptor mRNAs in leukocytes in response to microbes, their products, and cytokines.
J Immunol, 168 (2002), pp. 554-561
[fe de errores en: J Immunol. 2002;169:1136.]
[28.]
M.T. Ochoa, A.J. Legaspi, Z. Hatziris, P.J. Godowski, R.L. Modlin, P.A. Sieling.
Distribution of toll-like receptor 1 and toll-like receptor 2 in human lymphoid tissue.
Immunology, 108 (2003), pp. 10-15
[29.]
M. Muzio, D. Bosisio, N. Polentarutti, G. D’Amico, A. Stoppacciaro, R. Mancinelli, et al.
Differential expression and regulation of toll-like receptors (TLR) in human leukocytes: selective expression of TLR3 in dendritic cells.
J Immunol, 164 (2000), pp. 5998-6004
[30.]
V. Hornung, S. Rothenfusser, S. Britsch, A. Krug, B. Jahrsdörfer, T. Giese, et al.
Quantitative expression of toll-like receptor 1-10 mRNA in cellular subsets of human peripheral blood mononuclear cells and sensitivity to CpG oligodeoxynucleotides.
J Immunol, 168 (2002), pp. 4531-4537
[31.]
T. Compton, E.A. Kurt-Jones, K.W. Boehme, J. Belko, E. Latz, D.T. Golenbock, et al.
Human cytomegalovirus activates inflammatory cytokine responses via CD14 and toll-like receptor 2.
J Virol, 77 (2003), pp. 4588-4596
[32.]
M. Muroi, T. Ohnishi, K. Tanamoto.
Regions of the mouse CD14 molecule required for toll-like receptor 2- and 4-mediated activation of NF-kappa B.
J Biol Chem, 277 (2002), pp. 42372-42379
[33.]
M. Rehli.
Of mice and men: species variations of toll-like receptor expression.
Trends Immunol, 23 (2002), pp. 375-378
[34.]
H. Zhang, P.N. Tay, W. Cao, W. Li, J. Lu.
Integrin-nucleated toll-like receptor (TLR) dimerization reveals subcellular targeting of TLRs and distinct mechanisms of TLR4 activation and signaling.
FEBS Lett, 532 (2002), pp. 171-176
[35.]
O. Takeuchi, T. Kawai, H. Sanjo, N.G. Copeland, D.J. Gilbert, N.A. Jenkins, et al.
TLR6: a novel member of an expanding toll-like receptor family.
Gene, 231 (1999), pp. 59-65
[36.]
H. Heine, E. Lien.
Toll-like receptors and their function in innate and adaptive immunity.
Int Arch Allergy Immunol, 130 (2003), pp. 180-192
[37.]
A. Dunne, L.A. O’Neill.
The interleukin-1 receptor/toll-like receptor superfamily: signal transduction during inflammation and host defense.
Sci STKE, 171 (2003), pp. re3
[38.]
T.H. Chuang, R.J. Ulevitch.
Cloning and characterization of a sub-family of human toll-like receptors: hTLR7, hTLR8 and hTLR9.
Eur Cytokine Netw, 11 (2000), pp. 372-378
[39.]
G.H. Skrepnek, S.V. Skrepnek.
Epidemiology, clinical and economic burden, and natural history of chronic obstructive pulmonary disease and asthma.
Am J Manag Care, 10 (2004), pp. S129-S138
[40.]
D.Y. Leung, T. Bieber.
Atopic dermatitis.
[41.]
S. Hoffjan, C. Ober.
Present status on the genetic studies of asthma.
Curr Opin Immunol, 14 (2002), pp. 709-717
[42.]
J.A. Castillo, J. Mullol.
Rhinitis and asthma comorbidity in Spain: the RINAIR study.
Arch Bronconeumol, 44 (2008), pp. 597-603
[43.]
A.M. Bowcock, W.O. Cookson.
The genetics of psoriasis, psoriatic arthritis and atopic dermatitis.
