Chemodenervating pharmaceutical as anti-inflammatory agent

Abstract

Pharmaceutical application of a chemodenervating agent, particularly botulinum toxin, reduces inflammatory response and serves as an anti-inflammatory agent without systemic side effects and with long duration action, on the order of 12-24 weeks. In one embodiment, the effective dosage for allergy provoked inflammation reduction is an order of magnitude less than dosages associated with treatment of regional movement diseases, since the agent works to reduce inflammation by reducing histamine and other preformed mediator releases associated with mast cell degranulation.

Description

FIELD OF INVENTION[0001]This invention relates to the use of chemodenervating agents in the treatment of disease, and more particularly to its use as an anti-inflammatory agent.BACKGROUND OF THE INVENTION[0002]Immunity and inflammation are forms of physiologic processes defined as the body's response against foreign substances such as antigens or, in some cases, itself, autoantigens, or some form of damaging biologic or mechanical insult. The process often involves the production of antibodies by type B lymphocytes which interact with foreign substances and subsequently destroy or inactivate the antigen using a number of cellular and chemical amplification systems and regulation systems such as complement, arachidonic acid metabolites such as prostaglandin and leukotrienes, cytokines, preformed mediators such as serotonin and histamine, and enzymes. Inflammatory responses occur in conjunction and as a result of the immune recognition process and functions to provide the basic tissue...

AI Technical Summary

Benefits of technology

[0010]It has been found that the use of botulinum toxin in doses from ⅓rd to several orders of magnitude less than those associated with treatment of regional movement diseases has been effective to reduce inflammation and adverse sensory experiences associated with the inflammatory response. These observations are explained by the fact that it has been found that low dosages of the subject chemodenervative agent reduces histamine releases and releases of other preformed mediators associated with mast cell degranulation. The subject bioeffect is noted at low dosages of the chemodenervative agent in one animal model of ocular surface disease well noted for histamine release and releases of other preformed mediators associated with mast cell degranulation and rapid inflammatory response.

[0016]It has been found that Type 1 hypersensitivity reactions are reduced with the subject anti-inflammatory agent. Such hypersensitivity reactions are classic for rapid expression of the inflammatory response often leading to edema with increased vascular permeability, erythema, abnormal sensory experiences, and increased heat release.

Problems solved by technology

Unfortunately, inflammatory reactions intrinsically may have destructive effects on tissue and organ structure and function, and may lead to painful or subjectively adverse sensory experiences.

Despite the known tissue effects from regional injections of botulinum toxin, certain medical observations regarding the use of chemodenervating agents can not be easily explained by such denervating tissue effects.

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