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PubMed1994

[Evaluation of regional analgesia and surgical trauma on selected factors of the human immune system].

The work attempted to explain the influence of epidural analgesia and operations on the behaviour of complement and lymphocyte systems. There are very few theses in the world anaesthetic literature which attempt to explain the influence of analgesia and operations on the immune system. Moreover, the problem is treated very superficially in these theses and research was conducted on a small number of patients. In the face of this fact it was decided to assess the behaviour of selected factors of the immune system during analgesia and operations. The research encompassed approximately 80 patients who underwent analgesia and operations. The operated patients were divided into two groups: a 40-person research group A and a 40-person control group K. In group A resection of the prostate gland was performed in epidural analgesia, whereas group K underwent analgesia of the brachial plexus to be operated within the hand and the upper limb. Because of the small extent of sympathetic interruption and of the operation the K group was the control group in relation to the A group where the sympathetic interruption and the operation were extensive. During the analgesia, operation and the 7-day post-operation period the concentration of immunoglobulins was examined (IgG, IgA, IgM), components of the complement (C3, C4), the total haemolithic activity of the complement (Kc) as well lymphocyte populations and sub-populations (B, T, CD4, CD8). Modern research techniques were used to carry out these examinations: monoclone antibody for examining lymphocytes, nephelometric technique for examining concentration of immunoglobulins and components of the complement and the hemolithic method for examination of the total activity of the complement. It was found that epidural analgesia acts deeply depressively on the concentration of endogenous immunoglobulins and of the components of the complement during the day of the operation. This type of analgesia also a similar effect on the level of total haemolithic activity of the complement. Operation trauma on the other hand causes depression of the auxiliary T lymphocyte population (CD4) and the stimulation of the cytotoxic T cell subpopulation (CD8) with a pathological reduction of the quotient factor of these lymphocyte sub-populations CD4/CD8. No statistically significant immunologic disorders were found in the area of the factors examined in patients who underwent operations in the area of the hand and the upper limb with application of plexus analgesia. The presented research results--although they do not have a correspondent in the world anaesthetic literature--seem to prove that epidural analgesia, hitherto regarded as a safe manner of anaesthetizing patients for operations is not devoid of negative influences on the immune system. With regard to immunity on the other hand, plexus analgesia seems to be a safe method anaesthetizing patients for operations in the area of the upper limb. It seems that the extent of sympathetic interruption caused by epidural analgesia affects selected immune factors depressively. This is a clinical question which still requires much research, especially in the area of effect on the immune system because post operative infection complications still constitute an important etiopathogenetic and medical problem.

Aged↗
PubMed1998

Activated complement component 3 (C3) is required for ultraviolet induction of immunosuppression and antigenic tolerance.

Complement component 3 (C3), a critical regulator of innate immunity, may also play a role in the regulation of cognate immunity, such as contact sensitivity responses. Because ultraviolet (UV) radiation also activates C3 in the skin, we determined whether the immunosuppressed state that results when a contact sensitizer is applied through UVB-exposed skin requires the presence and activation of C3. This question was addressed through the use of C3-deficient mice, blockade of C3 cleavage to C3b, and accelerated degradation of iC3b by soluble complement receptor 1 (sCR1). Both C3-modulated systems totally reversed the failure to induce a contact sensitivity response to dinitrofluorobenzene (DNFB) upon primary sensitization at the UV-exposed site, as well as immunologic tolerance to a second DNFB immunization through normal skin. Treatment with sCR1 reduced the infiltration of CD11b+ leukocytes into the epidermis and dermis of UV-irradiated skin but did not reverse the UV-induced depletion of epidermal class II MHC+CD11blo Langerhans cells. These data, taken together with previous results showing abrogation of locally induced UV immunosuppression by in vivo anti-CD11b treatment, suggest a novel mechanism by which ligation of the leukocyte beta2 integrin, CD11b, by iC3b molecules formed from C3 activation in UV-exposed skin, modifies cutaneous CD11b+ cells such that skin antigen-presenting cells are unable to sensitize in a primary immune response, but actively induce antigenic tolerance.

