Orvosi Hetilap
Volume/Issue:
Volume 158: Issue 13
Az asthma bronchiale fenotípusai
Author: László Béla Nagy 1
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  • 1 Felsődobsza, Thököly u. 1., 3847
DOI:
https://doi.org/10.1556/650.2017.30702
Page Count:
491–498
Publication Date:
01 Apr 2017
Online Publication Date:
Apr 2017
Article Category:
Review Article
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Absztrakt:

Egyre inkább felismerjük, hogy az asthma bronchiale heterogén entitás, amely különböző fenotípusokat ölel fel. A hatásosabb, személyre szabott terápia kulcsa a specifikus fenotípus azonosítása. Az asthma-fenotipizálás legkorábbi kísérleteként ajánlották extrinszik és intrinszik típusba sorolását. A klinikai asthmát elsődlegesen allergiás (atopiás) és nem allergiás (nem atopiás) asthmára oszthatjuk. Más fenotípusok a kiváltó tényezőkön alapulnak. Később a fenotipizálást a gyulladás domináló sejtes típusára alapozták. Ez lehet eosinophil vagy noneosinophil. A noneosinophil asthma lehet neutrophil, kevert vagy paucigranulocytás. Az IgE felfedezése nagy áttörést jelentett az asthmakutatásban. Az IgE egy immunglobulin, amelynek központi szerepe van a patomechanizmusban. Később újabb immunfenotípusokat azonosítottak: T helper-2 magas és T helper-2 alacsony altípus. A neutrophil asthma elsődlegesen T helper-17 indukálta mechanizmuson alapul. A fenotípusok azonosítására fokozódó mértékben alkalmazzák a klaszterelemzést. Az új adatok molekuláris utakat tártak fel. Azonban az asthma fenotipizálása komplex, mivel a különböző fenotípusok átfedik egymást. Ezért a kérdés további kutatásokat igényel. Biomarkerek, mint a vér és köpet eosinophilszintje, a kilégzett nitrogén-oxid-frakció, a szérum-immunglobulin-E, szérumperiostin azonosít különböző asthmafenotípusokat. Orv. Hetil., 2017, 158(13), 491–498.

  • 1

    Global Initiative for Asthma. 2016. http://www.ginaasthma.org
  • 2

    Coca, A. F., Cooke, R. A.: On the classification of the phenomena of hypersensitiviness. J. Immunol., 1923, 8, 163–182.

  • 3

    Keeney, E. I.: The history of asthma from Hippocrates to Meltzer. J. Allergy Clin. Immunol., 1964, 35, 215–226.

  • 4

    Auer, J., Lewis, P. A.: The physiology of the immediate reaction of anaphylaxis in the guinea-pig. J. Exp. Med., 1910, 12, 151–175.

  • 5

    Bousquet, J., Chanez, P., Lacoste, J. Y., et al.: Eosinophilic inflammation in asthma. NEJM, 1990, 323, 1033–1039.

  • 6

    Tiffeneau, R.: Hyperexcitabilité bronchomotrice de l’asthmatique, sequelle des agressions bronchosonstrictives allergiques. Allergy, 1959, 14, 416–432.

  • 7

    Walker, C., Bode, E., Boer, L., et al.: Allergic and nonallergic asthmatics have distinct patterns of T-cell activation and cytokine production in peripheral blood and bronchoalveolar lavage. Am. Rev. Respir. Dis., 1992, 146, 109–115.

  • 8

    Nair, P., Dasgupta, A., Brightling, C. E., et al.: How to diagnose and phenotype asthma. Clin. Chest Med., 2012, 33, 445–457.

  • 9

    Cooke, R. A.: Asthma in children. Its causes and treatment. JAMA, 1934, 102, 664–668.

  • 10

    Hajós, M.: The pathogenesis and therapy of asthma bronchiale. [Az asthma bronchiale pathogenezise és therapiája.] Orvtud. Akt. Probl., 1973, 1, 45–89. [Hungarian]

  • 11

    Kraszkó, P., Angyal, I.: Does “infectious” asthma bronchiale exist? [Van-e „infekt” asthma bronchiale?] Pneumol. Hung., 1984, 37, 495–499. [Hungarian]

  • 12

    Jackson, D. J., Makrinioti, H., Rana, B. M., et al.: IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo. Am. J. Respir. Crit. Care Med., 2014, 190, 1373–1382.