Hum Mol Genet, 13 (2004), pp. R43-R55
Spec No 1
[44.]
N.A. Molfino.
Genetics of COPD.
Chest, 125 (2004), pp. 1929-1940
[45.]
A. Arnedo-Pena, L. García-Marcos, I. Carvajal, R. Busquets, M. Morales, C. Miner, et al.
Air pollution and recent symptoms of asthma, allergic rhinitis, and atopic eczema in schoolchildren aged between 6 and 7 years.
Arch Bronconeumol, 45 (2009), pp. 224-229
[46.]
F.D. Martínez.
The coming-of-age of the hygiene hypothesis.
Respir Res, 2 (2001), pp. 129-132
[47.]
S.T. Weiss.
Eat dirt – the hygiene hypothesis and allergic diseases.
N Engl J Med, 347 (2002), pp. 930-931
[48.]
M.T. Elías, R. Sánchez, A. Cayuela, F.J. Álvarez, J.A. Romero, A. García, et al.
Risk factors for bronchial asthma in patients with rhinitis.
Arch Bronconeumol, 37 (2001), pp. 429-434
[49.]
L. Prieto, C. Morales.
Allergic rhinitis and asthma as probable clinical manifestations of the same process.
Arch Bronconeumol, 34 (1998), pp. 277-280
[50.]
M.J. Leckie, A. Ten Brinke, J. Khan, Z. Diamant, B.J. O’Connor, C.M. Walls, et al.
Effect of an interleukin-5 blocking monoclonal antibody on eosinophiles, airway hyperresponsiveness and the response to allergen in patients with asthma.
Lancet, 356 (2000), pp. 2144-2148
[51.]
S.A. Bryan, B.J. O’Connor, S. Matti, M.J. Leckie, V. Kanabar, J. Khan, et al.
Effects of recombinant human interleukin-12 on eosinophiles, airway hyper-responsiveness, and the late asthmatic response.
Lancet, 356 (2000), pp. 2149-2153
[52.]
The ENFUMOSA Study Group.
The ENFUMOSA cross-sectional European multicentre study of the clinical phenotype of chronic severe asthma.
Eur Resp J, 22 (2003), pp. 470-477
[53.]
M.M. Pizzichini, E. Pizzichini, A. Efthimiadis, A.J. Chauhan, S.L. Johnston, P. Hussack, et al.
Asthma and natural cold. Inflammatory indices in induced sputum: a feasibility study.
Am J Resp Crit Care Med, 158 (1998), pp. 1178-1184
[54.]
S. Sur, T.B. Crotty, G.M. Kephart, B.A. Hyma, T.V. Colby, C.E. Reed, et al.
Sudden-onset fatal asthma. A distinct entity with few eosinophiles and relatively more neutrophils in the airway submucosa.
Am Rev Respir Dis, 148 (1993), pp. 713-719
[55.]
F.J. Álvarez, F. Valenzuela, J.A. Rodríguez, R. Sánchez, E. Tabernero, J. Castillo.
Blood levels of eosinophil cationic protein in patients with allergic rhinitis. Evolution after treatment with corticoids.
Arch Bronconeumol, 33 (1997), pp. 6-11
[56.]
F.J. Álvarez, J.A. Rodríguez, F. Valenzuela, F. Capote, R. Sánchez, J. Castillo.
Inflammation mediators (eosinophilic cationic protein, ECP) in a normal population and in patients with bronchial asthma or allergic rhinitis.
Arch Bronconeumol, 31 (1995), pp. 280-286
[57.]
P.G. Gibson, J.L. Simpson, N. Saltos.
Heterogeneity of airway inflammation in persistent asthma.
Chest, 119 (2001), pp. 1329-1336
[58.]
I.D. Pavord, C.E. Brightling, G. Woltmann, A.J. Wardlaw.
Non-eosinophilic corticosteroid unresponsive asthma.
Lancet, 353 (1999), pp. 2213-2214
[59.]