Animals↗
PubMed1995

Human glomerular epithelial cells synthesize and secrete the third component of complement.

Complement proteins in serum are mainly synthesized by hepatocytes. Recently, many cell types have been reported to synthesize complement in various tissues. In this study, we report the synthesis and secretion of the third component of complement (C3) by cultured glomerular epithelial cells (GEC). Using reverse transcriptase polymerase reaction, we have found that GEC and whole kidney expressed the C3 mRNA for C3. By ELISA, we have found that C3 was secreted in culture supernatants harvested from cultured GEC. The secretion of C3 is regulated by proinflammatory cytokines (IL-1 beta, TNF-alpha and IL-6). IL-1 beta is shown to be the most potent stimulator of C3 secretion from GEC. The exact significance of C3 produced at glomerular site is not clear, but its upregulation by proinflammatory cytokines may suspect a role in local activation of complement which may lead to glomerular injury. We further studied the expression of C3 step regulatory proteins (membrane cofactor protein (MCP), decay-accelerating factor (DAF), CR-1 and CD59 (a terminal step regulatory protein) by cultured GEC. Treatment of GEC by proinflammatory cytokines IL-1 beta, TGF-beta, TNF-alpha and IL-6 did not modify the expression of MCP, DAF and CR-1 whereas an increase in the expression of CD59 could be observed after treatment with IL-1 beta and TGF-beta. These results indicate that the expression of these regulatory proteins is tissue specific and may be implicated in inflammatory processes.

Antigens, CD↗
PubMed1976

Cytotoxicity responses to melanoma cells by human lymphoid cell subpopulations.

Lymphoid cell subpopulations from normal donors and patients with malignant melanoma were assessed for cytotoxicity. Unfractionated mononuclear cells and T-cells from melanoma patients gave cell-mediated cytotoxic (CMC) responses to melanoma target cells but not to human fibroblasts. These specific CMC responses to melanoma cells were partially inhibited by autologous serum. Non-T-cells and nonrosetting cells from melanoma patients were not directly cytolytic for melanoma target cells; however these same subpopulations were cytotoxic in the presence of autologous serum, which indicated antibody-dependent cell cytotoxic responses. Non-T-cell subpopulations from normal donors were not cytotoxic when incubated with autologous serum. A third cytotoxic mechanism was demonstrated with complement (C3) receptor-activated lymphocytes. From both melanoma patients and normal donors, cells forming rosettes with erythrocyte-antibody-complement were nonspecifically cytotoxic for lung fibroblasts and melanoma target cells, These responses were independent of antibody, since melanoma serum presumably containing antibody to melanoma target cells neither enhanced nor blocked cytotoxicity mediated by C3 receptor-bearing lymphocytes. The results indicated that lymphoid cell subpopulations from the same melanoma patient could express at least three different lymphocyte-mediated cytotoxicity mechanisms against melanoma target cells.

Antibodies↗
PubMed1990

Complement-mediated immune complex solubilization and precipitation inhibition in sera of patients with non-Hodgkin's lymphoma.

The complement functions of 42 patients with non-Hodgkin's lymphoma have been examined. The patients were divided into groups according to the severity of their disease: 1st--patients with high-grade lymphomas, 2nd--with low-grade lymphomas and 3rd--with chronic lymphocytic leukaemia. The adopted methods were the measurements of complement-mediated immune complex solubilizing capacity (CMSC) and the complement-mediated immune complex precipitation inhibition capacity (IPIC). The CMSC and IPIC values were examined parallel with CH50, C3 complement levels and with levels of circulating immune complexes (CIC) in the sera of patients. The results indicated that the acquired deficiency of complement functions could be established by CMSC and IPIC measurements in the sera of patients with high-grade lymphomas. These defects were found to be milder in the group with low-grade lymphomas, and were not detectable in CLL. The changes of CH50 levels were found to be similar to that of IPIC values and the decrease in C3 levels was detectable in high-grade and low-grade lymphomas too. Elevated CIC levels were found in those cases in which both CMSC and IPIC were decreased.

