Inflammation, Allergy and Asthma, Complex Immune Origin Diseases: Mechanisms and Therapeutic Agents

Abstract

Inflammation, allergy and asthma are the manifestation of multitude reactions of biological, cellular and immunological events. The various associated biological, cellular, and molecular events with inflammation, allergy and asthma participate to induce increased vascular permeability, vasodilatation, cellular migration, increased mucus secretion, broncho-constriction, structural changes of airway architecture, decline in pulmonary functions, release of intracellular mediators, increased formation of reactive oxygen species, cartilage degradation and loss of function. The participation of variety of effector cells viz. leukocytes, neutrophils, eosinophils, basophils, monocytes, macrophages, mast cells, dendritic cells, T-cells, B-cells, NK-cells, lead to cascade of events trigger of intracellular mediators (cytokines, chemokines etc.) activating diverse biological effects and immune responses. Eicosanoids are major precursors in cyclooxygenase and lipooxygenase pathways and play an important role in inflammation, allergy and asthma. Such biological and cellular events are further enhanced by stress related effects. The wide varieties of synthetic and natural compounds have been showed to act on different molecular targets (receptor, enzymes, mediators, and cells) involved in inflammation, allergy and asthma and to alter produce specific/definite therapeutic activity. The present review describes pathogenesis and etiological aspects of inflammation, allergy and asthma with few relevant patents which would be immensely useful for researchers in the field of immunology and molecular pharmacology to explore new avenues/strategies for development of new generation of therapeutically active agents for treatment of inflammation and allergic disorders.

Rheumatoid Arthritis and the Risk of Bipolar Disorder: A Nationwide Population-Based Study

“…Evidence has indicated that chronic inflammatory processes in asthma and liver cirrhosis, like the pathophysiology of RA, involve cytokine interactions [29]–[31], and this combined and augmented chronic inflammatory effect might subsequently induce bipolar disorder. Moreover, cytokines that potentially cause depression and anxiety in liver cirrhosis [32] might also be associated with the development of bipolar disorder [33].…”

Characteristics of Proinflammatory Cytokines and Chemokines in Airways of Asthmatics

“…[ 1 2 3 4 ] Increased expression of these proinflammatory cytokines and various chemokines, at mRNA or protein levels, is observed in different clinical samples of asthmatics compared with controls, such as peripheral blood, sputum, bronchoalveolar lavage fluid (BALF), and bronchial biopsies. [ 5 6 7 8 ] However, these observations vary from individual studies and sometimes are even contradictory, possibly because of the limitation of numbers of subjects, different kinds of samples, and noncorrespondence between transcription and translation of certain molecules. In this case, little is known about the systemic evaluation of whether these proinflammatory cytokines and chemokines are all equally important and what is the associated status of other biomarkers in human asthmatic airways.…”

Boehmeria niveaAttenuates the Development of Dextran Sulfate Sodium-Induced Experimental Colitis

“…Leucocyte infiltration induces mucosal tissue damage in colons, resulting in an inflammatory response involving cytokines and the chemokine MCP-1 [15]. Anticolitis medications such as sulfasalazine significantly decrease colitis and neutrophil/macrophage infiltration by reducing cytokine and chemokine levels [16, 17]. Polyphenol-rich extra-virgin olive oil has been shown to modulate macrophage activation and decrease cytokine production in UC [18].…”