Immune-Modulation in Chronic Obstructive Pulmonary Disease: Current Concepts and Future Strategies

Abstract

Chronic obstructive pulmonary disease (COPD) is caused by the chronic inhalation of toxic particles and gases that are primarily but not exclusively derived from cigarette smoke that may be either actively or passively inhaled, which initiates a persistent innate and adaptive immune response in the lung. This immune response is associated with an aberrant tissue repair and remodeling process that results in varying degrees of chronic inflammation with excess production of mucus in the central airways and permanent destruction of the smaller conducting airways and gas exchanging surface in the peripheral lung. Currently, the primary aims of treatment in COPD are bronchodilation (inhaled short-and long-acting β-agonist and antimuscarinic therapies), to control symptoms and nonspecific broad-acting anti-inflammatory agents (inhaled and oral corticosteroids, phosphor-di-esterase inhibitors, and macrolides). That provide symptomatic relief but have little or no impact on either disease progression or mortality. As our understanding of the immune pathogenesis of the COPD improves, available immune modulation therapies have the potential to alter or interfere with damaging immune pathways, thereby slowing relentless progression of lung tissue destruction. The purpose of this brief review is to discuss our current understanding of the immune pathogenesis of both the airways and parenchymal injury as well as the dysfunctional tissue repair process to propose immune modulating interventions in an attempt to stabilize or return these pathological changes to their normal state. The ultimate goal of the immune modulation therapy is to improve both morbidity and mortality associated with COPD.

Clinical Characteristics of Patients with Severe Pneumonia Caused by the SARS-CoV-2 in Wuhan, China

“…A previous study reported that hypoalbuminemia is a potent, dose-dependent predictor of poor outcomes for pneumonia with COVID-19 infection [ 12 ]. An elevated level of CRP may be associated with the inflammatory response and cytokine storms caused by SARS-CoV-2 in the blood vessels [ 13 ]. These results were consistent with a previous study, which showed that the CRP level was positively correlated with the pneumonia severity [ 14 ].…”

Immune Modulation in Lung Cancer: Current Concepts and Future Strategies

“…In most patients, COPD is characterized by T-helper 1 (Th1) and Th17-polarized inflammation, with local production of interferon (IFN)γ, tumor necrosis factor (TNF)α, interleukin (IL)-1b, IL-8, and other cytokines [20, 27, 28]. These recruit neutrophils, M1-polarized macrophages, and cytotoxic T cells, whose reactive oxygen species not only destruct the extracellular matrix to cause emphysema [29], but also aggravate smoking-induced DNA damage to initiate tumorigenesis in bronchial and alveolar epithelial cells (Fig.…”

Overview of clinical outcome and therapeutic effectiveness of Favipiravir in patients with COVID-19 admitted to intensive care unit, Riyadh, Saudi Arabia

“…The inflammatory response and cytokine storms caused by SARS-CoV-2 in the blood vessels lead to an increased level of CRP [52] .This is in accordance with previous studies, which showed that the CRP level was positively correlated with the pneumonia severity [53] .Our data showed CRP values in COVID – 19 patients in the FVP therapy arm (106.03 ± 85.58) is much less than the control arm without FVP treatment (170.55 ± 282.69); P=0.016. However, a study by Mortaz et al [54] , on the effect of antiviral therapy (FVP or Kaletra) for 7 days on COVID-19 infected individuals showed a significant elevation in serum levels of IL-8 in non-ICU patients and TNFα, IL-1β, and IL-6 in ICU patients.…”