Table 2.

Inflammatory mediators released during the allergic response in the guinea pig asthma model

Inflamatory mediator	Funcion	References
IL-4	Creates an inflammatory environment for the recruitment of inflammatory cells, primarily eosinophils in responses Th2	[86]
IL-1	Recruitment of leukocytes such as neutrophils (severe neutrophilic asthma)	[79, 86]
IL-5	Increases eosinophilopoiesis	[85]
TNF-α	Associated with non-allergic severe inflammation. Recruitment of neutrophils	[86]
IFN-γ	Associated with non-allergic severe inflammation. Recruitment of neutrophils	[86]
IgE	Activates mast cells and basophils by binding to the FcεR receptor	[87]
IgG1	Immunoglobulin predominantly expressed in guinea pigs. Generates a mild obstructive response	[56]
PAF	Chemotactic for neutrophils and eosinophils. Enhances mast cell activation and CysLT release. Potentiates histamine-induced bronchoconstriction	[82, 88]
CysLT	Binding to its receptor on airway smooth muscle induces contraction. Considered the most potent bronchoconstrictors. Eosinophil chemotaxis, induce plasma extravasation, and cause tissue edema	[85, 86, 88]
TxA2	Binding to its specific receptor on smooth muscle causes contraction. Vasoconstriction	[89]
PGD2	Eosinophil and Th2 cell chemotaxis	[88]
Tryptases	Promote mast cell activation and histamine release. Leukocyte recruitment. Possible link to increased bronchoconstriction through bronchodilator degradation	[90]
Chymase	Increases mast cell degranulation	[90]
Histamine	Regulates granulocyte accumulation in the airways	[87]
Eotaxin	Activation and recruitment of eosinophils	[79]
Eosinophils	Release cytotoxic proteins, TxA2, PGD2, CysLT, PAF, oxygen free radicals, and inflammatory cytokines	[86–88]
Neutrophils	Activation increases severe neutrophilic asthma, generally non-allergic. Release of PAF	[86, 88]
Mast cells	Release histamine, TxA2, PGD2, CysLT, PAF, IL-1, IL-5, IFN-γ, TNF-α. Associated with early responses	[79, 85, 86, 88]