Antigen-Antibody Complex↗
PubMed2003

Cloning and expression of the complement receptor glycoprotein C from Herpesvirus simiae (herpes B virus): protection from complement-mediated cell lysis.

Simian herpes B virus (SHBV) is the herpes simplex virus (HSV) homologue for the species MACACA: Unlike in its natural host, and unlike other animal herpesviruses, SHBV causes high mortality in accidentally infected humans. SHBV-infected cells, like those infected with HSV-1 and equine herpesvirus types 1 and 4, express complement C3 receptor activity. To study immunoregulatory functions involved in susceptibility/resistance against interspecies transmission, the SHBV glycoprotein C (gC(SHBV)) gene (encoding 467 aa) was isolated. Sequence analysis revealed amino acid identity with gC proteins from HSV-2 (46.9 %), HSV-1 (44.5 %) and pseudorabies virus (21.2 %). Highly conserved cysteine residues were also noted. Similar to gC(HSV-2), gC(SHBV) is less glycosylated than gC(HSV-1), resulting in a molecular mass of 65 kDa if expressed in replication-deficient vaccinia virus Ankara. Stable transfectants expressing full-length gC(SHBV) on the cell surface induced C3 receptor activity and were substantially protected from complement-mediated lysis; no protection was observed with control constructs. This suggests that expression of the gC homologues on infected cell surfaces might also contribute to the survival of infected cells in addition to decreased virion inactivation. Interestingly, soluble gC(SHBV) isolated from protein-free culture supernatants did not interfere with the binding of the alternative complement pathway activator properdin to C3b, which is similar to our findings with gC(HSV-2) and could be attributed to major differences in the amino-terminal portion of the protein with extended deletions in both gC(SHBV) and gC(HSV-2). Binding of recombinant gC(SHBV) to polysulphates was observed. This, together with the heparin-sensitivity of the gC(SHBV)-C3 interaction on the infected cell surface, suggests a role in adherence to heparan sulphate, similar to the gC proteins of other herpesviruses.

Amino Acid Sequence↗
PubMed1986

Genetic expression of complement factors and alpha 1-acid glycoprotein by liver tissue during senescence.

The effect of age on several messenger RNAs coding for non-specific immune factors were determined in liver RNA isolated from 6-, 12-, 24-, 29- and 37-month-old male Fischer Rats. The levels of complement factors C3 and C4, complement protein factor B, and alpha 1-acid glycoprotein were determined by dot blot hybridization using cDNA probes. All four mRNAs increased slightly between 6 and 29 months of age. Only the mRNAs coding for complement factors C3 and C4 decreased significantly after 29 months of age. In addition, Northern blot analysis of the RNA preparations showed that the size of the four mRNA species did not change with increasing age. There was no evidence for age-related changes in the post-transcriptional processing or degradation of the mRNA species coding for complement factors C3 and C4, complement protein factor B, and alpha 1-acid glycoprotein.

Age Factors↗
PubMed1983

Conversion of the C3 component of complement in sera of hanseniasis patients.

The levels of total C3 (native C3 plus its degradation products) and the degree of conversion of native C3 into its breakdown products were studied in sera of Virchowian (V), tuberculoid (T), indeterminate (I), and Virchowian with erythema nodosum Hansenicum (ENH) patients. Sera from normal individuals (N) were also analysed. While the levels of total C3 were not significantly different among the groups, the percentage of conversion of C3 into its degradation products was significantly higher in V and ENH sera. The activation of the complement system and the involvement of immune complexes (IC) are discussed.

Antigen-Antibody Complex↗
PubMed2002

Redundant and alternative roles for activating Fc receptors and complement in an antibody-dependent model of autoimmune vitiligo.

