scholarly journals Local immune response to Escherichia coli pili in experimental pyelonephritis.

1981 ◽  
Vol 31 (1) ◽  
pp. 17-20 ◽  
Author(s):  
J W Smith ◽  
S Wagner ◽  
R M Swenson
1998 ◽  
Vol 4 (2) ◽  
pp. 71-75
Author(s):  
Takaoki Hirose ◽  
Akifumi Yokoo ◽  
Hiroshi Hotta ◽  
Yasuharu Kunishima ◽  
Taiji Tsukamoto

1999 ◽  
Vol 45 (9) ◽  
pp. 723-731 ◽  
Author(s):  
J Wayne Conlan ◽  
Rhonda KuoLee ◽  
Ann Webb ◽  
Malcolm B Perry

The present study was performed to assess the potential of a humoral mucosal immune response directed against the O157 antigen of Escherichia coli O157:H7 to prevent intestinal colonization by the pathogen. To this end, mice were gavaged with inocula of Salmonella landau, a Salmonella strain that naturally expresses the O157 antigen. Salmonella landau was avirulent for mice. Despite this, mice exposed to S. landau developed high titres of serum and coproantibodies against the O157 antigen. These mice, compared with controls, demonstrated some ability to resist transient intestinal colonization by an oral inoculum of an isolate of E. coli O157:H7. These findings suggest that a local immune response directed against the O157 antigen might increase host resistance to this pathogen.Key words: Salmonella landau, Escherichia coli O157:H7, mucosal immunity, mice.


1992 ◽  
Vol 66 (7) ◽  
pp. 964-973 ◽  
Author(s):  
Takaoki HIROSE ◽  
Yoshiaki KUMAMOTO ◽  
Masanori MATSUKAWA ◽  
Akibumi YOKOO ◽  
Takashi SATOH ◽  
...  

2021 ◽  
pp. 31-40
Author(s):  
M.R. Orazov ◽  
L.M. Mikhaleva ◽  
E.S. Silantieva ◽  
R.E. Orekhov

Recent evidence indicates that the endometrium plays a much more important role in successful implantation and clinical pregnancy than many other recognized factors. Chronic endometritis (CE) is associated with negative reproductive outcomes, including repeated implantation failures. Streptococcus spp., Escherichia coli, Enterococcus faecalis, Klebsiella pneumoniae, Staphylococcus spp., Corynebacterium and Mycoplasma / Ureaplasmaspp are currently considered the main pathogens of CE. This disease disrupts the architectonics of the endometrium at different levels: first of all, CE promotes changes in the population of immunocompetent cells and, therefore, contributes to the disruption of the local immune response in the endometrium at the time of implantation. Antibiotic treatment for CE improves implantation rates and decreases abortion rates, although there are no well-designed prospective studies to support this conclusion. Considering the insufficient effectiveness of antibiotic therapy for CE, especially in cases of resistance of pathogens, or in the case of viral chronic endometritis, it is necessary to develop schemes with additional use of drugs that affect other etiopathogenetic pathways of development and maintenance of CE. An example of such a treatment can be cytokine therapy, which requires further study regarding the efficacy and safety in CE therapy.


1968 ◽  
Vol 47 (11) ◽  
pp. 2541-2550 ◽  
Author(s):  
James D. Lehmann ◽  
James W. Smith ◽  
Thomas E. Miller ◽  
Jack A. Barnett ◽  
Jay P. Sanford

2000 ◽  
Vol 80 (8) ◽  
pp. 1299-1309 ◽  
Author(s):  
René van den Wijngaard ◽  
Anna Wankowicz-Kalinska ◽  
Caroline Le Poole ◽  
Bert Tigges ◽  
Wiete Westerhof ◽  
...  

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 110
Author(s):  
Anna K. Riebisch ◽  
Sabrina Mühlen ◽  
Yan Yan Beer ◽  
Ingo Schmitz

Autophagy is a highly conserved and fundamental cellular process to maintain cellular homeostasis through recycling of defective organelles or proteins. In a response to intracellular pathogens, autophagy further acts as an innate immune response mechanism to eliminate pathogens. This review will discuss recent findings on autophagy as a reaction to intracellular pathogens, such as Salmonella typhimurium, Listeria monocytogenes, Mycobacterium tuberculosis, Staphylococcus aureus, and pathogenic Escherichia coli. Interestingly, while some of these bacteria have developed methods to use autophagy for their own benefit within the cell, others have developed fascinating mechanisms to evade recognition, to subvert the autophagic pathway, or to escape from autophagy.


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