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LIST of ABBREVIATIONS ABP ADCC BPI C3 CAMP Cfu CGD CM I CR1

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LIST of ABBREVIATIONS ABP ADCC BPI C3 CAMP Cfu CGD CM I CR1 LIST OF ABBREVIATIONS ABP actin binding protein ADCC antibody-dependent cellular cytotoxicity BPI bactericidal permeability increasing protein C3 complement component 3 CAMP cyclic adenosine monophosphate cfu colony forming unit CGD chronic granulomatous disease CM I cell mediated immunity CR1 complement receptor type 1 CR2 complement receptor type 2 CR3 complement receptor type 3 CR4 complement receptor type 4 CRP C-reactive protein CSF colony stimulating factor CV coefficient of variation DAC diacylglycerol EBV Epstein-Barr virus EGTA ethylene glycol-bis(3-aminoethyl ether)N,N,N',N'-tetraacetic acid E-LAM endothelium leucocyte adhesion molecule ELISA enzyme-1 inked immunosorbent assay FcocR receptor for the Fc portion of IgA FMLP N-formyl-L-methionyl-L-leucyl-L-phenylalanine GABHS group A p-haemolytic streptococcus GBS Group B streptococcus G-PROTEIN guanine nucleotide binding protein G-CSF granulocyte colony stimulating factor GM-CSF granulocyte-monocyte colony stimulating fa c to r HMS hexose monophosphate shunt HNP human neutrophil peptide IC internal control IFNy interferon gamma IgA immunoglobulin A igG immunoglobulin G IL3 interleukin 3 inositol 1,4-5 trisphosphate l5a leucocyte adhesion deficiency LPS 1ipopolysaccharide LTB4 leukotriene B4 mAb monoclonal antibody MBP mannose binding p ro te in min minute MPO myeloperoxidase NA neutrophil antigen NADG N-acetyl-D-glucosamine NADPH nicotinamide adenine dinucleotide phosphate NAP neutrophil activating peptide PA p ro te in A PBS phosphate buffered saline PBSAT phosphate buffered saline-azide-tween PG peptidoglycan PIP- phosphoinositol 4,5-bisphosphate PKC protein kinase C PLC phospholipase C PMN polymorphonuclear leucocyte PNH paroxysmal nocturnal haemogloninuria RBC erythrocyte RCA regulator of complement activation RGD Arg i n i ne-Glyc i ne-Aspartate SAP serum amyloid protein STSS staph ylococcal to x ic shock syndrome TA teichoic acid TNF tumour necrosis factor TNF-oc tumour necrosis factor-alpha TSLS toxic shock-like syndrome WCH Westminster Children's Hospital 3A STATISTICAL ANALYSIS 3A.1 Staphylococcal Inhibition assay 3A.1.1 Reference Range 3A.1.2 Intra-assay variation 3A.1.3 In te r-a ssa y and b io lo g ic a l v a ria tio n 3A.1.4 Analysis of cross-over studies 3A.2 Staphylococcal inhibition assay in the presence of heat inactivated plasma 3A.3 Streptococcal inhibition assay 3A.4 Anti-staphylococcal ELISA 3A.5 Statistical analysis of patients 3A.5.1 Patients with staphylococcal infections 3A.5.1.1 Clinical characteristics of patients with staphylococcal infections 3A .5.1.2 The 27 p a tie n ts w ith S.aureus infections but normal opsonophagocytosis 3A .5.1.3 A comparison of Fc-mediated phagocytosis in patients with S.aureus infections, patients with other infections and normal volunteers 3A .5.1.4 A comparison of anti- S.aureus IgGl and IgG2 an tib o d ie s in p a tie n ts w ith S.aureus infections, patients with other in fe c tio n s and healthy volunteers 3A .5.1.5 Correlation between Fc-mediated phagocytosis and a n t i-S.aureus IgGl and IgG2 subclass an tib o d ie s LIST OF TABLES IN CHAPTER 3A 3A.1 Results showing the intra-assay variation of the staphylococcal inhibition assay 3 3A.2 Results of 13 consecutive tests of the S .aureus inhibition assay using PMNs and plasma from a single healthy volunteer 4 3A.3 A comparison of staphylococcal inhibition using patient plasma in the presence of p a tie n t (PcPp) and co n tro l PMN (NcPp) 7 3A.4 Variation in % inhibition when heat inactivated control plasma was incubated with PMN from 3 donors 8 3A.5 Serial dilution of 4 different broth cultures of S.pyogenes 10 3A.6 Fc-mediated opsonophagocytosis using plasma from patients with S.aureus infections, other infections and healthy normal controls 19 3A.7 A n t i- 5 .aureus to ta l IgG, IgGl and IgG2 le v e ls in patients with S.aureus infections, other p a tie n ts and normal volu n teers 21 LIST OF FIGURES IN CHAPTER 3A 3A.1 Frequency histogram of the results of S .aureus inhibition tests using PMN and plasma from 29 healthy volunteers 2 3A.2 Graph showing the relationship between broth b a c te ria l con cen tration and absorbance of S.pyogenes at 650nm 10 3A.3 Phagocytosis of 2 clinical isolates of S.pyogenes (JB & FS) using PMNs from 3 donors (Ncl-3) with plasma from 10 different healthy volunteers (A-J) 11 3A.4 Comparison of IgGl (A) and IgG2 (B) a n t i- S.aureus subclass antibodies in patient and reference plasma samples 14 