Complement and Fc receptor (FcR)-positive cells mediate effector functions of antibodies. Antibody-dependent immunity against the melanosome membrane glycoprotein gp75/tyrosinase-related protein-1 (TYRP-1) of melanocytes leads to autoimmune hypopigmentation (vitiligo) in mice. Hypopigmentation occurred in mice deficient in activating FcR containing the common gamma subunit (Fc gamma R gamma(-/-)) and in mice deficient in the C3 complement component. Mice doubly deficient in both Fc gamma R gamma and C3 did not develop hypopigmentation, suggesting that complement and Fc gamma R formed redundant mechanisms. Following passive immunization with antibody, no further adaptive immune responses were required. Chimeric Fc gamma R gamma(-/-),C3(-/-) mice reconstituted with bone marrow from either Fc gamma R gamma(-/-) or C3(-/-) mice or adoptively transferred with Fc gamma R gamma(+/-) macrophages did develop antibody-mediated hypopigmentation. Thus, either complement or macrophages expressing activating Fc gamma R can independently and alternatively mediate disease in a model of autoimmune vitiligo.

Adoptive Transfer↗
PubMed1980

Complement-independent adherence of Escherichia coli to complement receptors in vitro.

We studied adherence to human cells by a strain of Escherichia coli. Adherence to erythrocytes was assessed directly by phase-contrast microscopy and indirectly by hemagglutination; adherence to peripheral blood leukocytes, using radiolabeled bacteria and subsequent determination of leukocyte-associated radioactivity; and adherence to renal glomeruli, by microscopy of fluoresceinated bacteria and of Gram-stained nonfluoresceinated bacteria. In serum-free systems, E. coli of this strain adhered to human erythrocytes, which have surface receptors for the third component of complement (C3), but not to erythrocytes from species lacking this receptor. 1 mM trypan blue, a reagent that inhibits complement receptor function, inhibited adherence to human erythrocytes, as well as adherence to leukocytes and glomeruli. Preincubation of erythrocytes and leukocytes with complement-coated zymosan particles partially blocked subsequent bacterial adherence. Incubation of human erythrocytes with aging human serum, with trypsin-cleaved C3, or with C3 cleaved by the classical pathway convertase (EAC142)-all of which treatments deposited C3 on the erythrocyte surface, presumably at C3 receptors-inhibited subsequent E. coli adherence. Finally, incubation of E. coli with rabbit antiserum to human C3 blocked adherence to erythrocytes.Bacterial hemagglutination and erythrocyte adherence were not inhibited by mannose in concentrations up to 2.5%. And this strain of E. coli did not adhere to or agglutinate guinea pig erythrocytes, the usual test particle used for demonstration of common pili. Finally, electron microscopy of adherent bacteria showed only rare surface pili. In contrast, adherence to and agglutination of guinea pig erythrocytes by a stock piliated E. coli was inhibited by mannose but not by trypan blue. We conclude that organisms of this strain of E. coli adhere to human erythrocytes, leukocytes, and glomeruli at complement receptors. Complement is not required for this interaction. Adherence apparently involves a C3-like structure on the bacterial surface, but bacterial surface pili play no role. The physiological or pathological role of this adherence is not apparent, but study of this phenomenon may elucidate functions of complement receptors on various cells.

Animals↗
PubMed2004

IgM binding to injured tissue precedes complement activation during skeletal muscle ischemia-reperfusion.

BACKGROUND: Skeletal muscle reperfusion injury is mediated by IgM natural antibodies and by complement activation, as shown by the attenuation of reperfusion injury seen in mice with no natural IgM [] and in mice deficient in complement C3 and C4 []. We postulate that tissue, when ischemic, expresses neoantigens to which preformed natural IgM antibodies bind, in turn producing harmful complement activation and reperfusion injury. MATERIALS AND METHODS: C57Bl/6 mice were subjected to 2 h of tourniquet-induced hind limb ischemia followed by variable periods of reperfusion. Two hours of ischemia and 3 h of reperfusion produced severe muscle necrosis and edema. Deposition of IgM and C3 in tissue was assessed using immunohistochemistry on both frozen and Formalin-fixed tissue samples. RESULTS: IgM binding to the endothelium and muscle bundles of the hind limb began during the ischemic period and continued throughout reperfusion up to 6 h. C3 deposition was not present during ischemia and, in contrast, began to appear at 1 h of reperfusion and increased progressively thereafter. CONCLUSIONS: These data demonstrate that IgM binding to ischemic tissues precedes the damaging complement activation by a significant period of time. This has important therapeutic implications when considering anti-inflammatory therapy for reperfusion injury.

