Infections, Starch, Endotoxins, And Nitric Oxide

Amazoniac

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Some people have really bad reactions when they ingest starch, here are some more clues:

Klebsiella microbes, found in the bowel flora, might be the trigger factors in this disease and therefore reduction in the size of the bowel flora could be of benefit in the treatment of AS patients.
Microbes from the bowel flora depend on dietary starch for their growth and therefore a reduction in starch intake might be beneficial in AS patients. A "low starch diet" involving a reduced intake of "bread, potatoes, cakes and pasta" has been devised and tested in healthy control subjects and AS patients. The "low starch diet" leads to a reduction of total serum IgA in both healthy controls as well as patients, and furthermore to a decrease in inflammation and symptoms in the AS patients.”

“Elevated levels of total serum IgA are found in AS patients during active phases of the disease (6,7) and this correlates with elevations in acute phase reactants such as erythrocyte sedimentation rate (ESR) and serum C-reactive protein (CRP), as well as with increased isolation of Klebsiella microbes from fecal samples (8). Furthermore ileo-colonoscopic studies from Ghent in Belgium, have revealed that during active phases of the disease, over 50% of AS patients have microscopic Crohn's like lesions in the gut mucosa (9).

Clearly gut involvement is present during active phases of the disease in AS patients and the most likely trigger factor would appear to be Klebsiella bacteria found in the bowel flora. Thus one possible way of treating relapses or acute phases of the disease in AS could be by reducing the number of microorganisms in the bowel flora, including Klebsiella. The main source of substrates on which colonic microbes depend are the residual dietary nutrients entering the large bowel following incomplete digestion.”

“The source of these carbohydrates could be dietary starch. Nearly all normal subjects fail to absorb appreciable amounts (5 - 20%) of starch in wheat flour, commonly present in bread and pasta, as assessed by oral hydrogen excretion studies, following a test meal. This is due to the formation of insoluble complexes between some carbohydrate and protein components of wheat. Breath hydrogen concentrations were measured for 5 hours after an overnight fast, followed by a test meal containing equal amounts of either sucrose or bread/pasta. The sucrose meal produced no increase in oral hydrogen but significant amounts were detected at 4 and 5 hours after a test meal with either bread or pasta (14).

It would appear that dietary mono- and disaccharides can be readily absorbed in the stomach and upper part of the small bowel and therefore they are not available as substrates for bacterial fermentation in the colon. The carbohydrates detected in the "ileostomy fluids" would appear to be derived from complex carbohydrates. These observations could form the basis of a "low starch" diet for AS patients.”

From: KickAS.org - Low Starch Diet in the Treatment of Patients Suffering from Ankylosing Spondylitis

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Enters nitric oxide; I mean, the opposite :ss
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC175233/pdf/651870.pdf

“Nitric oxide has been demonstrated to be a crucial and versatile molecule in the regulation of vascular tone, neurotransmission, acute and chronic inflammation, and host defense mechanisms (24). The widespread expression of inducible nitric oxide synthase (iNOS) following inflammation or infection has been well characterized and accepted as a vital component of the host’s adaptive response to noxious stimuli and virulent pathogens (22). This increase in nitric oxide and its role in the control of a variety of intracellular organisms has been described in leishmaniasis (23) and malaria (30) and for trypanasomal (26), viral (4), and fungal (2) infections.”

“Despite the obvious significance of the rise in nitric oxide levels in the milieu of infection, the mechanisms by which nitric oxide aids in host defense remain unspecified. Potential mechanisms include direct microbicidal effect via the reaction of nitric oxide with iron or thiol groups on proteins forming iron-nitrosyl complexes that inactivate enzymes crucial in mitochondrial respiration or DNA replication. In addition, nitric oxide has been found to react with superoxide to form reactive oxidants capable of damaging target cells (29). On a cellular level, nitric oxide exerts varied effects on leukocyte cell function, including the induction of macrophage apoptosis (1), the stimulation of macrophage cytoplasmic motility (12), the modulation of neutrophil adhesion (19), and the differential regulation of cytokine synthesis by leukocytes (20).”

Their main purposes were observing how nitric oxide rises during this infection and what happens if you suppress it. If the situation gets worse (survival, bacterial clearance, inflammatory cell recruitment, and cytokine profiles) when it’s suppressed, then they hypothesize that it has also a protective function.

