Literature DB >> 3539389

Kupffer cell complement receptor clearance function and host defense.

D J Loegering.   

Abstract

Kupffer cells are well known to be important for normal host defense function. The development of methods to evaluate the in vivo function of specific receptors on Kupffer cells has made it possible to assess the role of these receptors in host defense. The rationale for studying complement receptors is based on the proposed important role of these receptors in host defense and on the observation that the hereditary deficiency of a complement receptor is associated with recurrent severe bacterial infections. The studies reviewed here demonstrate that forms of injury that are associated with depressed host defense including thermal injury, hemorrhagic shock, trauma, and surgery also cause a decrease in complement receptor clearance function. This decrease in Kupffer cell receptor clearance function was shown not to be the result of depressed hepatic blood flow or depletion of complement components. Complement receptor function was also depressed following the phagocytosis of particulates that are known to depress Kupffer cell host defense function. Endotoxemia and bacteremia also were associated with a depression of complement receptor function. Complement receptor function was experimentally depressed in uninjured animals by the phagocytosis of IgG-coated erythrocytes. There was a close association between the depression of complement receptor clearance function and increased susceptibility to the lethal effects of endotoxin and bacterial infection. These studies support the hypotheses that complement receptors on Kupffer cells are important for normal host defense and that depression of the function of these receptors impairs host defense.

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Year:  1986        PMID: 3539389

Source DB:  PubMed          Journal:  Circ Shock        ISSN: 0092-6213


  6 in total

1.  Increased serum enzyme levels associated with kupffer cell reduction with no signs of hepatic or skeletal muscle injury.

Authors:  Zaher A Radi; Petra H Koza-Taylor; Rosonald R Bell; Leslie A Obert; Herbert A Runnels; Jean S Beebe; Michael P Lawton; Seth Sadis
Journal:  Am J Pathol       Date:  2011-05-13       Impact factor: 4.307

2.  Effect of phagocytosis of erythrocytes and erythrocyte ghosts on macrophage phagocytic function and hydrogen peroxide production.

Authors:  L M Commins; D J Loegering; P W Gudewicz
Journal:  Inflammation       Date:  1990-12       Impact factor: 4.092

3.  Lysosomotropic agents ameliorate macrophage dysfunction following the phagocytosis of IgG-coated erythrocytes: a role for lipid peroxidation.

Authors:  M J Raley; M G Schwacha; D J Loegering
Journal:  Inflammation       Date:  1997-12       Impact factor: 4.092

4.  Respiratory burst capacity of activated macrophages is resistant to depression by erythrocyte phagocytosis.

Authors:  M G Schwacha; D J Loegering
Journal:  Inflammation       Date:  1992-08       Impact factor: 4.092

5.  Scavengers of reactive oxygen intermediates do not mediate the depression of macrophage hydrogen peroxide production caused by erythrocyte phagocytosis.

Authors:  M G Schwacha; D J Loegering; L M Commins; P W Gudewicz
Journal:  Inflammation       Date:  1991-12       Impact factor: 4.092

Review 6.  Clinical significance of translocation.

Authors:  P A Van Leeuwen; M A Boermeester; A P Houdijk; C C Ferwerda; M A Cuesta; S Meyer; R I Wesdorp
Journal:  Gut       Date:  1994-01       Impact factor: 23.059

  6 in total

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