Lipopolysaccharides deficiency

Mice that are homozygous for a disrupted Bx or B2 receptor gene are healthy, fertile and normotensive. In Bx-deficient mice, bacterial lipopolysaccharide-induced hypotension is diminished and the recruitment of polymorphonuclear leukocytes to the sites of tissue injury is impaired, and the animals show signs of hypoalgesia. Deletion of the B2 gene in mice leads to salt-sensitive hypertension and altered nociception. 

The alternative pathway may become activated by lipopolysaccharides, endotoxin (sepsis), virus, fungi, immunoglobulin A-antigen (IgA-Ag) immunocom-plexes, and foreign material. These activate C3, after which the common pathway of complement activation takes place (Fig. 4). There are also a number of inhibitors that regulate and control complement activation. The most important are the Cl-esterase inhibitor (Cl-Inh) and the membrane attack complex inhibitor factor (MACIF CD59). In sepsis a relative deficiency of Cl-Inh has been reported. Administration of Cl-Inh to patients with septic shock attenuates complement acti-... 

Hoshino K, Takeuchi O, Kawai T, Sanjo H, Ogawa T, Takeda Y, Takeda K, Akira S. Cutting edge toll-like receptor 4 (TLR4)-deficient mice are hypore-sponsive to lipopolysaccharide evidence for TLR4 as the Lps gene product. J Immunol 1999 162(7) 3749-3752. 

Hancock, R.E.W., Mutharia, L.M., Chan, L., Darveau, R.P., Speert, D.P., Pier, G.B. Pseudomonas aeruginosa isolates from patients with cystic fibrosis a class of serum sensitive, nontypable strains deficient in lipopolysaccharide side chains. Infect Immun 42 (1983) 170-177. 

Ridley, B.L., Jeyaretnam, B.S., Carlson, R.W. The type and yield of lipopolysaccharide from sym-biotically deficient Rhizobium hpopolysaccharide mutants vary depending on the extraction method. Glycobiology 10 (2000) 1013-1023. 

Vanderlinde, E.M., Muszynski, A., Harrison, J.J., Koval, S.F., Foreman, D.L., Ceri, H., Kannenberg, E.L., Carlson, R.W., Yost, C.K. Rhizobium leguminosarum biovar viciae 3841, deficient in 27-hydroxyoctacosanoate-modified lipopolysaccharide, is impaired in desiccation tolerance, biofilm formation and motility. Microbiology 155 (2009) 3055-3069. 

Reid RR, Prodeus AP, Khan W, Hsu T, Rosen FS, Carroll MC, Endotoxin shock in antibody-deficient mice unraveling the role of natural antibody and complement in the clearance of lipopolysaccharide, J. Immunol., 159 970-975, 1997. 

Causes The following causes are seen as being responsible for an acquired immune deficiency syndrome in liver cirrhosis (B.A. Runyon, 1995) (i.) hypofunction of the RES (a decrease in the filter or clearance function and phagocytosis capacity as well as reduced formation of immune modulators) (s. p. 65), (2.) reduction in hepatic synthesis of opsonins (s. p. 66), (3.) compromised function of leucocytes, (4.) impaired proliferation and activation of T lymphocytes, and (5.) increased mucosa permeability to bacteria. Both bacteria and bacterial lipopolysaccharides enter the organism in large numbers. They are responsible for increased serum levels of the cytokines (e. g. interleukins 1 and 6, TNF, y-interferon), and there is increased production of these substances together with their reduced breakdown in the cirrhotic liver. Cytokines are formed in the monocytes of blood and in the mononuclear cells of various organs (above all in ascites). 

Endothelial NOS deficient mice Mouse Lipopolysaccharide 5 mg/kg IP No. Worse AKI [98]... 

CD28, a costimulatory molecule for T cell activation. CD 28 deficient mice Lipopolysaccharide lOpg/g IP Yes. LessTcell infiltration in kidney [207]... 

Caspase-1 deficient mice Mouse Lipopolysaccharide 2.5mg/kg IP Yes. Protection independent of iL-1 p and iL-18 [100]... 

ThromboxaneA(2) receptor deficient mice Mouse Lipopolysaccharide 8.5mg/kg IP Yes. improved RBF and GFR [208]... 

Serologic diagnosis uses an agglutination test that detects antibodies to lipopolysaccharide. This test, however, is not useful to diagnose infection caused by B canis, a naturally O-polysaccharide deficient strain. Infection can be most reliably con-... 

Lipopolysaccharide (LPS) also induces chemokine expression in a Stall-dependent manner, although this may involve the intermediate production of lipopolysaccharide (LPS)-induced IFNs (19,20). In vitro, LPS or LPS in combination with IFN-y induces expression of CXCLlO/IP-10 and CCL12/MCP-5 in murine peritoneal macrophages from wild-type, but not Stall-deficient mice (19,20). Injection of LPS in vivo also leads to the expression of CXCLlO/IP-10 in liver and spleen tissues from wild-type but not Statl-deflcient mice (20). 

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