“..These studies confirm that inoculation with K. pneumoniae results in the time-dependent and compartmentalized expression of nitric oxide during Klebsiella pneumonia.”

“L-NAME was previously shown to effectively inhibit the synthesis of nitric oxide both in vitro and in vivo at the dose administered, while D-NAME was shown to be a reliable inert enantiomer (33).”

“A significant increase in early lethality was noted in L-NAMEtreated infected mice compared to D-NAME-treated mice. In addition, long-term survival in the L-NAME-treated group was significantly decreased, as 70% of the D NAME-treated mice remained alive at 21 days, whereas only 30% of the L-NAMEtreated mice survived to that time point, representing a greater- than-twofold increase in mortality in the L-NAME-treated infected mice (Fig. 2). These results indicate that the inhibition of the endogenous production of nitric oxide significantly decreased survival in mice infected with K. pneumoniae.”

They then tested if the inflammatory markers were being suppressed by that compound or if they were lower due to nitric oxide actually inhibiting to some extent the progression of the infection.

“..In addition, bacterial killing of ingested K. pneumoniae cells was significantly attenuated in L-NAME-treated alveolar macrophages compared to that in cells exposed to D-NAME (P , 0.01) (Fig. 6B). Incubation of K. pneumoniae cells with either L-NAME or D-NAME in the absence of macrophages did not alter bacterial viability (data not shown). These findings indicate that nitric oxide represents a very important regulator of alveolar macrophage phagocytic and microbicidal activity in vitro.”

“We have established the time-dependent expression of nitric oxide within the lung during the course of murine Klebsiella pneumonia. Furthermore, the inhibition of nitric oxide synthesis by L-NAME results in significant mortality due to impaired bacterial clearance after challenge with K. pneumoniae. To our knowledge, this is the first study to clearly demonstrate that inhibition of endogenous nitric oxide production significantly alters the survival of animals in a murine model of infection by gram-negative bacteria.”

“Importantly, nitric oxide does not alter the influx of inflammatory leukocytes in vivo, but in vitro studies suggest that endogenous nitric oxide may activate the inflammatory cells present at the site of infection. Inhibition of nitric oxide synthesis clearly impaired both the ingestion and killing of K.pneumoniae cells, suggesting that nitric oxide may play a crucial role in activation of resident alveolar macrophages. The mechanism(s) whereby nitric oxide regulates alveolar macrophage phagocytic and microbicidal activity has not yet been defined. Nitric oxide has been shown to augment macrophage cytoplasmic motility (12), which may be mediated by changes in cell surface expression of adhesion molecules that are also instrumental in the ingestion of bacterial organisms.”

“Nitric oxide has been shown to stimulate the respiratory burst in inflammatory cells (29), which may partially account for the impairment in bacterial killing observed in alveolar macrophages incubated with L-NAME.”

“Furthermore, the phagocytosis and killing of Candida albicans cells by rat peritoneal neutrophils has been shown to be dependent upon endogeneous nitric oxide production (11). In contrast, Deitch and colleagues noted in a Pseudomonas model that neutrophil bactericidal activity was oxidant rather than nitric oxide dependent (8).”

“In summary, our studies demonstrate that mice in which nitric oxide is depleted and which are challenged i.t. with K.pneumoniae develop an inflammatory response similar to that of their non-nitric-oxide-depleted counterparts but that nitric oxide-depleted mice clearly had impairment in bacterial clearance. We have reported that there are no differences in the recruitment of inflammatory cells and that there is an increased expression of proinflammatory cytokines during the evolution of Klebsiella pneumonia in nitric oxide-depleted mice, compared to those animals with intact nitric oxide synthesis. Furthermore, nitric oxide appears to be an important mediator of macrophage phagocytosis and killing in Klebsiella pneumonia. The crucial role of nitric oxide in antibacterial host defense should be evident in several pertinent arenas. As treatment of bacterial infections becomes increasingly more difficult, the augmentation of nitric oxide synthesis and/or the local administration of nitric oxide may improve the clinical management of patients with severe bacterial pneumonias (6). In addition, the use of nonselective nitric oxide inhibitors in disease states such as septic shock (17), diabetes (7), or graft-versus-host disease (13) may result in impairment of antibacterial host defense, putting these patients at increased risk for the development of life-threatening nosocomial bacterial infections.”

