What Would Your Recommendations Be For Gut Inflammation, Gas Formation, Infection?

[Amazoniac]

- A lay doctor's guide to the inflammatory process in the gastrointestinal tract
- A guide to immunometabolism for immunologists

- Resolution of Inflammation and Gut Repair in IBD: Translational Steps Towards Complete Mucosal Healing
- Activation of Resolution Pathways to Prevent and Fight Chronic Inflammation: Lessons From Asthma and Inflammatory Bowel Disease
- Actors and Factors in the Resolution of Intestinal Inflammation: Lipid Mediators As a New Approach to Therapy in Inflammatory Bowel Diseases
- Keep calm: the intestinal barrier at the interface of peace and war
- Targeting gut barrier dysfunction with phytotherapies: Effective strategy against chronic diseases

 

[Amazoniac]

- Modulation of cytokine expression by traditional medicines: A review of herbal immunomodulators (!)

 

[Amazoniac]

- The biology of mucus: Composition, synthesis and organization
- Structure of intestinal-mucus glycoprotein from human post-mortem or surgical tissue: Inferences from correlation analyses of sugar and sulfate composition of individual mucins
- The Carbohydrate Composition of Mucin in Colonic Cancer
- Bacterial Glycosulphatases and Sulphomucin Degradation

 

[Amazoniac]

- Is Resolution the End of Inflammation?

Spoiler

"Resolution is typically defined as a tightly regulated process that restores tissue homeostasis and prevents the development of chronic disease [59]. Recent studies however introduce an alternative model in which resolution is not the end of immune responses to infection/injury, but that there is immunological activity occurring after the resolution cascade is complete that alters the immune physiology of the affected tissue post-injury.

It has been demonstrated that even after the inciting stimulus has been removed and resolution processes have dampened proinflammatory signals and cleared the traditional innate type leukocytes, there is continued immunological activity occurring at the subclinical level. Using a model of resolving murine peritonitis induced by low-dose yeast cell extract, zymosan, or by bacterial infection with Streptococcus pneumoniae, elicited a hitherto overlooked second wave of leukocyte infiltration into the tissue that persisted for months [60]."

"[..]data showing immune activity after resolution are supported by a variety of studies. Da Fonseca et al. [62] observed that following clearance of Yersinia pseudotuberculosis infection in mice, innate immune cells, particularly DCs accumulated in the adipose tissue. Importantly, following resolution of the infection, there were prolonged defects in the physical integrity of the gut-draining lymphatics, highlighted by leakage of the fluorescent long-chain fatty acid, Bodipy FL C16. This defect was sustained up to 10 months post-infection. Additionally, interruptions in the molecular and cellular interactions between the gut and mesenteric lymph nodes (MLNs), led to impaired mucosal immune responses that persisted for 42 weeks in mice, including reduced generation of regulatory T (Treg) cells, decreased Th17 induction, and prolonged increased production of proinflammatory cytokines such as IL-1b and TNFa, indicating a shift toward type-1 immunity [62]. Additionally, Collins et al. reported that infection with herpes simplex virus (HSV)-1 in mice leads to infiltration of CCR2-dependent cells in the skin, peaking at day 7 post-infection; a time that coincides with viral clearance. Subsequently, there were twofold and fourfold elevated numbers of DCs and macrophages locally, respectively, 30 days post-inflammation, when compared with unaffected regions. The numerical increase in localised DC and macrophage populations was observed for at least 23 weeks post-infection, well after viral clearance, and enhanced interferon-g responses by virus-specific CD4+ T cells upon reinfection with HSV-1, thereby protecting the tissue from reinfection [63]. Furthermore, when the irritant 1-fluoro-2,4-dinitrobenzene (DNFB) was applied to murine flank skin 30 days post-HSV-1 infection, there were threefold more DCs and sixfold more macrophages compared with untreated skin. This highlights that the phenomenon of continued immune activity was not only confined to HSV-1 infection, but is found more generally following an inflammatory response in the skin [63]."

"Evidence of immune activity following resolution in humans has been investigated utilising a model of acute inflammation driven by intradermal UV-killed E. coli in healthy male volunteers [68]. Similar to what has been reported in mouse models, there was evidence of sustained further cellular infiltration into the tissue following resolution. Flow cytometric analyses revealed an approximately tenfold increase of both CD4+/CD45RO+/CCR7 and CD8+/CD45RO+/ CCR7 memory T cells. Histology also revealed a significant increase in the numbers of CD163+ macrophages at the site from day 7 up to at least 17 days post-infection, and these levels were significantly higher than those in naïve tissue [69]. Post-resolution conservation in both murine and human models adds credence to the emerging concept that resolution is not the end of immune-mediated response post-inflammation."

