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Abstract
The complement mediators are the major effectors of the immune balance, which operates at the interface between the innate and adaptive immunity, and is vital for many immunoregulatory functions. Activation of the complement cascade through the classical, alternative or lectin pathways thus generating opsonins like C3b and C5b, anaphylatoxins C3a and C5a, chemotaxin, and inflammatory mediators, which leads to cellular death. Complement mediators that accelerate the airway remodeling are not well defined; however, an uncontrolled Th2-driven adaptive immune response has been linked to the major pathophysiologic features of asthma, including bronchoconstriction, airway hyperresponsiveness, and airway inflammation. The mechanisms leading to complement mediated airway tissue remodeling, and the effect of therapy on preventing and/or reversing it are not clearly understood. This review highlights complement-mediated inflammation, and the mechanism through it triggers the airway tissue injury and remodeling in the airway epithelium that could serve as potential targets for developing a new drug to rescue the asthma patients.
Highlights
Asthma is a chronic inflammatory disease of the airways distinguished by the variable airflow obstruction and associated increase in airway hyperresponsiveness (AHR) to various stimuli [1,2,3]
Overactivated complement cascade play a key role as effectors of cell-mediated and humoral immune system in pulmonary tissue injury during asthma pathogenesis [15,16,17]
Complement activation has been demonstrated in mouse models of allergic asthma, which highlighted the role of C3a mediated airway hyperresponsiveness, and airway tissue remodeling [21]
Summary
Asthma is a chronic inflammatory disease of the airways distinguished by the variable airflow obstruction and associated increase in airway hyperresponsiveness (AHR) to various stimuli [1,2,3]. TGF-β is one of the leading mediator involved in airway tissue remodeling during asthmatic pathogenesis This profibrotic cytokine is secreted by different inflammatory and epithelial cells including ASM, endothelial cells, fibroblasts, macrophages, and eosinophils [44]. The complement system, with its crucial role in innate and adaptive immunity mediates a variety of effector functions [3, 32, 41] that play a key roles in airway tissue inflammation and injury It is a complex cascade involving proteolytic cleavage of anaphylatoxins (C3a and C5a), which are often activated by cell receptors. C3a stimulates smooth muscle contraction [83], lysozyme release from immune cells [84], platelet aggregation [85], and triglyceride synthesis in adipocytes [86]
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