  • 13

    Kowalski, M. L., Cieślak, M., Pérez-Novo, C. A., et al.: Clinical and immunological determinants of severe/refractory asthma (SRA): Association with Staphylococcal superantigen-specific IgE antibodies. Allergy, 2011, 66, 32–38.

  • 14

    Samter, M., Beers, R. F.: Intolerance to aspirin? Clinical studies and considerations of its pathogenesis. Ann. Intern. Med., 1968, 68, 975–983.

  • 15

    McNeill, R. S., Nairn, J. R., Ingram, M. G.: Exercise-induced asthma. QJM, 1966, 35, 55–67.

  • 16

    Lessard, A., Turcotte, H., Cormier, Y., et al.: Obesity and asthma. Chest, 2008, 134, 317–323.

  • 17

    Dixon, A. E., Pynter, M. E.: Mechanisms of asthma in obesity. Pleiotrop aspects of obesity produce distinc asthma phenotypes. Am. J. Respir. Cell Mol. Biol., 2016, 54, 601–608.

  • 18

    Gjomarkaj, M., Gaga, M., Bruselle, G., et al.: Frequent exacerbators – a distinc phenotype of severe asthma. Clin. Exp. Allergy, 2014, 44, 212–221.

  • 19

    Opina, M. D., Bleecker, E. R., Meyers, D. A., et al.: The very frequent exacerbator sub-phenotype is seen in all spectrum of asthma severity including milder disease in the Severe Asthma Research Program. Am. J. Respir. Crit. Care Med., 2015, 191, a4182.

  • 20

    Yii, A., Tan, J., Lapperre, T., et al.: Stability of the frequent-exacerbator phenotype in severe asthma: A longitudinal study. Am. J. Respir. Crit. Care Med., 2015, 191, A4149.

  • 21

    Ishizaka, K., Ishizaka, T., Hornbrook, M. M.: Physico-chemical properties of human reaginic antibody. J. Immunol., 1966, 97, 75–85.

  • 22

    Kraszko, P., Beregi, E.: Changes in the IgE content of the serum and bronchial mucosa in extrinsic and intrinsic bronchial asthma. Progr. Resp. Res., 1980, 14, 47–50.

  • 23

    Ying, S., Humbert, M., Meng, Q., et al.: Local expression of ε heavy chain of IgE in the bronchial mucosa in atopic and nonatopic asthma. J. Allergy Clin. Immunol., 2001, 107, 686–692.

  • 24

    Humbert, M., Grant, J. A., Taborda-Barata, L., et al.: High-affinity IgE receptor (FcεRI)-bearing cells in bronchial biopsies from atopic and nonatopic asthma. Am. J. Respir. Crit. Care Med., 1996, 153, 1931–1937.

  • 25

    Kay, A. B.: Leukocytes in asthma. Immunol. Investig., 1988, 17, 679–705.

  • 26

    Simpson, J. L., Scott, R., Boyle, M. J., et al.: Inflammatory subtypes in asthma: Assessment and identification using induced sputum. Respirology, 2006, 11, 54–61.

  • 27

    Horwitz, R. J., Busse, W. W.: Inflammation and asthma. Clin. Chest Med., 1995, 16, 583–602.

  • 28

    Liu, M. C., Hubbard, W. C., Proud, D., et al.: Immediate and late inflammatory responses to ragweed antigen challenge of the peripheral airways in allergic asthmatics. Am. Rev. Respir. Dis., 1991, 144, 51–58.

  • 29

    Korevaar, D. A., Westerhof, G. A, Wang, J., et al.: Diagnostic accuracy of minimally invasive markers for detection of airway eosinophilia in asthma: a systematic review and meta-analysis. Lancet Respir. Med., 2015, 3, 290–300.

