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J u n e 2 5 - 2 6 , 2 0 1 8 | A m s t e r d a m , N e t h e r l a n d s
International Journal of Respiratory Medicine | Volume 3
Page 12
LUNG CANCER AND COPD
5th International Congress on
Chronic obstructive pulmonary disease (COPD) is a slowly progressive
condition with high morbidity and mortality. Inhaled irritants are linked
to COPD development, with cigarette smoke being the important factor.
Manifestation of COPD includes two main components, emphysema and
chronic obstructive bronchitis. An important feature is persistent inflammatory
process, characterized by involvement of many immune cells, including
neutrophils, macrophages, T lymphocytes, B lymphocytes, and eosinophil’s.
Activation of these cells is mediated by different immune mediators. Several
pro-inflammatory cytokines play important roles during development and
progression of COPD. Cytokines identified as pathophysiological mediators of
COPDare interleukin (IL)-1β,IL-6, tumor necrosis factorTNF-α interferon (IFN)-γ,
IL-8, IL-17, IL-18 and IL-32. Cigarette smoke can directly activate multiple cells,
including cells such as pulmonary macrophages and bronchial epithelial cells,
resulting in release of pro-inflammatory cytokines. Increased levels of these
cytokines result in activation and recruitment of inflammatory cells, leading
to inflammation and eventually to pulmonary tissue destruction. Numbers of
immune cells reactive to IL-1β are increased in bronchial biopsies frompatients
with stable COPD along with elevated IL-1β levels in sputum, bronchoalveolar
lavage and serum. Systemic and local levels of IL-6 are elevated in patients
with stable COPD. IL-6may also significantly contribute to progression of COPD
by playing an important role in autoimmune response in patients with more
severe stable COPD. TNF-α activates immune cells and bronchial epithelial
and smooth muscle cells to release inflammatory mediators, such as oxidants,
resulting in progressive airway remodeling. Sputum levels of these cytokines
are elevated in patients during COPD exacerbation.
Biography
John Klir has completed his PhD in Physiology
fromUniversity of Illinois, MD fromSaba Universi-
ty School of Medicine and postgraduate training
fromUniversity of Michigan School of Medicine in
areas of Immune-Pathophysiology, namely roles
of cytokines as pro-inflammatory mediators. His
work resulted in significant contribution to area of
cytokine research, as evidenced by multiple pub-
lications.
E-BABE ROLE OF PRO-INFLAMMATORY
CYTOKINES IN DEVELOPMENT
AND PROGRESSION OF CHRONIC
OBSTRUCTIVE PULMONARY DISEASE
John Klir
American International Medical University
Saint Lucia
John Klir, Int J Respir Med 2018, Volume 3