Antigastric autoantibodies inHelicobacter pylori infection: role in gastric mucosal inflammation

2000 ◽  
Vol 30 (4) ◽  
pp. 173-178 ◽  
Author(s):  
D. Basso ◽  
N. Gallo ◽  
C. -F. Zambon ◽  
M. Baron ◽  
F. Navaglia ◽  
...  
Keyword(s):  
Mucosal Inflammation

A rapid method for the direct identification of paramyxovirus in canine CSF by ultracentrifugation and negative staining as a rule out for distemper

1990 ◽  
Vol 48 (3) ◽  
pp. 594-595
Author(s):  
W.L. Steffens ◽  
M.B. Ard ◽  
C.E. Greene ◽  
A. Jaggy
Keyword(s):  
Subacute Sclerosing Panencephalitis ◽  
Clinical Signs ◽  
Viral Disease ◽  
Etiologic Agent ◽  
Mucosal Inflammation ◽  
Worldwide Distribution ◽  
Negative Stain ◽  
Viral Particles ◽  
Systemic Manifestations ◽  
Rule Out

Canine distemper is a multisystemic contagious viral disease having a worldwide distribution, a high mortality rate, and significant central neurologic system (CNS) complications. In its systemic manifestations, it is often presumptively diagnosed on the basis of clinical signs and history. Few definitive antemortem diagnostic tests exist, and most are limited to the detection of viral antigen by immunofluorescence techniques on tissues or cytologic specimens or high immunoglobulin levels in CSF (cerebrospinal fluid). Diagnosis of CNS distemper is often unreliable due to the relatively low cell count in CSF (<50 cells/μl) and the binding of blocking immunoglobulins in CSF to cell surfaces. A more reliable and definitive test might be possible utilizing direct morphologic detection of the etiologic agent. Distemper is the canine equivalent of human measles, in that both involve a closely related member of the Paramyxoviridae, both produce mucosal inflammation, and may produce CNS complications. In humans, diagnosis of measles-induced subacute sclerosing panencephalitis is through negative stain identification of whole or incomplete viral particles in patient CSF.

Rabeprazole treatment increased the level of reduced form of glutathione and attenuated the H.pylori -associated gastric mucosal inflammation in mongolian gerbils

2001 ◽  
Vol 120 (5) ◽  
pp. A650-A650
Author(s):  
M MIYAZAWA ◽  
H SUZUKI ◽  
S NAGAHASHI ◽  
M SATO ◽  
M BESSHO ◽  
...  
Keyword(s):  
Reduced Form ◽  
Mucosal Inflammation ◽  
Mongolian Gerbils

The probiotic E. coli Nissle 1917 is a potent modulator of mucosal inflammation and visceral sensory function

2007 ◽  
Vol 45 (08) ◽  
Author(s):  
B Adam ◽  
T Liebregts ◽  
S Bertram ◽  
A Ruszkiewicz ◽  
A Schreiner ◽  
...  
Keyword(s):  
Sensory Function ◽  
Mucosal Inflammation ◽  
E Coli

scholarly journals Microbiota-mediated mucosal inflammation in arthritis

2019 ◽  
Vol 33 (6) ◽  
pp. 101492 ◽  
Author(s):  
Meagan E. Chriswell ◽  
Kristine A. Kuhn
Keyword(s):  
Mucosal Inflammation

Inflammatory cell numbers in the stomach of Japanese subjects with endoscopically normal mucosa without H. pylori infection

2021 ◽  
Author(s):  
Naoki Sumi ◽  
Ken Haruma ◽  
Tomoari Kamada ◽  
Mitsuhiko Suehiro ◽  
Noriaki Manabe ◽  
...  
Keyword(s):  
Inflammatory Cells ◽  
Normal Mucosa ◽  
Mucosal Inflammation ◽  
Upper Gastrointestinal Endoscopy ◽  
Fundic Gland ◽  
Eosinophilic Gastritis ◽  
Pyloric Mucosa ◽  
Sydney System ◽  
Updated Sydney System ◽  
H Pylori

Introduction: Since inflammatory cells, such as lymphocytes and plasma cells, normally inhabit the stomach, the border between normal and mild inflammation is difficult to visually determine using the updated Sydney system scale of gastritis. Additionally, eosinophils in the gastric mucosa must be counted to diagnose eosinophilic gastritis. We aimed to determine the normal number of inflammatory cells in patients with endoscopically normal mucosa and without H. pylori infections. Methods: We assessed patients aged 20–79 years, who had undergone upper gastrointestinal endoscopy at Kawasaki Medical School Hospital between January 2010 and December 2014. Inflammatory cells were counted in 1,000 μm2 fields of pyloric and fundic gland mucosal biopsy specimens. We finally included 325 (male, n = 141; female, n = 184; average age = 49.3 years) patients without inflammation who had H. pylori-negative endoscopic results and negative histological findings interpreted based on the updated Sydney System and the Kyoto classification of gastritis. Results: The average numbers of nucleated cells were 83.3 ± 14.2/mm2 and 65.4 ± 12.6/mm2 in the pyloric and fundic gland mucosae, respectively. Inflammatory cells were significantly more abundant in the pyloric mucosa than the fundic gland mucosa (p < 0.05). Age and sex distribution did not significantly differ. Eosinophils were absent or scanty in the gastric mucosae of both glands in all patients. Conclusion: We determined the absolute values of inflammatory cells, including eosinophils, in normal mucosae of pyloric and fundic glands. These findings could be important in defining gastric mucosal inflammation, including eosinophilic gastritis diagnosis.