  • 30

    Schleich, F. N., Chevremont, A., Paulus, V., et al.: Importance of concomittant local and systemic eosinophilia in uncontrolled asthma. Eur. Respir. J., 2014, 44, 97–108.

  • 31

    Kraszkó, P., Tomcsányi, A., Brunner, M.: The effect of allergen provocation on IgE level and on circulating eosinophil leukocyte count in bronchial asthma. [Allergén provokáció hatása az IgE szintre és a keringő eozinofil leukocitaszámra asthma bronchialéban.] Pneumol. Hung., 1980, 33, 481–486. [Hungarian]

  • 32

    Turner, M. O., Hussack, P., Sears, M. R., et al.: Exacerbations of asthma without sputum eosinophilia. Thorax, 1995, 50, 1057–1061.

  • 33

    Fahy, J. V., Kim, K. W., Liu, J., et al.: Prominent neutrophilic inflammation in sputum from subjects with asthma exacerbation. J. Allergy Clin. Immunol., 1995, 95, 843–852.

  • 34

    Wenzel, S. E., Schwartz, L. B., Langmack, E. L., 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., 1999, 160, 1001–1008.

  • 35

    Mc Grath, K. W., Icitovic, N., Boiushey, H. A., et al.: A large subgroup of mild-to-moderate asthma is persistent noneosinophilic. Am. J. Respir. Crit. Care Med., 2012, 185, 612–619.

  • 36

    Green, R. H., Brightling, C. E., Woltmann, G., et al.: Analysis of induced sputum in adults with asthma: neutrophilia and poor response to inhaled corticosteroids. Thorax, 2002, 57, 875–879.

  • 37

    Haldar, P., Pavord, D.: Noneosinophilic asthma: A distinct clinical and pathologic phenotype. J. Allergy Clin. Immunol., 2007, 119, 1043–1052.

  • 38

    Majewski, S., Ciebiada, M., Domagala, M., et al.: Short-term reproducibility of the inflammatory phenotype in different subgroups of adult asthma cohort. Mediators Inflamm., 2015, 2015, 419039.

  • 39

    Nadif, R., Siroux, V., Boudier, A., et al.: Blood granulocyte patterns as predictors of asthma phenotypes in adults from the EGEA study. Eur. Respir. J., 2016, 48, 1040–1051.

  • 40

    Boudier, A., Curjuric, I., Basagana, X., et al.: Ten-year follow-up of cluster-based asthma phenotypes in adults. Am. J. Respir. Crit. Care Med., 2013, 188, 550–560.

  • 41

    Siroux, V., González, J. R., Bouzigon, E., et al.: Genetic heterogenity of asthma phenotypes identified by a clustering approach. Eur. Respir. J., 2014, 43, 439–452.

  • 42

    Howrylak, J. A., Fuhlbrigge, A. L., Strunk, R. C., et al.: Classification of childhood asthma phenotypes and long-term clinical responses to inhaled antiinflammatory medications. J. Allergy Clin. Immunol., 2014, 133, 1289–1300.

  • 43

    Kim, T. B., Jang, A. S., Kwon, H. K., et al.: Identification of asthma clusters in two independent Korean adult asthma cohort. Eur. Respir. J., 2013, 41, 1308–1314.

  • 44

    Lavoie-Charland, É., Bérube, J. C., Laviolette, M., et al.: Multivariate asthma phenotypes in adults: The Quebec City Case- Control Asthma cohort. Open J. Respir. Dis., 2013, 3, 133–142.

  • 45

    Haldar, P., Pavord, I. D., Shaw, D. E., et al.: Cluster analysis and clinical asthma phenotypes. Am. J. Respir. Crit. Care Med., 2008, 178, 218–224.

  • 46

    Moore, W. C., Meyers, D. A., Wenzel, S. E., et al.: Identification of asthma phenotypes using cluster analysis in the Severe Asthma Research Program. Am. J. Respir. Crit. Care Med., 2010, 181, 315–323.

