Biocompatible devices, systems, and methods for reducing levels of pro-inflammatory or anti-inflammatory stimulators or mediators in the blood

Abstract

Devices, systems, and methods reduce levels of pro-inflammatory or anti-inflammatory stimulators or mediators in blood by selective adsorption. The devices, systems, and methods are useful in situations where abnormal levels of or unregulated or excessive interaction among pro-inflammatory or anti-inflammatory stimulators or mediators occur, or during events that do induce or have the potential for inducing abnormal production of pro-inflammatory or anti-inflammatory stimulators or mediators. The devices, systems, and methods serve to prevent, control, reduce, or alleviate the severity of the inflammatory response and disease states that are associated with abnormal levels of or unregulated or excessive interaction among pro-inflammatory or anti-inflammatory stimulators or mediators.

Description

RELATED APPLICATIONS [0001] This application is a divisional of co-pending U.S. patent application Ser. No. 10 / 036,758, which is a continuation-in-part U.S. patent application Ser. No. 09 / 832,159, filed Apr. 10, 2001, now abandoned, and entitled “System for Treating Patient with Bacterial Infections,” which is incorporated herein by reference. This application is also a continuation-in-part of U.S. patent application Ser. No. 09 / 829,252, filed Apr. 10, 2001, now abandoned, and entitled “Method of Treating Patient with Bacterial Infections,” which is also incorporated herein by reference. This application claims, under 35 U.S.C. § 120, the benefit of the filing date of co-pending U.S. patent application Ser. No. 09 / 294,224, filed Apr. 19, 1999, (now U.S. Pat. No. 6,416,487) and entitled “Method for Removing Beta-2 Microglobulin from Blood,” which is a continuation-in-part of U.S. patent application Ser. No. 08 / 902,727, filed Jul. 30, 1997 (now U.S. Pat. No. 5,904,663).FIELD OF THE IN...

AI Technical Summary

Benefits of technology

[0023] However, while this traditional view is true, these intense inflammatory response conditions may also be viewed as a syndrome of immune suppression. Immune effector cells become dysfunctional and are no longer capable of normal immune surveillance. Such a condition results in increased susceptibility to recurrent infection, prolonged inflammation and continued tissue injury. This condition can be referred to as “immuno-paralysis” and can be easily demonstrated. When either intact septic animals or whole blood taken from septic patients is exposed to an inflammatory stimulus (e.g. endotoxin) the normal host response is severely inhibited.

[0032] As another example, organs harvested for transplantation, e.g., kidney, liver, or heart, are typically stored for period of time in a suitable preservation solution until transplantation takes place. Storage of the organ in preservation solution can lead to the generation of cytokines or other species of pro-inflammatory or anti-inflammatory stimulators or mediators, which accumulate in the preservation solution. In such situations, the devices, systems, and methods that embody this aspect of the invention remove cytokines or other species of pro-inflammatory or anti-inflammatory stimulators or mediators from the preservation solution during organ storage and / or before transplantation of the organ occurs. In this way, the invention serves to prevent or at least ameliorate inflammatory response conditions or disease states as a result of organ transplantation.

Problems solved by technology

Immune effector cells, especially neutrophils, possess potent cytotoxic capacity and when unchecked, this response can cause significant tissue injury.

Immune effector cells become dysfunctional and are no longer capable of normal immune surveillance.

Such a condition results in increased susceptibility to recurrent infection, prolonged inflammation and continued tissue injury.

From this perspective, therapy aimed at reducing an inflammatory response by targeting removal of some of the pro-inflammatory stimulus may not restore normal immune responsiveness and thus, may not improve outcome.

Finally, the desirable strategy might well be limited in its effect to the circulating pool of mediators rather than influencing the tissue levels where their activity may be beneficial.

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