scholarly journals The Relative Role of Bacterial Cell Wall and Capsule in the Induction of Inflammation in Pneumococcal Meningitis

1985 ◽  
Vol 151 (3) ◽  
pp. 535-540 ◽  
Author(s):  
E. Tuomanen ◽  
A. Tomasz ◽  
B. Hengstler ◽  
O. Zak
2002 ◽  
Vol 22 (1-2) ◽  
pp. 209-222 ◽  
Author(s):  
Bénédicte Flambard

1991 ◽  
Vol 260 (2) ◽  
pp. G213-G219 ◽  
Author(s):  
R. A. DeLa Cadena ◽  
K. J. Laskin ◽  
R. A. Pixley ◽  
R. B. Sartor ◽  
J. H. Schwab ◽  
...  

The plasma kallikrein-kinin system is activated in Gram-negative sepsis and typhoid fever, two diseases in which bacterial products have been shown to initiate inflammation. Because a single intraperitoneal injection of bacterial cell wall peptidoglycan-polysaccharide polymers from group A steptococci (PG-APS) into a Lewis rat produces a syndrome of relapsing polyarthritis and anemia, we investigated changes in the role of the kallikrein-kinin system in this model of inflammation. Coagulation studies after injection of PG-APS revealed an immediate and persistent decrease in prekallikrein levels. High-molecular-weight kininogen levels decreased significantly during the acute phase and correlated with the severity of arthritis. Factor XI levels were decreased only during the acute phase. Antithrombin III levels remained unchanged, indicating that neither decreased hepatic synthesis nor disseminated intravascular coagulation caused the decreased plasma contact factors. Plasma T-kininogen (an acute phase protein) was significantly elevated during the chronic phase. PG-APS failed to activate the contact system in vitro. Thus the kallikrein-kinin system plays an important role in this experimental model of inflammation, suggesting that activation of this system may play a role in the pathogenesis of inflammatory bowel disease and rheumatoid arthritis in which bacterial products might be etiologically important.


Biochemistry ◽  
2000 ◽  
Vol 39 (9) ◽  
pp. 2164-2173 ◽  
Author(s):  
Ernst Schönbrunn ◽  
Susanne Eschenburg ◽  
Florian Krekel ◽  
Karolin Luger ◽  
Nikolaus Amrhein

2013 ◽  
Vol 16 (6) ◽  
pp. 760-766 ◽  
Author(s):  
Timothy K Lee ◽  
Kerwyn Casey Huang

1987 ◽  
Vol 53 (8) ◽  
pp. 1893-1897 ◽  
Author(s):  
M C van Loosdrecht ◽  
J Lyklema ◽  
W Norde ◽  
G Schraa ◽  
A J Zehnder

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Lauren Genova ◽  
James Melnyk ◽  
Vishnu Mohanan ◽  
Catherine Grimes

2019 ◽  
Author(s):  
Garima Rani ◽  
Issan Patri

AbstractThe bacterial cell wall is primarily composed of a mesh of stiff glycan strands cross-linked by peptide bridges and is essential for safeguarding the cell. The structure of the cell wall has to be stiff enough to bear the high turgor pressure and sufficiently tough to ensure protection against failure. Here we explore the role of various design features of the cell in enhancing the toughness of the cell wall. We explain how the glycan strand length distribution and the degree of cross-linking can play a vital role in ensuring that the cell wall offers sufficient resistance to propagation of cracks. We suggest a possible mechanism by which peptide bond hydrolysis can also help mitigate this risk of failure. We also study the reinforcing effect of MreB on the cell wall and conclude that the cross-linked structure of the cell wall plays the more important role in safeguarding against mechanical failure due to cracking.


2000 ◽  
Vol 68 (8) ◽  
pp. 4688-4698 ◽  
Author(s):  
Michael P. Kozar ◽  
Mark T. Krahmer ◽  
Alvin Fox ◽  
Barry M. Gray

ABSTRACT Muramic acid serves as a marker for the presence of bacterial cell wall debris in mammalian tissues. There have been a number of controversial and sometimes conflicting results on assessing the levels of muramic acid in health and disease. The present report is the first to use the state-of-the art technique, gas chromatography-tandem mass spectrometry, to identify and quantify the levels of muramic acid in tissues. Muramic acid was not found in normal rat brain or spleen. However, when tissues were spiked with muramic acid, it was readily identified. The detection limit was <1 ng of muramic acid/100 mg (wet weight) of tissue. The levels of muramic acid reported in diseased human spleen and spleen of arthritic rats, previously injected with bacterial cell walls, were 100- to 1,000-fold higher. In the present study, muramic acid was also readily detected in the cerebrospinal fluid of patients with pneumococcal meningitis (6.8 to 3,900 ng of muramic acid/ml of cerebrospinal fluid). In summary, there can be an enormous difference in the levels of muramic acid found in different mammalian tissues and body fluids in health and disease. This report could have great impact in future studies assessing the role of bacterial cell wall remnants in the pathogenesis of certain human inflammatory diseases.


Author(s):  
T. Kossmann ◽  
C. Manthey ◽  
J. B. Allen ◽  
C. Morganti-Kossmann ◽  
K. Ohura ◽  
...  

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