"Da Fonseca et al. [62] proposed that a long-gone infection may set the stage for the development of chronic disease due to alterations in the immune system. They show that a single transient encounter with Y. pseudotuberculosis has profound effects on tissue-specific immunity. The post-resolution environment in this case is characterised by lymphatic leakage in the mesenteric adipose tissue that redirects DCs to the adipose compartment, thereby preventing their proper accumulation in the MLNs. Chronic mesenteric lymphadenopathy is not limited to Yersinia infection, but is also evident in in a variety of other diseases including Crohn’s disease and coeliac disease [99,100]. The precise mechanism by which Y. pseudotuberculosis triggers these alterations to the lymphatic system is not understood; however, mucosal functions including tolerance and protective immunity are compromised. A key finding in this study is that Y. pseudotuberculosis infection may predispose to food allergy. Mice that displayed mesenteric lymphadenopathy induced by Y. pseudotuberculosis failed to acquire oral tolerance following oral ovalbumin (OVA) exposure and displayed a delayed type hypersensitivity reaction to OVA challenge. The breaking of tolerance in this case can be linked to a failure of migratory DCs to access the MLNs. A dramatic decrease of DCs in the MLNs, generation of Treg cells and IgA, which are important for maintaining a tolerogenic environment, results in profound consequences for the normally tolerogenic mucosal environment. Thus, the authors propose that infections, despite effective resolution result in immunological scarring, and that following a simple infection, the complex balance between the immune system and the gastrointestinal microbiota is compromised, creating a context for an otherwise innocuous microbe to become a chronic pathogen [62]. This connection between the immune system and the microbiome is frequently reported in the gastrointestinal tract, which is home to the largest population of commensal organisms in the human body. It therefore maintains a unique immunoregulatory phenotype that prevents inappropriate immune activation to innocuous microbes. Upsetting this balance can create an environment favourable to chronic conditions. For example, the development of IBD is associated with genes that are critical in maintenance of the epithelial barrier and regulation of innate and adaptive immune responses. In this instance, failure of intestinal defence and immunoregulatory functions leads to sustained immune activation by commensal bacterial species such as members of the Enterobacteriaceae family [101,102]."

"Da Fonseca’s observations that acute infections may lead to chronic disease are supported by earlier evidence that in the murine lungs, clearance of a viral infection still leads to chronic airway inflammation. A single paramyxoviral infection in mice not only produced an episode of acute bronchiolitis, but also triggered airway hyper-reactivity and goblet cell hyperplasia that lasted for at least 1 year after complete viral clearance [103]. Following complete clearance of Sendaivirus-induced parainfluenza, mice progressed to develop an asthma like disease, involving increased airway hyper-reactivity, mucus production, and eosinophilia. The cause of such asthma-like disease was mediated by sustained activity of NK T cells that drive macrophages to produce IL-13; a cytokine previously shown to mediate chronic allergic asthma disease [104,105]. Thus, even if the inciting stimulus is cleared, there is evidence of local immunological maladaption, leading to a predisposition to chronic inflammation in the affected tissues."

"It is therefore proposed that the ‘adapted homeostatic’ environment is important for the maintenance of immune tolerance. However, evidence also suggests that the way in which inflammation resolves may dictate the post-resolution environment. Newson et al. described an alternative resolution pathway elicited by high-dose zymosan-induced peritonitis in which there was overexuberant inflammation; a more severe response associated with systemic inflammation [61]. In this pathway, resolution no longer leads to post-resolution and adapted homeostasis, but instead results in the implementation of ‘maladapted homeostasis’, an environment conducive to the development of chronic disease (Figure 1)."

 

[richofden]

Abdominal Inflammation on rifeplayer.com works for me.

 

[Rinse & rePeat]

Hey all. As the title describes what would your recommendations be for gut inflammation, abdominal bloating, gas formation, and intestinal bacterial infection?

Thanks.

Avoidance of starches for awhile, would be my first choice of action, switch to sprouted grains instead. I would only drink fresh pressed juice too instead of whole fruit.

 

[Rinse & rePeat]

Need help I'm dealing with the side effects of taking a generic form of Tums lowered my stomach acid year ago 1 year persists burning feet constipation frequent urination cracking knees and no ability to build muscle I'm hpylori + 2nd round of antiboitics couldn't clear it since horrible symptoms still remain

TUMs cause a lot of trouble. My father’s EXTREME heartburn issues went away when he got off the TUM’s, and his heartburn medication, and switched to baking soda instead. People get addicted to those TUM’s. They are delicious!