M.O. Turner, P. Hussack, M.R. Sears, J. Dolovich, F.E. Hargreave.
Exacerbations of asthma without sputum eosinophilia.
Thorax, 50 (1995), pp. 1057-1061
[60.]
W. Anees, V. Huggins, I.D. Pavord, A.S. Robertson, P.S. Burge.
Occupational asthma due to low molecular weight agents:eosinophilic and non-eosinophilic variants.
Thorax, 57 (2002), pp. 231-236
[61.]
S.E. Wenzel, L.B. Schwartz, E.L. Langmack, J.L. Halliday, J.B. Trudeau, R.L. Gibbs, et al.
Evidence that severe asthma can be divided pathologically into two inflammatory subtypes with distinct physiologic and clinical characteristics.
Am J Respir Crit Care Med, 160 (1999), pp. 1001-1008
[62.]
I. Helenius, A. Lumme, T. Haahtela.
Asthma, airway inflammation and treatment in elite athletes.
Sport Med, 35 (2005), pp. 565-574
[63.]
A. Lumme, T. Haahtela, J. Ounap, P. Rytilä, Y. Obase, M. Helenius, et al.
Airway inflammation, bronchial hyperresponsiveness and asthma in elite ice hockey players.
Eur Respir J, 22 (2003), pp. 113-117
[64.]
S.E. Wenzel, S. Balzar, M. Cundall, H.W. Chu.
Subepithelial basement membrane immunoreactivity for matrix, metalloproteinase 9:association with asthma severity, neutrophilic inflammation and wound repair.
J Allergy Clin Immunol, 111 (2003), pp. 1345-1352
[65.]
M. Cundall, Y. Sun, C. Miranda, J.B. Trudeau, S. Barnes, S.E. Wenzel.
Neutrophil-derived matrix metalloproteinase-9 is increased in severe asthma and poorly inhibited by glucocorticoids.
J Allergy Clin Immunol, 112 (2003), pp. 1064-1071
[66.]
J.L. Simpson, R. Scott, M.J. Boyle, P.G. Gibson.
Inflammatory subtypes in asthma: assessment and identification using sputum.
[67.]
J. Douwes, P. Gibson, J. Pekkanen, N. Pearce.
Non-eosinophilic asthma: importance and posible mechanisms.
Thorax, 47 (2002), pp. 643-648
[68.]
C.A. Janeway, R. Medzhitov.
Innate immune recognition.
Annu Rev Immunol, 20 (2002), pp. 197-216
[69.]
J. Simpson, T. Grissell, J. Douwes, R. Scott, M. Boyle, P. Gibson.
Innate immune activation in neutrophilic asthma and bronquiectasis.
Thorax, 62 (2007), pp. 211-218
[70.]
W.C. Tan.
Viruses in asthma exacerbations.
Curr Opin Pulm Med, 11 (2005), pp. 21-26
[71.]
J.N. Kline, A.M. Krieg.
Toll-like receptor 9 activation with CpG oligodeoxynucleotides for asthma therapy.
Drug News Perspect, 21 (2008), pp. 434-439
[72.]
D.E. Fonseca, J.N. Kline.
Use of CpG oligonucleotides in treatment of asthma and allergic disease.
Adv Frug Deliv Rev, 61 (2009), pp. 256-262
[73.]
J.N. Kline.
Inmunotherapy of asthma using CpG oligodeoxynucleotides.
Immunol Res, 39 (2007), pp. 279-286
[74.]
Peter Fritsch.
Dermatologie Venerologie: Grundlagen.
Springer, (2004),
[75.]
Q. Du, L.F. Zhou, Z. Chen, X.Y. Gu, M. Huang, K.S. Yin.
Imiquimod, a toll like receptor 7 ligand, inhibits airway remodeling in a murine model of chronic asthma.
Clin Exp Pharmacol Physiol, 36 (2009), pp. 43-48
[76.]