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Magnesium Deficiency, A Brief Review


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In other words:

“For people with really sensitive intestines or bad bacteria, starch should be zero.”


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PakPik

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Just my non-expert take on nitric oxide and infections:
The problem with Nitric Oxide is that once it rises beyond physiological levels -and many many factors can contribute to the excess- two paradoxical things happen: 1) it generates immunossuppression and 2) stimulates formation of biofilms. So a little, physiological amount of N.O is good for infections, but anything beyond that will leave you more prone to immune deficiency, chronic infections and harder to treat infections (besides the well-known metabolic damage by N.O). In fact, lowering N.O can improve resistance to infections.

Nitric Oxide Leads to Biofilms

Inducible nitric oxide synthase deficiency in mice increases resistance to chronic infection with Echinococcus multilocularis. - PubMed - NCBI
"...Consequently, the high level of NO production observed during chronic infection in WT mice appears to contribute more to immunosuppression than to limitation of parasite growth. This is also reflected by the fact that splenocyte proliferation was significantly higher and parasite masses lower in iNOS-KO mice (at 1 and 4 months postinfection) than in WT mice."

In vivo blockage of nitric oxide with aminoguanidine inhibits immunosuppression induced by an attenuated strain of Salmonella typhimurium, potentia... - PubMed - NCBI
"... Collectively, these in vivo results underscore the dual biological consequences of NO production following Salmonella infection, with NO being necessary for host defense, but also having the potentially adverse effect of immunosuppression."

Macrophage nitric oxide mediates immunosuppression in infectious inflammation. - PubMed - NCBI
"...Evidence is presented that supports a relationship between the microbial burden in the spleen, the degree of nitric oxide produced, and the extent of immunosuppression. It is proposed that this model of microbial immunosuppression mediated by nitric oxide is generalizable for understanding immunosuppression and loss of delayed-type hypersensitivity induced by other microbes, such as Mycobacteria and measles virus

Possible role of nitric oxide in malarial immunosuppression. - PubMed - NCBI
 
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Amazoniac

Amazoniac

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Joined
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Messages
8,583
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Just my non-expert take on nitric oxide and infections:
The problem with Nitric Oxide is that once it rises beyond physiological levels -and many many factors can contribute to the excess- two paradoxical things happen: 1) it generates immunossuppression and 2) stimulates formation of biofilms. So a little, physiological amount of N.O is good for infections, but anything beyond that will leave you more prone to immune deficiency, chronic infections and harder to treat infections (besides the well-known metabolic damage by N.O). In fact, lowering N.O can improve resistance to infections.

Nitric Oxide Leads to Biofilms

Inducible nitric oxide synthase deficiency in mice increases resistance to chronic infection with Echinococcus multilocularis. - PubMed - NCBI
"...Consequently, the high level of NO production observed during chronic infection in WT mice appears to contribute more to immunosuppression than to limitation of parasite growth. This is also reflected by the fact that splenocyte proliferation was significantly higher and parasite masses lower in iNOS-KO mice (at 1 and 4 months postinfection) than in WT mice."

In vivo blockage of nitric oxide with aminoguanidine inhibits immunosuppression induced by an attenuated strain of Salmonella typhimurium, potentia... - PubMed - NCBI
"... Collectively, these in vivo results underscore the dual biological consequences of NO production following Salmonella infection, with NO being necessary for host defense, but also having the potentially adverse effect of immunosuppression."

Macrophage nitric oxide mediates immunosuppression in infectious inflammation. - PubMed - NCBI
"...Evidence is presented that supports a relationship between the microbial burden in the spleen, the degree of nitric oxide produced, and the extent of immunosuppression. It is proposed that this model of microbial immunosuppression mediated by nitric oxide is generalizable for understanding immunosuppression and loss of delayed-type hypersensitivity induced by other microbes, such as Mycobacteria and measles virus

Possible role of nitric oxide in malarial immunosuppression. - PubMed - NCBI
Interesting. So, I guess it's not only related to accumulation.
It works in a similar way as antibiotic overuse, that if you don't eradicate, with each round the infection become more and more resistant?
 

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