Induction of Intestinal Th17 Cells by Segmented Filamentous Bacteria

Evolution of Protein Molecules

Gut microbiota is an assortment of microorganisms inhabiting the length and width of the mammalian gastrointestinal tract. The composition of this microbial community is host specific, evolving throughout an individual's lifetime and susceptible to both exogenous and endogenous modifications. Recent renewed interest in the structure and function of this "organ" has illuminated its central position in health and disease. The microbiota is intimately involved in numerous aspects of normal host physiology, from nutritional status to behavior and stress response. Additionally, they can be a central or a contributing cause of many diseases, affecting both near and far organ systems. The overall balance in the composition of the gut microbial community, as well as the presence or absence of key species capable of effecting specific responses, is important in ensuring homeostasis or lack thereof at the intestinal mucosa and beyond. The mechanisms through which microbiota exerts its beneficial or detrimental influences remain largely undefined, but include elaboration of signaling molecules and recognition of bacterial epitopes by both intestinal epithelial and mucosal immune cells. The advances in modeling and analysis of gut microbiota will further our knowledge of their role in health and disease, allowing customization of existing and future therapeutic and prophylactic modalities.

Gut Microbiota in Health and Disease

White adipose tissue is no longer considered an inert tissue mainly devoted to energy storage but is emerging as an active participant in regulating physiologic and pathologic processes, including immunity and inflammation. Macrophages are components of adipose tissue and actively participate in its activities. Furthermore, cross-talk between lymphocytes and adipocytes can lead to immune regulation. Adipose tissue produces and releases a variety of proinflammatory and anti-inflammatory factors, including the adipokines leptin, adiponectin, resistin, and visfatin, as well as cytokines and chemokines, such as TNF-α, IL-6, monocyte chemoattractant protein 1, and others. Proinflammatory molecules produced by adipose tissue have been implicated as active participants in the development of insulin resistance and the increased risk of cardiovascular disease associated with obesity. In contrast, reduced leptin levels might predispose to increased susceptibility to infection caused by reduced T-cell responses in malnourished individuals. Altered adipokine levels have been observed in a variety of inflammatory conditions, although their pathogenic role has not been completely clarified.

https://www.jacionline.org/article/S0091-6749(05)00417-3/pdf

Adipose tissue, adipokines, and inflammation.

Helicobacter pylori is the first formally recognized bacterial carcinogen and is one of the most successful human pathogens, as over half of the world's population is colonized with this gram-negative bacterium. Unless treated, colonization usually persists lifelong. H. pylori infection represents a key factor in the etiology of various gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Disease outcome is the result of the complex interplay between the host and the bacterium. Host immune gene polymorphisms and gastric acid secretion largely determine the bacterium's ability to colonize a specific gastric niche. Bacterial virulence factors such as the cytotoxin-associated gene pathogenicity island-encoded protein CagA and the vacuolating cytotoxin VacA aid in this colonization of the gastric mucosa and subsequently seem to modulate the host's immune system. This review focuses on the microbiological, clinical, immunological, and biochemical aspects of the pathogenesis of H. pylori.

Pathogenesis of Helicobacter pylori Infection

https://www.gastrojournal.org/article/S0016-5085(97)70155-0/pdf

A standardized mouse model of Helicobacter pylori infection: introducing the Sydney strain.

Bitcoin: Medium of Exchange or Speculative Assets?

Stomach biopsy specimens from M0 individuals with Campylobacterpyloridis-assodated gastritis were examined by light and electron microscopy. The bacteria were consistently seen in two locations: within the gastric mucus and associated with intercellular junctions of gastric epithelial cells. C. pyloridis is suggested to be one of a broad group of spiral bacteria that are adapted to the peculiar niche provided by intestinal mucus. The spiral morphology and the form of motility of these organisms give them a selective advantage in a viscous environment. This point has been demonstrated in vitro by measurement of the velocity of clinical isolates in solutions of methyl cellulose of varying viscosity. The localization of C. pyloridis close to intercellular junctions is proposed to be due to the presence of preferred metabolites or growth factors, e.g., urea and hemin. All isolates show an extremely high urease activity and require hemin for growth.

https://www.jstor.org/stable/pdfplus/30104864.pdf

Campylobacter pyloridis and Gastritis: Association with Intercellular Spaces and Adaptation to an Environment of Mucus as Important Factors in Colonization of the Gastric Epithelium

A large cross-sectional study to investigate the prevalence and possible modes of transmission of Helicobacter pylori was done in southern China. Serum samples (1727) were collected from Guangzhou city and three rural areas of Guangdong Province, and the prevalence of H. pylori infection was determined using an ELISA. Each subject completed a questionnaire. The overall prevalence of H. pylori infection was 44.2%; a significantly higher prevalence was found in Guangzhou (52.4%) than in the rural areas (38.6%). This difference was generally reflected in the group 0-5 years old, but the rate of increase in seroprevalence for H. pylori over 5 years of age was similar (1%/year). This study provides important new data on the acquisition of H. pylori, particularly in the early years of life, and shows that density of living conditions is a prime determinant in the acquisition of H. pylori.

Adrian Lee

Papers

A standardized mouse model of Helicobacter pylori infection: introducing the Sydney strain.

Bitcoin: Medium of Exchange or Speculative Assets?

Campylobacter pyloridis and Gastritis: Association with Intercellular Spaces and Adaptation to an Environment of Mucus as Important Factors in Colonization of the Gastric Epithelium

Epidemiology of Helicobacter pylori in southern China: identification of early childhood as the critical period for acquisition.

Campylobacter pyloridis, urease, hydrogen ion back diffusion, and gastric ulcers