S. Davila, M. Hibberd, R. Hari, H. Wong, E. Sahiratmadja, C. Bonnard, et al.
Genetic association and expression studies indicate a role of toll-like receptor 8 in pulmonary tuberculosis.
PLoS Genet, 4 (2008), pp. e1000218
[77.]
Y. Imai, K. Kuba, G. Neely, R. Yaghubian-Malhami, T. PerKmann, G. Loo, et al.
Identification of oxidative stress and toll-like receptor 4 signaling as a key pathway of acute lung injury.
[78.]
L. Murray, D. Knight, L. McAlonan, R. Argentieri, A. Joshi, F. Shaheen, et al.
Deleterious role of TLR3 during hyperoxia-induced acute lung injury.
Am J Respir Crit Care Med, 178 (2008), pp. 1227-1237
[79.]
J.P. Wong, M.F. Christopher, S. Viswanathan, N. Karpoff, X. Dai, D. Das, et al.
Activation of toll-like receptor signaling pathway for protection against influenza virus infection.
Vaccine, 27 (2009), pp. 3481-3483
[80.]
H. Sarir, P.A. Henricks, A.H. Van Houwelingen, F.P. Nijkamp, G. Folkerts.
Cells, mediators and toll-like receptors in COPD.
Eur J Pharmacol, 585 (2008), pp. 346-353
[81.]
S.I. Rennard, J. Vestbo.
COPD: the dangerous underestimate of 15%.
Lancet, 367 (2006), pp. 1216-1219
[82.]
G. Devereux.
ABC of chronic obstructive pulmonary disease. Definition, epidemiology, and risk factors.
BMJ, 332 (2006), pp. 1142-1144
[83.]
P.A. Martorana, T. Brand, C. Gardi, P. Van Even, M.M. De Santi, P. Calzoni, et al.
The pallid mouse. A model of genetic alpha 1-antitrypsin deficiency.
Lab Invest, 68 (1993), pp. 233-241
[84.]
R.D. Hautamaki, D.K. Kobayashi, R.M. Senior, S.D. Shapiro.
Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice.
Science, 277 (1997), pp. 2002-2004
[85.]
M. Kuro-o, Y. Matsumura, H. Aizawa, H. Kawaguchi, T. Suga, T. Utsugi, et al.
Mutation of the mouse klotho gene leads to a syndrome resembling ageing.
Nature, 390 (1997), pp. 45-51
[86.]
S.E. Wert, M. Yoshida, A.M. LeVine, M. Ikegami, T. Jones, G.F. Ross, et al.
Increased metalloproteinase activity, oxidant production, and emphysema in surfactant protein D gene-inactivated mice.
Proc Natl Acad Sci U S A, 97 (2000), pp. 5972-5977
[87.]
C.A. Smith, D.J. Harrison.
Association between polymorphism in gene for microsomal epoxide hydrolase and susceptibility to emphysema.
[88.]
T. Rangasamy, C.Y. Cho, R.K. Thimmulappa, L. Zhen, S.S. Srisuma, T.W. Kensler, et al.
Genetic ablation of Nrf2 enhances susceptibility to cigarette smoke-induced emphysema in mice.
J Clin Invest, 114 (2004), pp. 1248-1259
[89.]
W. MacNee.
Pulmonary and systemic oxidant/antioxidant imbalance in chronic obstructive pulmonary disease.
Proc Am Thorac Soc, 2 (2005), pp. 50-60
[90.]
X. Zhang, P. Shan, G. Jiang, L. Cohn, P. Lee.
Research article. Toll-like receptor 4 deficiency causes pulmonary emphysema.
J Clin Invest, 116 (2006), pp. 3050-3059
[91.]
B. Fuchs, A. Braun.
Modulation of asthma and allergy by addressing toll-like receptor 2.
J Occup Med Toxicol, 3 (2008), pp. S5
[92.]
J. Pons, J. Sauleda, V. Regueiro, C. Santos, M. López, J. Ferrer, et al.
Expression of toll-like receptor 2 is up-regulated in monocytes from patients with chronic obstructive pulmonary disease.