Animals↗
PubMed1981

Potentiation of opsonization and phagocytosis of Streptococcus pyogenes following growth in the presence of clindamycin.

Streptococcus pyogenes, bearing M-protein on its surface, resists opsonization by normal human serum and subsequent phagocytosis by human polymorphonuclear leukocytes. Previous studies have shown that M-protein positive organisms are poorly opsonized by the alternate pathway of complement. In an attempt to define further the role of the surface components of S. pyogenes in this process, we examined the ability of clindamycin, an antibiotic that inhibits protein biosynthesis, to alter bacterial opsonization. An M-protein positive strain of S. pyogenes was grown in varying concentrations of clindamycin at levels lower than those which inhibited growth, i.e., at levels less than the minimal inhibitory concentration. These bacteria were incubated with purified human polymorphonuclear leukocytes and peripheral blood monocytes. Significant enhancement of bacterial opsonization, phagocytosis, and killing resulted. Measurement of complement consumption and binding of the third component of complement (C3) onto the bacterial surface demonstrated that organisms grown in the presence of clindamycin activated complement more readily and fixed more C3 on their surface. Electron microscopy revealed the probable basis for these findings. Streptococci exposed to clindamycin during growth were largely denuded of surface "fuzz," the hairlike structures bearing M-protein. We conclude that the incorporation of clindamycin at concentrations that fail to inhibit growth of S. pyogenes nevertheless causes significant changes in the capacity of these bacteria to resist opsonization by serum complement. These findings support the hypothesis that M-protein inhibits bacterial opsonization by interfering with effective complement activation on the bacterial surface.

Antigens, Bacterial↗
PubMed1985

Deficiency of the complement regulatory protein, "decay-accelerating factor," on membranes of granulocytes, monocytes, and platelets in paroxysmal nocturnal hemoglobinuria.

Erythrocytes from patients with paroxysmal nocturnal hemoglobinuria are deficient in decay-accelerating factor, a membrane protein that inhibits the complement C3 convertases. We studied the expression of this protein on leukocytes and platelets from four patients with paroxysmal nocturnal hemoglobinuria, using cytofluorographic analysis and antibody to decay-accelerating factor. The granulocytes and monocytes had a bimodal distribution of fluorescence, indicating antigen-deficient and antigen-positive subpopulations of cells. In contrast, granulocytes and monocytes from normal donors and patients with other diseases had no antigen-deficient cells. Platelets from the four patients with paroxysmal nocturnal hemoglobinuria had less fluorescence than normal platelets. Furthermore, surface-radiolabeled granulocytes and platelets from one of the four patients, which were maximally deficient in decay-accelerating factor, also lacked antigen that was immunoprecipitable by specific antibody to this protein. Thus, paroxysmal nocturnal hemoglobinuria is a clonal disorder characterized by deficient membrane expression of decay-accelerating factor on granulocytes, monocytes, and platelets, as well as on erythrocytes.

Adult↗
PubMed1973

Measurement of the third component of complement bound to red blood cells in patients with the cold agglutinin syndrome.

The amount of the third component of complement (C3) bound to red cells of patients with the cold agglutinin syndrome was determined by a quantitative assay, measuring the fixation of the first component of complement by anti-C3. Abrupt reduction in the serum concentration of cold agglutinin by plasmapheresis markedly decreased the hemolytic rate, but the amount of C3 bound to circulating cells did not change appreciably. When this patient was transfused with normal cells. C3 accumulated on the transfused cells within 48 h to the level present on his own cells, but selective destruction of the transfused cells did not occur. When patients were subjected to acute cold stress, cell-bound C3 rose abruptly and intravascular hemolysis occurred. These studies suggest that most of the C3 detected on the circulating red cells of cold agglutinin patients is in an inactive form, and that the rate of attachment of C3 to the membrane is important in determining hemolysis.

Aged↗