Staphylococcus epidermidis - virulence factors and innate ... - Munin

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Lectin pathway Classical pathway Alternative pathway Activators Saccharides on microbial surfaces Microbial surface, CRP, antibodies Host- or microbial surface MBL/Ficolins C1q C3 C4 Bb C3 C3a C5 C5a C5b-9 TCC Figure 3: The complement cascade with its three initial pathways; the lectin pathway, the classical pathway and the alternative pathway. All three initial pathways converge in the final common pathway. The classical pathway can be initiated by three mechanisms; i) antibodies recognizing a microbial target with subsequent binding to the complement component C1q creating a complex (C1qrs), ii) binding of bacterial surface structures directly to the C1q component or iii) binding of C-reactive proteins (CRP) to bacterial surfaces and C1 (85, 88-90). Immunoglobulin M and G 14
(IgM and IgG) are the only groups of antibodies that are able to activate the classical pathway (91). Among the IgG subgroups, IgG1 and IgG3 activate complement most efficiently, while IgG2 is less efficient (92). Furthermore, immunoglobulins can influence the complement cascade in many steps, both as activators and inhibitors, indicating their important role in maintaining homeostasis in the inflammatory response (91). The lectin pathway is initiated by recognition of specific patterns composed of saccharides on microbial surfaces. The recognition molecules of this pathway are the acute phase proteins, mannose-binding lectin (MBL) and ficolins (93, 94). From C4 the classical and lectin pathway share the same route. The alternative pathway is activated by spontaneous cleavage of C3. However, the alternative pathway will only proceed when non-self surfaces (without inhibitory factors) or “own” surfaces lacking inhibiting factors (such as some tumor cells) are close to the cleaved components. Activators of the alternative pathway are lipids, carbohydrates and proteins (95-97). Another important function of the alternative pathway is amplification of the final complement response initiated by the other two pathways (98, 99). Recently, the alternative pathway has also been suggested to control and balance other parts of the innate immune system (100). All three pathways converge at C3 and follow the same final pathway, from where the main inflammatory components are created. The end-product of the complement cascade is the terminal complement complex (TCC). TCC exists both in the fluid-phase and inserted into membranes where it is often called the membrane-attack complex (MAC) (101). The TCC is important in the defense against Gram negative bacteria, such as meningococci (102). In Gram 15
Page 1 and 2: Staphylococcus epidermidis - virule
Page 3 and 4: List of papers Paper I Hildegunn No
Page 5 and 6: 1. Introduction 1.1 Clinical releva
Page 7 and 8: The innate immune system, also know
Page 9 and 10: For neonates to survive the transit
Page 11 and 12: 41). There is cross-talk between th
Page 13: ecently published two reviews on th
Page 17 and 18: levels in plasma are: i) generation
Page 19 and 20: Levels of factor B (153, 164) and p
Page 21 and 22: Neutrophils are short lived cells,
Page 23 and 24: activating transcription factors an
Page 25 and 26: In contrast, other authors describe
Page 27 and 28: 1.2.7 Inflammation When danger is o
Page 29 and 30: affecting the whole body is a doubl
Page 31 and 32: due to the increasing use of broad-
Page 33 and 34: these findings are applicable to cl
Page 35 and 36: Table 2: Immune modulating strategi
Page 37 and 38: 1.3.6 Biofilm Biofilms are microorg
Page 39 and 40: Figure 6: Formation of S. epidermid
Page 41 and 42: (335, 342, 371). Proteins such as A
Page 43 and 44: of anionic AMP protection is still
Page 45 and 46: ACME is divided into three allotype
Page 47 and 48: 3. Material and methods 3.1. Materi
Page 49 and 50: Paper III The regional committee fo
Page 51 and 52: indistinguishable strains and isola
Page 53 and 54: the substance inert (29). This NaIO
Page 55 and 56: times with PBS/0.1% Tween (also use
Page 57 and 58: were then analyzed on a FACS Calibu
Page 59 and 60: 4. Summary of the main results Pape
Page 61 and 62: Paper III: • Both S. epidermidis
Page 63 and 64: methicillin resistant and -sensitiv
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increase in serum somewhat later an
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knock-out mutant was treated as a n
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5.4 The neonatal versus the adult i
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iofilms with a longer incubation ti
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6. Main conclusions The Arginine Ca
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Animal models It is a long way from
Page 77 and 78:
(15) Zarember KA, Godowski PJ. Tiss
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(41) Shaw MH, Reimer T, Kim YG, Nun
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(68) Gahr M, Speer CP, Damerau B, S
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(95) Bexborn F, Andersson PO, Chen
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(120) Riedemann NC, Neff TA, Guo RF
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(145) Thurman JM, Holers VM. The ce
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(171) Frakking FN, Brouwer N, van E
Page 91 and 92:
(197) Wynn JL, Levy O. Role of inna
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(224) Schultz C, Temming P, Bucsky
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type 1 and T cytotoxic type 1 cell
Page 97 and 98:
(275) Vuong C, Otto M. Staphylococc
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hematological malignancies during t
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(323) Avila-Figueroa C, Goldmann DA
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(347) Christner M, Franke GC, Schom
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(374) Hennig S, Nyunt Wai S, Ziebuh
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(397) Miragaia M, de Lencastre H, P
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for the quantification of complemen
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importance of surface hydrophobicit
Page 113:
Paper 1
Page 117:
Paper 3
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ISBN xxx-xx-xxxx-xxx-x
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Staphylococcus epidermidis - virulence factors and innate ... - Munin

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