Disease relevance of Corynebacterium

• These vaccines consisted of Hib capsular polysaccharide polyribosyl-ribitol phosphate (PRP) conjugated to the meningococcal outer membrane protein (OMP) complex (PRP-OMP) and H influenzae oligosaccharide conjugated to a mutant toxin (CRM197) isolated from Corynebacterium diphtheriae (HbOC) [1].
• Intralesional immunotherapy of brain tumors with combined Corynebacterium parvum and recombinant interleukin-2 in mice [2].
• The hydroxamic acid siderophore ferrioxamine B [FeIII(HDFB)+] and the iron complex of diethylenetri-aminepentaacetic acid [FeIII(DTPA)2-] protected mice against death by septic shock induced by Corynebacterium parvum + lipopolysaccharide [3].
• In vivo activation of natural killer cells by treatment of mice with polyinosinic-polycytidylic acid or Corynebacterium parvum, 24 hr prior to tumor challenge rendered th 3-week-old nude mice resistant to development of metastases [4].
• Weekly i.p. injections of killed Corynebacterium parvum and of cyclophosphamide (given on different days) strongly inhibited growth of a transplantable murine mammary adenocarcinoma [5].

Psychiatry related information on Corynebacterium

• A randomized prospective therapy trial in patients with stage III optimal epithelial carcinoma of the ovary was accomplished by the Gynecologic Oncology Group. Therapy with melphalan or melphalan plus immuno-adjuvant, Corynebacterium parvum (C. parvum), was utilized as adjuvant treatment following surgical therapy [6].

High impact information on Corynebacterium

• Factor B represented approximately 0.5% of newly synthesized protein and 4-6% of the secreted protein of resident peritoneal macrophages and macrophages elicited with thioglycollate broth, pyran copolymer, NaIO4, bacillus Calmette-Guerin, or Corynebacterium parvum [7].
• NK activity against both targets is stimulated 3 d after injection of Corynebacterium parvum, and 24 h after challenge with polyinosinic:polycytidylic acid [8].
• Ingestion of EA was similarly stimulated by lipopolysaccharide or killed Corynebacterium parvum [9].
• To determine how alpha-MSH acts in vivo, we induced acute hepatic inflammation by administering endotoxin (LPS) to mice pretreated with Corynebacterium parvum, alpha-MSH prevented liver inflammation even when given 30 min after LPS administration [10].
• The tumor necrosis-inducing factor (TNF) found in sera of Corynebacterium parvum-treated, endotoxin-stressed BALB/C and outbred albino CD-1 mice has been purified to a single band of protein by polyacrylamide gel electrophoresis after identification and removal of contaminating albumin and transferrin [11].

Chemical compound and disease context of Corynebacterium

• Further observations on the inhibition of tumor growth by Corynebacterium parvum with cyclophosphamide. IX. Macrophage content of tumors in mice [12].
• Further observations on the inhibition of tumor growth by Corynebacterium parvum with cyclophosphamide. II. Effect of cortisone acetate [13].
• Effect of adriamycin and Corynebacterium parvum in tumor-bearing mice: modulation of response to sheep red blood cells [14].
• Dose, route, and time dependence of serum lysozyme and antitumor activity following administration of glucan, Corynebacterium parvum, pyran, or lipopolysaccharide to mice [15].
• Requirement for macrophages in in vitro augmentation, by interferon (IFN), polyinosinic-polycytidylic acid (poly I:C), or Corynebacterium parvum, of rat, mouse, and human natural killer (NK) activities was examined [16].

Biological context of Corynebacterium

• Molecular cloning and DNA sequence analysis of a diphtheria tox iron-dependent regulatory element (dtxR) from Corynebacterium diphtheriae [17].
• Of the immunomodulating agents, mycobacterial preparations (Bacillus Calmette-Guérin or interphase material), Corynebacterium parvum, and polyinosinic-polycytidylic acid moderately prolonged the survival time of mice bearing J774 or 70Z/2; the EL-4 lymphoma was refractory to all 10 immunomodulating agents [18].
• Data mining of the Corynebacterium glutamicum genome identified 4 genes analogous to the mshA, mshB, mshC, and mshD genes that are involved in biosynthesis of mycothiol in Mycobacterium tuberculosis and Mycobacterium smegmatis [19].
• Solution 1H NMR investigation of the active site molecular and electronic structures of substrate-bound, cyanide-inhibited HmuO, a bacterial heme oxygenase from Corynebacterium diphtheriae [20].
• Nucleotide sequence of the erythromycin resistance gene from the Corynebacterium plasmid pNG2 [21].

