Sandbox: spontaneous bacterial peritonitis: Difference between revisions

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Revision as of 21:04, 26 January 2017

Overview

Spontaneous bacterial peritonitis(SBP) is an advanced clinical expression of a pathological bacterial translocation as it develops from normal inhabitant gut bacteria through breakage of immune barriers.[1]

Pathogenesis

Bacterial Translocation

It is defined as the translocation of either bacteria or bacterial products such as lipopolysacharides (LPS), bacterial DNA, peptidoglycans, muramyl-dipeptides from gut into mesenteric lymph nodes.[2]

Physiological: It is the normal bacterial translocation in healthy individuals due to lack of pro-inflammatory responses against commensal bacteria. Physiological translocation is crucial for the development of host immunity response.

Pathological: It is developed due to abnormal increase in physiological translocation in both rate and degree by breaking the normal immunological barriers.

Barriers that limit pathological transmission:

  1. Interstinal lumen and it's secretory components such as inner and outer mucus layer, antimicrobial peptides: This is the primary barrier that limit direct contact between the intestinal bacteria and the epithelial cell surface
  2. Epithelial barrier with the gut-associated lymphatic tissue (GALT) and autonomic nervous system: This is a mechanical barrier with local immunological response elements (e.g., TNF and other pro-inflammatory cytokines) that rapidly detects and kill the pathogen that manage to penetrate
  3. Systemic immune system: This includes hematogenous (portal venous) and lymphatic (ductus thoracicus) route of delivery that acts as a third immune barrier to prevent or minimize the pathogen to disseminate systemically from local immune system such as lymph nodes.

Mechanism of pathological bacterial translocation

Breaking these immune barriers can progress physiological BT into pathological BT.

Bacterial Translocation
I. Immune response by gut associated lymphoid tissue A. Innate immunity Innate immunity is the first line of defense mechanism against invading pathogen that detects common bacterial motifs such as microbial-associated molecular patterns (MAMPs) through germline-coded pattern-recognition receptors (PRR) on intestinal cells.[3]

Mechanism of breaking of innate immunity

  1. Dendritic cells below the epithelial layer allows pathogen via dendritic processes with out affecting tight junction function.
  2. Disruption of epithelial barrier by antigenic properties of the pathogen with the underlying epithelial layer and compromises its epithelial integrity.
  3. Access provided by M- cells overlying payers patches with in the villous epithelium through antigen presenting cells.[4]
B. Adaptive immunity Bacterial translocation through epithelial cells

References

  1. ↑ Benten D, Wiest R (2012) Gut microbiome and intestinal barrier failure--the "Achilles heel" in hepatology? J Hepatol 56 (6):1221-3. DOI:10.1016/j.jhep.2012.03.003 PMID: 22406521
  2. ↑ Berg RD, Garlington AW (1979) Translocation of certain indigenous bacteria from the gastrointestinal tract to the mesenteric lymph nodes and other organs in a gnotobiotic mouse model. Infect Immun 23 (2):403-11. PMID: 154474
  3. ↑ Akira S, Takeda K, Kaisho T (2001) Toll-like receptors: critical proteins linking innate and acquired immunity. Nat Immunol 2 (8):675-80. DOI:10.1038/90609 PMID: 11477402
  4. ↑ Hase K, Kawano K, Nochi T, Pontes GS, Fukuda S, Ebisawa M et al. (2009) Uptake through glycoprotein 2 of FimH(+) bacteria by M cells initiates mucosal immune response. Nature 462 (7270):226-30. DOI:10.1038/nature08529 PMID: 19907495
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