Candida and Probiotics
Probiotics provide Candida-inhibiting activities of commensal bacteria that reside in the alimentary and vaginal tracts of humans. Probiotic microbes not only suppress the growth of Candida spp in the alimentary tract and vagina, but they also inhibit the adherence of Candida spp to epithelial surfaces(11).
Lactobacilli and Bifidobacteria have the capacity to inhibit Candida spp.
Each strain can have a different effect. That is the reason, Custom Probiotics formulates and supplies single and multistrain highest potency and quality probiotic bacteria for maximum effectiveness. We perform rigorous independent lab testing to verify the bacterial count of every batch to guarantee the potency of our probiotic dietary supplements.
A variety of mechanisms have been evoked to explain the anti-Candida activity of the probiotics. Nutritional competition, blocking receptors to Candida spp., adhesions on epithelial cells, production of anti-Candida compounds, increasing intestinal peristalsis, increasing intestinal epithelial cell renewal rates, alteration of pH and the production of an anaerobic oxidation-reduction potential (C. albicans is an aerobic microbe) have all been proposed as mechanisms that probiotic bacteria use to inhibit pathogens on mucosal surfaces.
The ability of probiotic bacteria to stimulate innate and acquired immune systems in the host and activate phagocytic cells is also thought to play a role in the inhibition of Candida spp. It is very likely that because of the recognized complexity of the aerobic and anaerobic normal flora, all the above factors are involved in the suppression of Candida spp. on mucosal surfaces. As a result, the inhibition of Candida spp. by probiotic bacteria, in the alimentary and vaginal tracts, represents a key, first-line defense against mucosal and systemic candidiasis.
http://www.customprobiotics.com/candida.htm
Friday, September 10, 2010
Systemic bacterial invasion induced by sleep deprivation
Systemic bacterial invasion induced by sleep deprivation
Am J Physiol Regul Integr Comp Physiol 278: R905-R916, 2000;
0363-6119/00 $5.00
Vol. 278, Issue 4, R905-R916, April 2000
Carol A. Everson1 and Linda A. Toth2
1 Department of Physiology, University of Tennessee College of Medicine and 2 Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis Tennessee 38163
Profound sleep disruption in humans is generally believed to cause health impairments.
Through comparative research, specific physical effects and underlying mechanisms altered by sleep deprivation are being elucidated.
Studies of sleep-deprived animals previously have shown a progressive, chronic negative energy balance and gradual deterioration of health, which culminate in fatal bloodstream infection without an infectious focus.
The present study investigated the conditions antecedent to advanced morbidity in sleep-deprived rats by determining the time course and distribution of live microorganisms in body tissues that are normally sterile.
The tissues cultured for microbial growth included the blood, four major organs, six regional lymph nodes, the intestine, and the skin.
The principal finding was early infection of the mesenteric lymph nodes by bacteria presumably translocated from the intestine and bacterial migration to and transient infection of extraintestinal sites.
Presence of pathogenic microorganisms and their toxins in tissues constitutes a septic burden and chronic antigenic challenge for the host.
Bacterial translocation and pathogenic sequelae provide mechanisms by which sleep deprivation appears to adversely affect health.
http://ajpregu.physiology.org/cgi/content/abstract/278/4/R905
Sleep Deprivation and Host Defense
Am J Physiol Regul Integr Comp Physiol 280: R602-R603, 2001;
0363-6119/01 $5.00
Vol. 280, Issue 2, R602-R603, February 2001
To the Editor: Rechtschaffen and Bergmann cite studies that they contend counter our suggestion that systemic bacterial invasion and antigenic challenge are a likely cause of physiological signs induced by sleep deprivation (5). A number of issues must be considered in the interpretation of those studies and the extent to which they are germane to the present study.
