Abstract

POTENTIAL THERAPEUTIC TARGETS FOR ALLERGIC ASTHMA SUPPRESSOR AIRWAYS: COMPLEMENT COMPONENTS (ANAPHYLOTOXIN C3A & C5A) A NOVEL APPROACH TO TREATING ASTHMA THROUGH HYPERRESPONSIVENESS AND AIRWAYS INFLAMMATION

Davande C. C.* and Shinde S. G.

ABSTRACT

Asthma is the most common respiratory disorder, and is characterized by distal airway inflammation and hyperresponsiveness. This disease challenges human health because of its increasing prevalence, severity, morbidity, and the lack of a proper and complete cure. Asthma is characterized by Th2 - skewed inflammation with elevated pulmonary levels of IL-4, IL-5, and IL-13 levels. A role for the complement anaphylatoxins C3a and C5a in allergic asthma was suggested, as deficiencies of the C3a receptor (C3aR) and of complement factor C5 modulate airway hyperresponsiveness, airway inflammation, and Th2 cytokine levels. In early time targeting Th2 cytokines by corticosteroids remains immunomodulators of choice. Innate immune injury mediated by complement components also act as potent mediators of the allergic inflammatory responses and offer a new and exciting possibility for asthma immunotherapy. The complement cascade consists of a number of plasma- and membrane-bound proteins, and the cleavage products of these proteins (C3 and C5) regulate the magnitude of adaptive immune responses. This topic highlights the complement-mediated injury during asthma inflammation, and how blockade of active complement mediators may have therapeutic application. The complement cascade is made up of many plasma- and membrane-bound proteins, and the cleavage products of these proteins (C3 and C5) control the amount of adaptive immunological responses. This issue focuses on complement-mediated harm during asthma inflammation and how active complement mediator blocking may have therapeutic applications.

Keywords: Complement mediated injury, Asthma, Anaphylatoxins, Innate immunity mediated injury, C3aR.