  • 47

    Siroux, V., Basagana, X., Boudier, A., et al.: Identifying adult asthma phenotypes using a clustering approach. Eur. Respir. J., 2011, 38, 310–317.

  • 48

    Amelink, M., de Nijs, S. B., de Groot, J. C., et al.: Three phenotypes of adult-onset asthma. Allergy, 2013, 68, 674–680.

  • 49

    Robinson, D. S., Hamid, Q., Ying, S., et al.: Predominant TH2 – like bronchoalveolar T-lymphocyte population in atopic asthma. NEJM, 1992, 326, 298–304.

  • 50

    Woodruff, P. G., Modrek, B., Choy, D. F., et al.: T-helper type 2-driven inflammation defines major subphenotypes of asthma. Am. J. Respir. Crit. Care Med., 2009, 180, 388–395.

  • 51

    Sun, Y., Zhou, Q., Yao, W.: Sputum interleukin-17 is increased and associated with airway neutrophilia in patients with severe asthma. Chin. Med. J., 2005, 118, 953–956.

  • 52

    Al-Ramli, W., Préfontaine, D., Chouiali, F., et al.: TH 17-associated cytokines (IL-17A and IL-17F) in severe asthma. J. Allergy Clin. Immunol., 2009, 123, 1185–1187.

  • 53

    Ramirez-Velazquez, C., Castillo, E. C., Guido-Bayardo, L., et al.: IL-17-producing peripherial blood CD177+ neutrophils increase in allergic asthmatic subjects. Allergy Asthma Clin. Immunol., 2013, 9, 23.

  • 54

    Cosmi, L., Maggi, L., Santgarlasci, V., et al.: Identification of a novel subset of human circulating memory CD4+ T cells that produce both IL-17A and IL-4. J. Allergy Clin. Immunol., 2010, 125, 222–230.

  • 55

    Sven, S., Scheers, H., Marijsse, G., et al.: Th2-high asthma: a heterogenous asthma population? Clin. Transl. Allergy, 2015, 5(Suppl. 2), 01.

  • 56

    Wenzel, S. E.: Emergence of biomolecular pathways to define novel asthma phenotypes. Typ-2 immunity and beyond. Am. J. Respir. Cell Mol. Biol., 2016, 55, 1–4.

  • 57

    Pelaia, G., Vatgrella, A., Busceti, M. T., et al.: Cellular mechanisms underlying eosinophilic and neutrophilic airway inflammation in asthma. Mediators Inflamm., 2015, 2015, 879783.

  • 58

    Akdis, C. A., Akdis, M.: Mechanisms of allergen-specific immunotherapy and immun tolerance to allergens. World Allergy Organ. J., 2015, 8, 17.

  • 59

    Raedler, D., Ballenberger, N., Klucker, E., et al.: Identification of novel immune phenotypes for allergic and nonallergic childhood asthma. J. Allergy Clin. Immunol., 2015, 135, 81–91.

  • 60

    Baines, K. J., Simpson, J. L., Wood, L. G., et al.: Sputum gene expression signature of 6 biomarkers discriminates asthma inflammatory phenotypes. J. Allergy Clin. Immunol., 2014, 133, 997–1007.

  • 61

    Modena, B. D., Tedrow, J. R., Milosevic, J., et al.: Gene expression in relation to exhaled nitric oxide identifies novel asthma phenotypes with unique biomolecular pathways. Am. J. Respir. Crit. Care Med., 2014, 190, 1363–1372.

  • 62

    Baines, K. J., Simpson, J. L., Wood, L. G., et al.: Transcriptional phenotypes of asthma defined by gene expression profiling of induced sputum samples. J. Allergy Clin. Immunol., 2011, 127, 153–160.

  • 63

    Yan, X., Chu, J. H., Gomez, J., et al.: Noninvasive analysis of the sputum transcriptome discriminates clinical phenotypes of asthma. Am. J. Respir. Crit. Care Med., 2015, 191, 1116–1125.

  • 64

    Kidd, C. D., Thompson, P. J., Barrett, L., et al.: Histone modifications and asthma. Am. J. Respir. Cell Mol. Biol., 2016, 54, 3–12.

