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Review
. 2017 Jun 22:12:1857-1865.
doi: 10.2147/COPD.S136592. eCollection 2017.

Th17 profile in COPD exacerbations

Marco Antonio Ponce-Gallegos  1   2   3 , Alejandra Ramírez-Venegas  4 , Ramcés Falfán-Valencia  1
Affiliations
Review

Th17 profile in COPD exacerbations

Marco Antonio Ponce-Gallegos et al. Int J Chron Obstruct Pulmon Dis. .

Abstract

COPD is characterized by an ongoing inflammatory process of the airways that leads to obstruction or limitation of airflow. It is mainly associated with exposure to cigarette smoke. In addition, it is considered, at present, a serious public health problem, ranking fourth in mortality worldwide. Many cells participate in the pathophysiology of COPD, the most important are neutrophils, macrophages and CD4+ and CD8+ T cells. Neutrophil migration to the inflammation area could be mediated largely by cytokines related to CD4+ Th17 lymphocytes, because it has been shown that IL-17A, IL-17F and IL-22 act as inducers for CXCL8, CXCL1, CXCL5, G-CSF, and GM-CSF secretion by epithelial cells of the airways. The aims of these molecules are differentiation, proliferation and recruitment of neutrophils. Furthermore, it is believed that CD4+ lymphocytes Th17 may be involved in protection against pathogens for which Th1 and Th2 are not prepared to fight. In COPD exacerbations, there is an increased cellularity in the lung region and respiratory tract. Therefore, the increase in the number of neutrophils and macrophages in the airways and the increase in proinflammatory cytokines are directly related to the severity of exacerbations and that is the importance of the functions of Th17 profile in this entity.

Keywords: IL-17A; IL-17F; IL-22; bacteria; tobacco smoking; virus.

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Conflict of interest statement

Disclosure The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
When airway epithelium is exposed to harmful substances, such as those contained in cigarette smoke, it changes its structure. Note: These changes include the loss of close junctions between ciliated epithelial cells, shortening of cilia, hyperplasia of goblet-producing goblet cells and basal cells, in addition to squamous epithelial cell metaplasia. Abbreviation: DAMPs, damage-associated molecular patterns.
Figure 2
Figure 2
With exposure to harmful agents, epithelial cells present in the airways release DAMPs, such as HSPs that are recognized by membrane receptors (TLRs, for example) present in leukocytes, such as DCs. Note: This leads to an intracellular signaling cascade commanded by MyD88 and the transcription factor NF-κB, culminating in the release of proinflammatory cytokines such as IL-1β and IL-18, important mediators in the pathophysiology of COPD. Abbreviations: DAMPs, damage-associated molecular patterns; HSP, heat shock protein; TLR, Toll-like receptor; DC, dendritic cell; HMGB1, high mobility group box 1; IL, interleukin.
Figure 3
Figure 3
When dendritic cells pick up DAMPs, they travel to the lymph nodes where they are presented to the virgin T lymphocytes through the class II MHC-11, which binds to the TCR present on the cell membrane. Notes: Along with the existing cytokine microenvironment, polarization to Th17 CD4+ occurs. One of its main functions is the differentiation, activation and recruitment of neutrophils to the zone of inflammation, which contribute to the destruction of the lung parenchyma with the release of NE and other metalloproteases. Abbreviations: DAMPs, damage-associated molecular patterns; IL, interleukin; MHC, major histocompatibility complex; TCR, T cell receptor; NE, neutrophil elastase; DC, dendritic cell; IL, interleukin.
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