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

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(embp) accumulation. Immune evasion Poly-γ-glutamic Acid (PGA) (capA/B/C/D) VraF/G (vraF/G) Aps system (aps) Metalloprotease (sepA) Resistance to AMPs and neutrophil phagocytosis. Increased survival during high salt concentrations AMP resistance AMP sensing system, AMP resistance Exoenzyme. Lipase maturation, AMP degradation and resistance Immune stimulatory strategies PIA Peptidoglycan Lipopetides Phenol-soluble Modulins (hld, psm α/β/γ/ε/δ) Cytokine secretion Component of cell wall, induce cytokine secretion Component of cell wall, induce cytokine secretion Chemotaxis, decreased apoptosis of leukocytes, cytokine secretion, degranulation, oxidative burst. Colonization. Cell lysis. Biofilm maturation Based on references: (29, 183, 333-353). 36
1.3.6 Biofilm Biofilms are microorganisms encased in an extracellular matrix consisting of components produced by the microorganism and derived from the environment they grow in. They can be formed by both bacteria and fungi (277). It has been estimated that 99% of all bacteria live in biofilms (354). In nature, biofilms are primarily multispecies communities, where the different species engage in favorable metabolic interactions. For many organisms biofilms actually seems to be their preferred mode of growth. Biofilms are found in the everyday life; in the drain, on shower curtains, in the oil industry and deposited on our teeth. In clinical medicine, biofilms are usually monospecies, and they are considered an evil in that they complicate a range of infections. Many bacteria are associated with biofilm-associated infections, and most are hospital acquired (277, 278, 355-359). Living in a biofilm gives the bacteria the advantage of a better adaptation to environmental factors and increased resistance to hostile conditions (272, 277). Additionally, increased levels of horizontal gene transfer in biofilm can be important for the survival of a species, giving it new tools to adapt to environmental changes and driving evolution forward (360, 361). There is a significant metabolic shift from the planktonic to the biofilm mode of growth (352), towards anaerobic or micro aerobic metabolism, decreased transcription and translation, and induction of a dormant state of life for the bacteria (362). Most likely these changes are a result of the low concentration of oxygen in biofilms and the restricted availability of nutrients (352). 37
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 and 14: ecently published two reviews on th
Page 15 and 16: (IgM and IgG) are the only groups o
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: Table 2: Immune modulating strategi
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
Page 65 and 66: increase in serum somewhat later an
Page 67 and 68: knock-out mutant was treated as a n
Page 69 and 70: 5.4 The neonatal versus the adult i
Page 71 and 72: iofilms with a longer incubation ti
Page 73 and 74: 6. Main conclusions The Arginine Ca
Page 75 and 76: Animal models It is a long way from
Page 77 and 78: (15) Zarember KA, Godowski PJ. Tiss
Page 79 and 80: (41) Shaw MH, Reimer T, Kim YG, Nun
Page 81 and 82: (68) Gahr M, Speer CP, Damerau B, S
Page 83 and 84: (95) Bexborn F, Andersson PO, Chen
Page 85 and 86: (120) Riedemann NC, Neff TA, Guo RF
Page 87 and 88:
(145) Thurman JM, Holers VM. The ce
Page 89 and 90:
(171) Frakking FN, Brouwer N, van E
Page 91 and 92:
(197) Wynn JL, Levy O. Role of inna
Page 93 and 94:
(224) Schultz C, Temming P, Bucsky
Page 95 and 96:
type 1 and T cytotoxic type 1 cell
Page 97 and 98:
(275) Vuong C, Otto M. Staphylococc
Page 99 and 100:
hematological malignancies during t
Page 101 and 102:
(323) Avila-Figueroa C, Goldmann DA
Page 103 and 104:
(347) Christner M, Franke GC, Schom
Page 105 and 106:
(374) Hennig S, Nyunt Wai S, Ziebuh
Page 107 and 108:
(397) Miragaia M, de Lencastre H, P
Page 109 and 110:
for the quantification of complemen
Page 111 and 112:
importance of surface hydrophobicit
Page 113:
Paper 1
Page 117:
Paper 3
Page 121:
ISBN xxx-xx-xxxx-xxx-x
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