  • 65

    Nicodemus-Johnson, J., Naughton, K. A., Sudi, J., et al.: Genome-wide methylation study identifies an IL-13-induced epigenetic signature in asthmatic airways. Am. J. Respir. Crit. Care Med., 2016, 193, 376–385.

  • 66

    Simpson, J. L., Phipps, S., Baines, K. J., et al.: Elevated expression of the NLRP3 inflammasome in neutrophilic asthma. Eur. Respir. J., 2014, 43, 1067–1076.

  • 67

    Panganiban, R. P., Wang, Y., Howrylak, J., et al.: Circulating microRNAs as biomarkers in patients with allergic rhinitis and asthma. J. Allergy Clin. Immunol., 2016, 137, 1423–1432.

  • 68

    Westerhof, G. A., Korevaar, D. A., Amelink, M., et al.: Biomarkers to identify sputum eosinophilia in different adult asthma phenotypes. Eur. Respir. J., 2015, 46, 688–696.

  • 69

    Wagener, A. H., de Nijs, S. B., Lutter, R., et al.: External validation of blood eosinophil, FENO and serum periostin as surrogate for sputum eosinophils in asthma. Thorax, 2015, 70, 115–120.

  • 70

    Izuhara, K., Conway, S. J., Moore, B. B., et al.: Roles of periostin in respiratory disorders. Am. J. Respir. Crit. Care Med., 2016, 193, 949–956.

  • 71

    Simpson, J. L., Yang, I. A., Upham, J. W., et al.: Periostin levels and eosinophilic inflammation in poorly-controlled asthma. BMC Pulm. Med., 2016, 16, 67.

  • 72

    Jia, G., Erickson, R. W., Choy, D. F., et al.: Periostin is a sytemic biomarker of eosinophilic airway inflammation in asthmatic patients. J. Allergy Clin. Immunol., 2012, 130, 647–654.

  • 73

    Matsusaka, M., Kabata, H., Fukunaga, K., et al.: Phenotype of asthma related with high serum periostin levels. Allergol. Internat., 2015, 64, 175–180.

  • 74

    Nagasaki, T., Matsumoto, H., Kanemitsu, Y., et al.: Using exhaled nitric oxide and serum periostin as a composite marker to identify severe/steroid-insensitive asthma. Am. J. Respir. Crit. Care Dis., 2016, 191, A2494.

  • 75

    Peters, M. C., Mekkonen, Z. K., Yuan, S., et al.: Measures of gene expression in sputum cells can identify TH2-high and TH2-low subtypes of asthma. J. Allergy Clin. Immunol., 2014, 133, 388–394.

  • 76

    Ray, A., Oriss, T. B., Wenzel, S. E.: Emerging molecular phenotypes of asthma. Am. J. Physiol. Lung Cell. Mol. Physiol., 2015, 308, L130–L140.

  • 77

    Silkoff, P. E., Strambu, I, Laviolette, M., et al.: Asthma characteristics and biomarkers from the Airway Disease Endotyping for Personalized Therapeutics (ADEPT) longitudinal profiling study. Respir. Res., 2015, 16, 142.

  • 78

    Little, S. A., Chalmers, G. W., MacLeod, K. J., et al.: Non-invasive markers of airway inflammation as predictors of oral steroid responsiveness in asthma. Thorax, 2000, 55, 232–234.

  • 79

    Jang, A. S., Lee, J. H., Péark, S. W., et al.: Factors influencing the responsiveness to inhaled glucocorticoids of patients with moderate-to-severe asthma. Chest, 2005, 128, 1140–1145.

  • 80

    Barbaro, M. P., Spanevello, A., Palladino, G. P., et al.: Exhaled matrix metalloproteinase-9 (MMP-9) in different biological phenotypes of asthma. Eur. J. Intern. Med., 2014, 25, 92–96.
Cover Orvosi Hetilap
Orvosi Hetilap
Print ISSN:
0030-6002
Online ISSN:
1788-6120
Keywords:
asthma bronchiale; fenotípusok; bronchial asthma; phenotypes

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