3A.5 Frequency histogram of the S.aureus inhibition results of patients with significant staphylococcal infections 15 3A.6 Frequency distribution of patients' ages 16 3A.7 Frequency distribution of the ages of patients with non-staphylococcal in fe c tio n s 19 CHAPTER 3A: STATISTICAL ANALYSIS 3A.1 STAPHYLOCOCCAL INHIBITION ASSAY 3A.1.1 REFERENCE RANGE The staphylococcal inhibition assay (see 3.9, page 67) was used to measure staphylococcal opsonization by patient and control plasma and phagocytosis of this organism by p a tie n t and c o n tro l PMNs. The r e s u lt s were expressed as % inhibition. PMNs in autologous plasma from 29 healthy adult volu n teers were tested by t h is method and produced a range of 88-99% in h ib it io n w ith a median o f 95.7%. A p lo t o f the frequency distribution of these results suggested a skewed distribution (Fig 3A.1). This reference range agrees well with that of Foroozanfar who defined the lower lim it of her normal range as 88% {Foroozanfar,1976}. A separate reference range for children was not established because of the difficulty in obtaining adequate quantities of blood from healthy children. Sporadic sibling studies and measurement of staphylococcal phagocytosis by PMNs obtained from 21 children with non-staphylococcal infections fell within the adult reference range, thereby suggesting that this reference range is also valid for phagocytic studies with children. 1 FIGURE 3A.1. Frequency histogram o f the re s u lts o f S.aureus inhibition tests using PMNs and plasma from 29 healthy volunteers. 2 3A.1.2. INTRA-ASSAY VARIATION The intra-assay variation of the staphylococcal inhibition test was determined by testing one sample of PMNs and plasma from a s in g le healthy vo lu n teer. The re s u lts set out in Table 3A.1 are the averages obtained from triplicate determinations. The mean was found to be 98.15% with a standard error of the mean (SEM) of 0.3. TABLE 3A.1. Results showing the intra-assay variation of the staphylococcal inhibition assay. % S.aureus TEST NO. INHIBITION 1. 95.0 2 . 97.3 3 . 97.7 4 . 98.0 5 . 98.1 6 . 98.3 7 . 98.4 8 . 98.5 9 . 98.5 10. 98.6 11. 98.7 12. 98.7 13. 98.8 14. 98.9 15. 99.1 3 3A.1.3. INTER-ASSAY AND BIOLOGICAL VARIATION The results of 13 consecutive tests performed over 2 years using freshly prepared PMNs and plasma from a single healthy volunteer are shown in Table 3A.2. The mean was found to be 95.9% with a SEM of 0.5. TABLE 3A.2 Results of 13 consecutive tests of the S. aureus in h ib itio n assay using PMNs and plasma from a single healthy volunteer % S.aureus TEST NO. INHIBITION 1 95.0 2 96.4 3 93.0 4 96.4 5 93.0 6 95.0 7 99.0 8 97.7 9 96.0 10 96.4 11 95.0 1 2 96.8 13 96.6 4 It is difficult to assess separately the inter-assay and biological variations in the staphylococcal inhibition assay because two components, the PMNs and the S. aureus organisms, were always freshly prepared before use. However, the contribution of plasma storage to inter-assay variability was assessed by comparing staphylococcal phagocytosis in the presence of stored and freshly separated plasma from a single individual. The % in h ib itio n obtained using fresh plasma and samples stored fo r 4 months and 18 months were 98%, 97% and 95%, resp ectively. Therefore, plasma storage does not appear to contibute s ig n ific a n tly to inter-assay variation. Nevertheless, most patient plasma are fre s h ly obtained and in the few cases where stored plasma were used, these were always tested w ithin a month of receiving them. The reproducibi lty of an assay is dependent on the effects of intra-assay, inter-assay and biological variations. In the staphylococcal inhibition assay, the intra-assay v a ria b ilty was low (CV 1.04%) and factors such as plasma storage contributed minimally to the inter-assay variation. Thus, the range of 7% obtained when fresh samples from a single individual were tested (Table 3A.2) was probably due to biological variation. Some factors which could have contributed to biological variation in the staphylococcal inhibition assay include: 1) Variation in the physiology of the PMN. 2) Activation of the PMN by the separation procedure. 5 3) Variation in the quantity and quality of humoral factors. 4) Variation in the growth characteristics of S,aureus micro-organisms which are phagocytosed. 3A.1.4.ANALYSIS OF CROSS-OVER STUDIES Staphylococcal inhibition tests were usually set up to d istin g u ish humoral and c e llu la r defects by using four combinations of control PMNs with control (NcNp) and patient plasma (NcPp), as well as patient neutrophils with patient (PcPp) and control plasma (PcNp).
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