Respir Res, 7 (2006), pp. 64
[93.]
M.J. Paul-Clark, S.K. McMaster, R. Sorrentino, S. Sriskandan, L.K. Bailey, L. Moreno, et al.
Toll-like receptor 2 is essential for the sensing of oxidants during inflammation.
Am J Respir Crit Care Med, 179 (2009), pp. 299-306
[94.]
D. Droemann, T. Goldmann, T. Tiedje, P. Zabel, K. Dalhoff, B. Schaaf.
Toll-like receptor 2 expression is decreased on alveolar macrophages in cigarette smokers and COPD patients.
Respir Res, 6 (2005), pp. 68
[95.]
M. Zhou, H.Y. Wan, S.G. Huang, B. Li, M. Li.
Expression of toll-like receptor 4 in human alveolar epithelial cells and its role in cellular inflammation.
Zhoghua Y Xue Za Zhi, 88 (2008), pp. 2112-2116
[96.]
J. Pons, J. Sauleda, V. Regueiro, C. Santos, M. López, J. Ferrer, et al.
Expression of toll-like receptor 2 is up-regulated in monocytes from patients with chronic obstructive pulmonary disease.
Respir Res, 7 (2006), pp. 64
[97.]
E. Doz, N. Noulin, E. Boichot, I. Guénon, L. Fick, M. Le Bert, et al.
Cigarette smoke-induced pulmonary inflammation is TLR4/MyD88 and IL-1R1/MyD88 signaling dependent.
J Immunol, 180 (2008), pp. 1169-1178
[98.]
P.S. Noakers, J. Hale, R. Thomas, C. Lane, S.G. Devadason, S.L. Prescott.
Maternal smoking is associated with impaired neonatal toll-like receptor mediated immune responses.
Eur Respir J, 28 (2006), pp. 675-677
[99.]
S. Hoffjan, S. Stemmler, Q. Parwez, E. Petrasch-Parwez, A. Umut, G. Rohde, et al.
Evaluation of the toll-like receptor 6 Ser249Pro polymorphism in patients with asthma, atopic dermatitis and chronic obstructive pulmonary disease.
BMC Med Genet, 6 (2005), pp. 34
[100.]
D.A. Meyers, M.J. Larj, L. Lange.
Genetics of asthma and COPD. Similar results for different phenotypes.
[101.]
T. Homma, A. Kato, N. Hashimoto, J. Batchelor, M. Yoshikawa, S. Imai, et al.
Corticosteroid and cytokines synergistically enhance toll-like receptor 2 expression in respiratory epithelial cells.
Am J Respir Cell Mol Biol, 31 (2004), pp. 463-469
[102.]
C.J. Blohmake, R.E. Victor, A.F. Hirschfeld, I.M. Elias, D.G. Hancock, C.R. Lane, et al.
Innate immunity mediated by TLR5 as a novel antiinflamatory target for cystic fibrosis lung disease.
J Immunol, 180 (2008), pp. 7764-7773
[103.]
B. Koller, M. Kappler, P. Latzin, A. Gaggar, M. Schreiner, S. Takyar, et al.
TLR expression on neutrophils at the pulmonary site of infection: TLR1/TLR2-mediated up-regulation of TLR5 expression in cystic fibrosis lung disease.
J Immunol, 181 (2008), pp. 2753-2763
[104.]
C. Greene, P. Branagan, N. McElvaney.
Toll-like receptors as therapeutic targets in cystic fibrosis.
Expert Opin Ther Targets, 12 (2008), pp. 1481-1495
[105.]
M. Vaneker, L. Joosten, L. Heuks, D. Snijdelaar, F. Halbertsma, J. Egmond, et al.
Low-tidal-volume mechanical ventilation induces a toll like receptor 4-dependent inflammatory response in healthy mice.
Anesthesiology, 109 (2008), pp. 465-472
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