Zusammenfassung der Ressource
Cellular Communication and Inflammation
- Cytokines
- Activity
- Autocrine
- Paracrine
- Endocrine
- IL-4
- B-cell
- Activation
- Proliferation
- Differentiation
- Thymocyte and Mast cell
- Proliferation
- IL-2 and IL-5
- B-cell proliferation
- IL-4 + IL-5
- Induces B-cell class switch to IgE
- Recognition and assessment
- PRR activation
- TLR receptors sense infection
inside and outside the cell
- TLR 4 and TLR1:TLR2 heterodimer
sense bacterial infection outside the
cell
- TLR3 detects viruses
- Horseshoe shaped
- Transmembrane
- Can be homo or hetero-dimers
- Assessment
- 1. Soluble pathogen-associated molecular
patters (PAMPs) and dead microorganisms
pose a low threat
- Recognised by pattern-recognition receptors PRRs
- Induces the production of pro-inflammatory
cytokines (IL-6, IL-12 and TNF), as well as other
cellular responses
- PAMPs and microbial debris removed from the tissue
- 2. Viable microorganisms, which are by definition
infectious, pose a significant threat and elicit robust
inflammatory responses
- Bacterial viability is sensed through detection of
'vita-PAMPs', and possibly though other
mechanisms
- Leads to the activation of additional PRR pathways, including those
involving interferon-regulatory factors, NOD-, LRR- and pyrin
domain-comtainin 3
- Induces IL-1-beta production and pyroptosis
- Increased IFN-beta production
- 3. Classical pathogens are extremely dangerous for the
host organism and usually trigger immediate and strong
inflammatory responses
- PRR activation
- Direct and indirect effects of virulence
are sensed triggering rapid mobilisation
of multiple PRR systems
- Include TLRs and NLRs
- Inflammatory response is scaled
to the microbial threat
- Activation of cytokine signalling and
recruitment of neutrophils and diapedesis
- General PRR activation activates an intracellular signal
cascade that turns on relevant gene transcription of cytokines
- Initiation of inflammatory response
- Activated macrophages release pro-inflammatory cytokines
- Neutrophils migrate to the site of inflammation by
'rolling'
- Rolling along the capillary
endothelium slows leukocytes down
and facilitates stronger intractions
- Diapedesis (extravation)
- Neutrophils follow the IL-8 gradient to
the site of the infection
- Systemic signalling
- Initiation of the inflammatory resopnse
- Activated macrophages release pro-inflammatory cytokines
- IL-6
- Fever. Induces acute-phase protein production by hepatocytes
- TNF-alpha
- Activates vascular endothelium and increases vascular permeability,
which leads to increased entry of complement and cells to tissues
- Increased fluid drain to lymph nodes
- Fever. Mobilisation of metabolites. Sock
- 185 amino acid glycoprotein peptide
released by many leukocytes
- Increases vascular permeability for cells and
humoral components (IgG and complement)
- Also acts on hypothalamus
- stimulates release of corticotropon
releasing hormone (CRH)
- suppresses appetite
- Causes a fever
- Enough TNF is good
- Too much TNF is bad
- IL-1-beta
- Activates vascular endothelium
- Activates lymphocytes
- Local tissue destruction
- Increases access of effector cells
- Fever. Produciton of IL-6
- CXCL8
- Chemotactic factor recruits neutrophils and basophils to site of infection
- IL-12
- Activates NK cells