A 1989 publication by Benca and colleagues (2) reported the results of in vitro proliferation and antibody tests on spleen cells collected from rats late in the experimental period. The findings showed that as compared with the responses of yoked rats, about half of the sleep-deprived rats showed reduced cellular responsiveness and half showed greater responsiveness in both assays. Thus the effects were not consistent. Moreover, bacterial translocation is not dependent on impaired lymphoproliferation, and in vitro antibody production by B cells is not necessarily reflective of sepsis.
The report of an increased rate of regression of experimentally induced subcutaneous tumors in sleep-deprived versus yoked rats (4) is an intriguing finding, but this effect is nonspecific and could be related to metabolic rather than immunologic mechanisms. The report therefore did not influence how we interpreted our findings.
Impaired host defense, accompanied by systemic infections and the many physiological and metabolic changes associated with septic states, provides a plausible explanation for signs of sleep deprivation, including hypercatabolism, a well-known consequence of infectious disease states (1). We measured numbers of live bacteria and not the many intermediary physiological responses that would link the presence of bacteria to the development of other signs. Therefore, our study was not designed to reveal correlations that might establish relationships between bacterial invasion and the progressive development of other signs associated with chronic sleep deprivation.
In a study designed to show that elimination of aerobic bacteria does not markedly alter the physiological signs associated with chronic sleep deprivation, Bergmann and colleagues (3) administered an antibiotic cocktail to rats during the baseline period and the first 4 days of sleep deprivation.
Despite this prophylactic treatment, however, eight sleep-deprived or yoked rats were excluded from analysis due to positive bacterial cultures, suggesting that the antibiotic regimen was largely ineffective.
Data from the remaining four bacteria-negative sleep-deprived rats, combined with similar data from rats given the antibiotic cocktail late during the course of sleep deprivation, were the basis for the reported negative correlation.
An absence of positive cultures of aerobic bacteria in a subset of antibiotic-treated sleep-deprived rats does not negate the finding or the implications of positive cultures of pathogenic microorganisms in untreated or even treated sleep-deprived rats.
Furthermore, the absence of positive blood or tissue cultures in septicemic patients is a well-known clinical phenomenon and does not negate the state of sepsis.
Moreover, factors other than aerobic bacteria (e.g., endotoxins derived from gut contents or killed translocated bacteria) can cause similar metabolic derangements.
Our data indicate impaired host defense, evidenced by the presence of live bacteria in normally sterile tissues.
We hypothesize that physiological changes induced by sleep deprivation allow bacteria to leave the gut, evade antimicrobial systems, and cause transient infections and finally septicemia, which leads to the death of the animal.
We thus view the presence of bacteria as a sign of a more fundamental abnormality. Clinically significant bacterial translocation and posttranslocation survival of bacteria typically does not occur in the absence of local or systemic immune impairment.
http://ajpregu.physiology.org/cgi/content/full/280/2/R602
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Am J Physiol Regul Integr Comp Physiol 278: R905-R916, 2000;
0363-6119/00 $5.00
Vol. 278, Issue 4, R905-R916, April 2000
Carol A. Everson1 and Linda A. Toth2
1 Department of Physiology, University of Tennessee College of Medicine and 2 Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis Tennessee 38163
Profound sleep disruption in humans is generally believed to cause health impairments.
Through comparative research, specific physical effects and underlying mechanisms altered by sleep deprivation are being elucidated.
Studies of sleep-deprived animals previously have shown a progressive, chronic negative energy balance and gradual deterioration of health, which culminate in fatal bloodstream infection without an infectious focus.
The present study investigated the conditions antecedent to advanced morbidity in sleep-deprived rats by determining the time course and distribution of live microorganisms in body tissues that are normally sterile.
The tissues cultured for microbial growth included the blood, four major organs, six regional lymph nodes, the intestine, and the skin.
The principal finding was early infection of the mesenteric lymph nodes by bacteria presumably translocated from the intestine and bacterial migration to and transient infection of extraintestinal sites.
Presence of pathogenic microorganisms and their toxins in tissues constitutes a septic burden and chronic antigenic challenge for the host.
