Lung inflammation caused by inhaled toxicants: a review

Figures & data

Figure 1 Common pathways involved in the production of IL-1β by inhaled toxicants.

Abbreviations: IL, interleukin; MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor-kappa B.

Table 1 Expression of cytokines and chemokines induced by inhaled toxicants in vivo

Toxicant	Cytokines and chemokines	References
Cigarette smoke	IL-1β, IL-4, IL-5, IL-13, TNF-α, CCL11, CCL17	^Citation84, ^Citation167, ^Citation168
Trichothecene (mycotoxin)	IL-1β, IL-6, TNF-α	^Citation105, ^Citation169
Ricin	IL-1β, IL-6, TNF-α, CXCL1, CCL2	^Citation125, ^Citation130
Toluene diisocyanate (VOC)	IL-1β, IL-4, TNF-α	^Citation170, ^Citation171
Asbestos	IL-1β, IL-6, TNF-α, CCL4, CCL6, CCL10	^Citation172, ^Citation173
Crystalline silica	IL-1β, IL-6, IL-12, IFN-γ, TNF-α, CXCL1, CXCL2, CCL2	^Citation140, ^Citation174–Citation176
Nanotubes	IL-1β, IL-6, IL-10, IL-33, TNF-α, CCL2, CCL7, CCL17	^Citation177–Citation180

Abbreviations: IL, interleukin; TNF-α, tumor necrosis factor-alpha; VOC, volatile organic compound.

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