scholarly journals Gut Microbiota and Acute Diverticulitis: Role of Probiotics in Management of This Delicate Pathophysiological Balance

2021 ◽  
Vol 11 (4) ◽  
pp. 298
Author(s):  
Andrea Piccioni ◽  
Laura Franza ◽  
Mattia Brigida ◽  
Christian Zanza ◽  
Enrico Torelli ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Diverticular Disease ◽  
Acute Diverticulitis ◽  
Bacterial Species ◽  
Mucosal Inflammation ◽  
Abdominal Symptoms ◽  
Pubmed Database ◽  
Anti Inflammatory ◽  
Key Terms

How can the knowledge of probiotics and their mechanisms of action be translated into clinical practice when treating patients with diverticular disease and acute diverticulitis? Changes in microbiota composition have been observed in patients who were developing acute diverticulitis, with a reduction of taxa with anti-inflammatory activity, such as Clostridium cluster IV, Lactobacilli and Bacteroides. Recent observations supported that a dysbiosis characterised by decreased presence of anti-inflammatory bacterial species might be linked to mucosal inflammation, and a vicious cycle results from a mucosal inflammation driving dysbiosis at the same time. An alteration in gut microbiota can lead to an altered activation of nerve fibres, and subsequent neuronal and muscular dysfunction, thus favoring abdominal symptoms’ development. The possible role of dysbiosis and mucosal inflammation in leading to dysmotility is linked, in turn, to bacterial translocation from the lumen of the diverticulum to perivisceral area. There, a possible activation of Toll-like receptors has been described, with a subsequent inflammatory reaction at the level of the perivisceral tissues. Being aware that bacterial colonisation of diverticula is involved in the pathogenesis of acute diverticulitis, the rationale for the potential role of probiotics in the treatment of this disease becomes clearer. For this review, articles were identified using the electronic PubMed database through a comprehensive search conducted by combining key terms such as “gut microbiota”, “probiotics and gut disease”, “probiotics and acute diverticulitis”, “probiotics and diverticular disease”, “probiotics mechanism of action”. However, the amount of data present on this matter is not sufficient to draw robust conclusions on the efficacy of probiotics for symptoms’ management in diverticular disease.

Faecal cytokines provide novel insights into the role of gut mucosal inflammation in acute decompensation of cirrhosis

2020 ◽  
Vol 73 ◽  
pp. S215-S216
Author(s):  
Vishal C Patel ◽  
Elizabeth H Gray ◽  
Antonio Riva ◽  
Sarah Azarian ◽  
Mark J W McPhail ◽  
...  
Keyword(s):  
Mucosal Inflammation ◽  
Acute Decompensation

scholarly journals Cognitive impairments induced by necrotizing enterocolitis can be prevented by inhibiting microglial activation in mouse brain

2018 ◽  
Vol 10 (471) ◽  
pp. eaan0237 ◽  
Author(s):  
Diego F. Niño ◽  
Qinjie Zhou ◽  
Yukihiro Yamaguchi ◽  
Laura Y. Martin ◽  
Sanxia Wang ◽  
...  
Keyword(s):  
Necrotizing Enterocolitis ◽  
Microglial Activation ◽  
Gastrointestinal Disease ◽  
Cognitive Impairments ◽  
High Mobility ◽  
Neurological Dysfunction ◽  
Mucosal Inflammation ◽  
Signaling Axis ◽  
The Brain

Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease of the premature infant. One of the most important long-term complications observed in children who survive NEC early in life is the development of profound neurological impairments. However, the pathways leading to NEC-associated neurological impairments remain unknown, thus limiting the development of prevention strategies. We have recently shown that NEC development is dependent on the expression of the lipopolysaccharide receptor Toll-like receptor 4 (TLR4) on the intestinal epithelium, whose activation by bacteria in the newborn gut leads to mucosal inflammation. Here, we hypothesized that damage-induced production of TLR4 endogenous ligands in the intestine might lead to activation of microglial cells in the brain and promote cognitive impairments. We identified a gut-brain signaling axis in an NEC mouse model in which activation of intestinal TLR4 signaling led to release of high-mobility group box 1 in the intestine that, in turn, promoted microglial activation in the brain and neurological dysfunction. We further demonstrated that an orally administered dendrimer-based nanotherapeutic approach to targeting activated microglia could prevent NEC-associated neurological dysfunction in neonatal mice. These findings shed light on the molecular pathways leading to the development of NEC-associated brain injury, provide a rationale for early removal of diseased intestine in NEC, and indicate the potential of targeted therapies that protect the developing brain in the treatment of NEC in early childhood.

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