Bacterial translocation and pathogenic sequelae provide mechanisms by which sleep deprivation appears to adversely affect health.
http://ajpregu.physiology.org/cgi/content/abstract/278/4/R905
Sleep Deprivation and Host Defense
Am J Physiol Regul Integr Comp Physiol 280: R602-R603, 2001;
0363-6119/01 $5.00
Vol. 280, Issue 2, R602-R603, February 2001
To the Editor: Rechtschaffen and Bergmann cite studies that they contend counter our suggestion that systemic bacterial invasion and antigenic challenge are a likely cause of physiological signs induced by sleep deprivation (5). A number of issues must be considered in the interpretation of those studies and the extent to which they are germane to the present study.
A 1989 publication by Benca and colleagues (2) reported the results of in vitro proliferation and antibody tests on spleen cells collected from rats late in the experimental period. The findings showed that as compared with the responses of yoked rats, about half of the sleep-deprived rats showed reduced cellular responsiveness and half showed greater responsiveness in both assays. Thus the effects were not consistent. Moreover, bacterial translocation is not dependent on impaired lymphoproliferation, and in vitro antibody production by B cells is not necessarily reflective of sepsis.
The report of an increased rate of regression of experimentally induced subcutaneous tumors in sleep-deprived versus yoked rats (4) is an intriguing finding, but this effect is nonspecific and could be related to metabolic rather than immunologic mechanisms. The report therefore did not influence how we interpreted our findings.
Impaired host defense, accompanied by systemic infections and the many physiological and metabolic changes associated with septic states, provides a plausible explanation for signs of sleep deprivation, including hypercatabolism, a well-known consequence of infectious disease states (1). We measured numbers of live bacteria and not the many intermediary physiological responses that would link the presence of bacteria to the development of other signs. Therefore, our study was not designed to reveal correlations that might establish relationships between bacterial invasion and the progressive development of other signs associated with chronic sleep deprivation.
In a study designed to show that elimination of aerobic bacteria does not markedly alter the physiological signs associated with chronic sleep deprivation, Bergmann and colleagues (3) administered an antibiotic cocktail to rats during the baseline period and the first 4 days of sleep deprivation.
Despite this prophylactic treatment, however, eight sleep-deprived or yoked rats were excluded from analysis due to positive bacterial cultures, suggesting that the antibiotic regimen was largely ineffective.
Data from the remaining four bacteria-negative sleep-deprived rats, combined with similar data from rats given the antibiotic cocktail late during the course of sleep deprivation, were the basis for the reported negative correlation.
An absence of positive cultures of aerobic bacteria in a subset of antibiotic-treated sleep-deprived rats does not negate the finding or the implications of positive cultures of pathogenic microorganisms in untreated or even treated sleep-deprived rats.
Furthermore, the absence of positive blood or tissue cultures in septicemic patients is a well-known clinical phenomenon and does not negate the state of sepsis.
Moreover, factors other than aerobic bacteria (e.g., endotoxins derived from gut contents or killed translocated bacteria) can cause similar metabolic derangements.
Our data indicate impaired host defense, evidenced by the presence of live bacteria in normally sterile tissues.
We hypothesize that physiological changes induced by sleep deprivation allow bacteria to leave the gut, evade antimicrobial systems, and cause transient infections and finally septicemia, which leads to the death of the animal.
We thus view the presence of bacteria as a sign of a more fundamental abnormality. Clinically significant bacterial translocation and posttranslocation survival of bacteria typically does not occur in the absence of local or systemic immune impairment.
http://ajpregu.physiology.org/cgi/content/full/280/2/R602
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Partial sleep deprivation compromises gastric mucosal integrity in rats
Partial sleep deprivation compromises gastric mucosal integrity in rats
Copyright © 2005 Elsevier Inc. All rights reserved.
Jin Sheng Guoa, b, Jenny Fung Ling Chaua, Chi Hin Choa and Marcel Wing Leung Kooa, ,
aDepartment of Pharmacology, Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong, China
bDivision of Digestive Diseases, Department of Internal Medicine, Zhong Shan Hospital, Fu Dan University, Shanghai, 200032, China
Received 27 June 2004; accepted 29 December 2004. Available online 3 February 2005.
