Abstract
Evidence demonstrates the involvement of hormones in the development of inflammatory response. Inflammation evokes marked structural alterations of microvasculature, besides migration of leukocytes from microcirculation to the site of lesion. These alterations are caused primarily by release or activation of endogenous mediators, in which hormones play an integral role in this regulatory system. Binding sites for many hormones may be characterized by vascular structures and hematogenous cells involved with the inflammatory response. Quantitative alterations of inflammatory events involving the decrease in microvascular response to inflammatory mediators, deficiency in the leukocyte-endothelium interaction, reduction of cell concentration in the inflammatory exudate, and failure of the phagocyte function of mononuclear cells were observed in insulin- deficient states. Therefore, inflammation is not merely a local response, but rather a process controlled by hormones in which insulin plays an essential role in modulation of these phenomena, and assures tissue repair and remodeling within the limits of normality.
Highlights
Animal kingdom organisms, vertebrates, are involved in a constant challenge in which external aggressors, such as trauma and infections, should be neutralized
In order to effectively respond to the challenge imposed, the organism activates a series of strictly conditioned events, characteristic of the inflammatory response, including structural and functional alterations of vessels, migration of hematogenous cells to the damaged area, phagocytosis, and local pain
In classic studies conducted by Miles and Niven, pyogenic bacteria were utilized as noxious stimulus, demonstrating convincingly the defensive aspect of the inflammatory response
Summary
Vertebrates, are involved in a constant challenge in which external aggressors, such as trauma and infections, should be neutralized. In order to effectively respond to the challenge imposed, the organism activates a series of strictly conditioned events, characteristic of the inflammatory response, including structural and functional alterations of vessels, migration of hematogenous cells to the damaged area, phagocytosis, and local pain. This reaction may be accentuated by means of recruitment of immune system components[1]. In classic studies conducted by Miles and Niven, pyogenic bacteria were utilized as noxious stimulus, demonstrating convincingly the defensive aspect of the inflammatory response. The present article aimed to demonstrate the interaction between the insulin hormone and modulation of inflammatory response
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