Effect of cyclopiazonic acid on delayed hypersensitivity to Mycobacterium tuberculosis, complement activity, serum enzymes, and bilirubin in guinea pigs

1986 ◽  
Vol 96 (2) ◽  
pp. 73-77 ◽  
Author(s):  
John L. Richard ◽  
W. Michael Peden ◽  
Rod E. Fichtner ◽  
Richard J. Cole
1951 ◽  
Vol 29 (2) ◽  
pp. 48-58
Author(s):  
Christine E. Rice ◽  
Paul Boulanger ◽  
P. J. G. Plummer

To determine whether liver injury would result in a parallel decline in the complement titer and coagulative properties of the blood, groups of guinea pigs were given series of injections of the liver poison, carbon tetrachloride. Marked fatty degeneration of the liver, a decline in total serum protein and albumin, a decrease in complement activity, and a prolongation of coagulation time was observed in the treated animals. A general relationship was noted between the albumin-globulin ratio and the complement titer of the serum and between the complement titer and the coagulation time of the plasma.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Mamta Singh ◽  
Prabhakar Tiwari ◽  
Garima Arora ◽  
Sakshi Agarwal ◽  
Saqib Kidwai ◽  
...  

Abstract Inorganic polyphosphate (PolyP) plays an essential role in microbial stress adaptation, virulence and drug tolerance. The genome of Mycobacterium tuberculosis encodes for two polyphosphate kinases (PPK-1, Rv2984 and PPK-2, Rv3232c) and polyphosphatases (ppx-1, Rv0496 and ppx-2, Rv1026) for maintenance of intracellular PolyP levels. Microbial polyphosphate kinases constitute a molecular mechanism, whereby microorganisms utilize PolyP as phosphate donor for synthesis of ATP. In the present study we have constructed ppk-2 mutant strain of M. tuberculosis and demonstrate that PPK-2 enzyme contributes to its ability to cause disease in guinea pigs. We observed that ppk-2 mutant strain infected guinea pigs had significantly reduced bacterial loads and tissue pathology in comparison to wild type infected guinea pigs at later stages of infection. We also report that in comparison to the wild type strain, ppk-2 mutant strain was more tolerant to isoniazid and impaired for survival in THP-1 macrophages. In the present study we have standardized a luciferase based assay system to identify chemical scaffolds that are non-cytotoxic and inhibit M. tuberculosis PPK-2 enzyme. To the best of our knowledge this is the first study demonstrating feasibility of high throughput screening to obtain small molecule PPK-2 inhibitors.


Vaccine ◽  
2012 ◽  
Vol 30 (9) ◽  
pp. 1572-1582 ◽  
Author(s):  
Shaobin Shang ◽  
Crystal A. Shanley ◽  
Megan L. Caraway ◽  
Eileen A. Orme ◽  
Marcela Henao-Tamayo ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (6) ◽  
pp. e66310 ◽  
Author(s):  
Ciaran Skerry ◽  
Supriya Pokkali ◽  
Michael Pinn ◽  
Nicholas A. Be ◽  
Jamie Harper ◽  
...  

1972 ◽  
Vol 59 (4) ◽  
pp. 345-348 ◽  
Author(s):  
William L. Weston ◽  
Mickey J. Mandel ◽  
Gerald G. Krueger ◽  
Henry N. Claman

1957 ◽  
Vol 105 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Jonathan W. Uhr ◽  
A. M. Pappenheimer ◽  
M. Yoneda

Guinea pigs infected by intradermal injection of living toxigenic diphtheria bacilli and protected by horse antitoxic globulin, given either before or after infection, develop delayed hypersensitivity of the tuberculin type to diphtherial proteins. The highest degree of hypersensitivity is specifically directed against diphtheria toxin (or toxoid) itself, although smaller delayed skin reactions may be evoked in sensitized animals by other diphtherial proteins common to both toxigenic and non-toxigenic strains. Animals sensitized to diphtheria toxin by infection with a toxigenic strain in this way react positively to the Schick test and their serum usually contains no detectable antitoxin 2 to 3 weeks after the initial infection. Animals infected with living non-toxigenic diphtheria bacilli become sensitized to proteins common to both toxigenic and non-toxigenic strains but do not show sensitivity to toxin. The observations suggest that a minute amount of toxoid, or of toxin comparable to that which might be liberated during infection, might induce the hypersensitive state if injected in the form of a complex with excess antitoxin. This prediction is verified by the results reported in the following paper (23).


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