Abstract
The gastric mucosa is most susceptible to stress that has been shown to induce mucosal damage in humans and animals.
This study aims to explore the underlying mechanisms of partial sleep deprivation, as a source of psychophysiological stress, on gastric functions and its effect on mucosal integrity.
Sprague-Dawley rats were partially sleep deprived (PSD) for 7 or 14 days by housing inside slowly rotating drums.
Gastric tissues and plasma were sampled at the end of the sleep deprivation periods and mucosal lesion scores were evaluated.
Morphological examination was performed after Hematoxylin and Eosin staining.
Plasma levels of noradrenaline, adrenaline, gastrin, histamine and somatostatin were determined with enzyme immunoassays.
Gastric acidity was measured with acid-base titration in pylorus ligated rats.
Gastric mucosal blood flow was evaluated with Laser Doppler Flowmetry.
It was found that gastric lesions were induced in about 30%–50% of the PSD rats.
Gastric acidity as well as plasma levels of noradrenaline, gastrin and histamine were elevated.
Gastric mucosal blood flow and plasma somatostatin level were on the contrary reduced, especially in rats with PSD for 14 days.
It is concluded that partial sleep deprivation compromises gastric mucosal integrity by increasing gastric acidity, plasma levels of noradrenaline, gastrin, histamine, and decreasing gastric mucosal blood flow.
These results provided experimental evidence on the gastric damaging effects of PSD and it could be one of the risk factors contributing to gastric ulcer formation.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T99-4FD9T34-2&_user=10&_coverDate=05%2F27%2F2005&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1457174832&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=f9811966dbe182c07f98894c3124fd8b&searchtype=a
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Copyright © 2005 Elsevier Inc. All rights reserved.
Jin Sheng Guoa, b, Jenny Fung Ling Chaua, Chi Hin Choa and Marcel Wing Leung Kooa, ,
aDepartment of Pharmacology, Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong, China
bDivision of Digestive Diseases, Department of Internal Medicine, Zhong Shan Hospital, Fu Dan University, Shanghai, 200032, China
Received 27 June 2004; accepted 29 December 2004. Available online 3 February 2005.
Abstract
The gastric mucosa is most susceptible to stress that has been shown to induce mucosal damage in humans and animals.
This study aims to explore the underlying mechanisms of partial sleep deprivation, as a source of psychophysiological stress, on gastric functions and its effect on mucosal integrity.
Sprague-Dawley rats were partially sleep deprived (PSD) for 7 or 14 days by housing inside slowly rotating drums.
Gastric tissues and plasma were sampled at the end of the sleep deprivation periods and mucosal lesion scores were evaluated.
Morphological examination was performed after Hematoxylin and Eosin staining.
Plasma levels of noradrenaline, adrenaline, gastrin, histamine and somatostatin were determined with enzyme immunoassays.
Gastric acidity was measured with acid-base titration in pylorus ligated rats.
Gastric mucosal blood flow was evaluated with Laser Doppler Flowmetry.
It was found that gastric lesions were induced in about 30%–50% of the PSD rats.
Gastric acidity as well as plasma levels of noradrenaline, gastrin and histamine were elevated.
Gastric mucosal blood flow and plasma somatostatin level were on the contrary reduced, especially in rats with PSD for 14 days.
It is concluded that partial sleep deprivation compromises gastric mucosal integrity by increasing gastric acidity, plasma levels of noradrenaline, gastrin, histamine, and decreasing gastric mucosal blood flow.
These results provided experimental evidence on the gastric damaging effects of PSD and it could be one of the risk factors contributing to gastric ulcer formation.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T99-4FD9T34-2&_user=10&_coverDate=05%2F27%2F2005&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1457174832&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=f9811966dbe182c07f98894c3124fd8b&searchtype=a
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