Anatomical context of Corynebacterium

• In vivo cortisone sensitivity of nonspecific antitumor activity of Corynebacterium parvum-activated mouse peritoneal macrophages [22].
• The present investigations have assessed the effects of prolonged cyclophosphamide (CY) and Corynebacterium (CP) treatment on the production of bone marrow macrophage precursors [colony-forming cells (CFC)] and on the cytotoxicity of macrophages comprising colonies produced by the CFC [23].
• Previous studies showed that the prostaglandin-forming macrophages (M phi) induced in the spleens of CBA/J mice by intraperitoneal administration of Corynebacterium parvum (CP) could not be demonstrated following the depletion of bone marrow and blood monocytes with 89Sr [24].
• Splenic suppressor M phi, defined by PGE-mediated inhibition of Con A-induced T lymphocyte proliferation are induced by the i.p. administration of Corynebacterium parvum (CP) [25].
• We have shown previously that, in the heterologous host, Corynebacterium glutamicum, FbpA, FbpB and FbpC can all add mycoloyl residues to the cell wall arabinogalactan and that, in M. tuberculosis, the cell wall mycoloylation decreases by 40% when fbpC is knocked out [26].

Gene context of Corynebacterium

• To determine whether TNF inhibition of IFN-gamma-induced IL-12 production contributed to the resolution of an inflammatory response in vivo, the response of TNF+/+ and TNF-/- mice injected with Corynebacterium parvum were compared [27].
• Upon treatment with heat-inactivated Corynebacterium parvum, urinary nitrite plus nitrate excretion of p53 KO mice exceeded that of wt controls by approximately 200% [28].
• In Corynebacterium parvum-primed mice, lipopolysaccharide injection resulted in elevated serum tumor necrosis factor-alpha levels early and increased hepatic enzyme release (641 +/- 80 IU AST/L; 22.7 +/- 1.9 IU ornithine carbamoyltransferase per liter) and plasma nitrite and nitrate (804 +/- 84 mumol/L) 5 hr after lipopolysaccharide injection [29].
• B7-1/CD80-transduced tumor cells elicit better systemic immunity than wild-type tumor cells admixed with Corynebacterium parvum [30].
• Roles of distal Asp in heme oxygenase from Corynebacterium diphtheriae, HmuO: A water-driven oxygen activation mechanism [31].

Analytical, diagnostic and therapeutic context of Corynebacterium

• Effect of immunotherapy with Corynebacterium parvum and methanol extraction residue of BCG administered intravenously on host defense function in cancer patients [32].
• Other programs of combination chemotherapy are under active study, especially programs that include nonspecific immune stimulation with Corynebacterium parvum or bacillus Calmette-Guérin (BCG) [33].
• Meth A fibrosarcoma-bearing BALB/c mice given intratumoral injections of 0.5 mg of Corynebacterium parvum showed a highly and tumor-specific transplantation antigen specifically potentiated concomitant immunity to a subsequent tumor challenge [34].
• Western blotting with 125I-WGA identifies a restricted set of glycoproteins in elicited peritoneal macrophages (M phi) (recruited with thioglycollate or periodate) and fully activated M phi (recruited with live Bacille Calmette-Guérin, or heat-killed Corynebacterium parvum); the major species migrates with Mr 89-115 kDa in 10% acrylamide gels [35].
• Pretreatment of BALB/c mice with Corynebacterium parvum inhibited the induction of tolerance to the contact sensitizing agent 2,4-dinitrofluorobenzene induced by intravenous injection of DNBSO3 [36].

References