Redness, swelling, heat, pain, and loss of function
Microscopic characteristics of acute pulmonary inflammation
Vasodilation, increased vascular permeability, and inflammatory cell infiltration
Inflammatory responses of acute pulmonary inflammation
To destroy and remove, as well as wall off and confine the injurious agents; The response stimulates the immune response to promote recovery
Acute lung inflammation
Is dominated by neutrophils, whereas chronic reactions involve mainly macrophages and lymphocytes
Acute respiratory distress syndrome; An example of acute inflammation not only persisting yet also becoming amplified to involve the entire organ; Pro-inflammatory cytokines (TNF-alpha and IL-1 beta) are increased, and the increment of anti-inflammatory cytokines like IL-10 may not keep up with their production; It has been reported that IL-10 is lower in this than in critically ill non-this patients; The imbalance of pro- and anti-inflammatory cytokines may promote the disease
When lungs are exposed to minimal bacterial loads
Pathogen clearance operates through innate defenses and the event is generally subclinical
What does acute infection result from?
When higher loads of bacteria overcome the local defenses, leading to acute inflammation and involving both innate and adaptive defenses
What does bacterial colonization result from?
Abnormal innate defenses, establishing an equilibrium between bacterial replication and clearance
When does a chronic infection occur?
When marked a inflammatory response generated by host defense mechanisms fails to clear the bacteria, with continued tissue destruction
Adhere to the epithelium
In response to bacteria
Dendritic cells, alveolar macrophages, and epithelial cells are activated as pathogen markers are identified through toll like receptors (TLRs)
4 Phases that progress through recognition of pathogen initiating inflammation
Initiation, amplification, phagocytosis, and resolution
Toll like receptors (TLRs) are membrane-bound pattern-recognition receptors (PRRs) that recognize specific conserved molecular patterns broadly shared by pathogens, known as pathogen-associated molecular patterns (PAMPs)
Pattern-recognition receptors (membrane-bound); Cytosolic (this) consist mainly of nucleotide oligomerization domain (NOD)-like receptors (NLRs), and function as regulators of innate immune response against microbial pathogens
Specific components of bacteria, and form a cytoplasmic signaling complex with other proteins known as the inflammasome
Inflammasomes are crucial actors of the innate immunity; A multiprotein cytoplasmic complex which activates one or more caspases, leading to the processing and secretion of pro-inflammatory cytokines—e.g., IL-1 beta, IL-18 and IL-33
In some cells, inflammasome activation
May lead to rapid host cell death (pyroptosis), which may protect the host by preventing bacterial replication
Pathogen-associated molecular patterns that are molecules essential for microorganism survival, and innate and adaptive immunity ensue when they are engaged by pattern-recognition receptors (PRRs)
After PAMPs are recognized, cell activation increases transcription factors like NF-_beta, producing growth factors, chemokines, adhesion molecules and pro-inflammatory cytokines including IL-8 and TNF-alpha.
Increases expression of lung capillary endothelial cell adhesion molecules for increased neutrophil adhesion
Acts as a neutrophil agent
Release more IL-8, which in turn increases neutrophil recruitment, with elastase from this inducing epithelial IL-8 production
After successfully evading mechanical barriers and ciliary removal, and surviving the actions of surfactants and antibodies, bacteria may encounter complement proteins; Complements facilitate recognition by alveolar macrophages of bacteria through PRRs and prepare bacteria for this phase
At least 2 additional mechanisms can be activated to enhance killing and clearance of a microbe
Alveolar macrophages and bacteria triggered T cells
Alveolar macrophage mechanisms activated to enhance killing and clearance of a microbe
These cells have the ability to liberate chemotactic factors that attract nearby neutrophils and initiate inflammatory responses
Bacteria triggered T cell mechanisms activated to enhance killing and clearance of a microbe
Released cytokines that stimulate the phagocytic and bacterial capacity of alveolar macrophages
Occurs after a successful host response; Complete bacterial phagocytosis, and killing by reactive oxygen species, bacteriocidal permeability-inducing protein, lactoferrin, elastase, and neutrophil extracellular trap, down regulates the host defense system
Resolving lung inflammation depends upon
Apoptosis as well as timely and adequate removal of acute inflammatory cells by macrophases
Neutrophils and eosinophils undergo surface changes enabling phagocytes to recognize and ingest them; The process is modulated through extracellular signaling; For example, neutrophils cultured in the bronchial alveolar lavage fluid from acute respiratory distress syndrome (ARDS) patients have a longer lifespan than those from patients with normal lungs
What may be responsible for apoptosis delay?
Pro-inflammatory cytokines such as GM-CSF
In some cases with conversely regulated apoptosis
Apoptosis of eosinophils and neutrophils is conversely regulated; For example, dexamethasone enhances apoptosis of eosinophils, yet inhibits that of neutrophils, prolonging neutrophil viability
What does resolution of inflammation depend on?
The removal of apoptotic cells, and also the suppression of inflammatory mediator production
What can incomplete resolution lead to?
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