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Receptor activator of nuclear factor kappa-B ligand (RANKL), robustly induced at 4 weeks, has direct mitogenic activity in mammary epithelial cells and, as a potent inducer of NF-κB activity, may induce inflammatory genes.
Based on this, C60s may induce inflammatory responses in the lung of mice.
Although current evidence suggests that these bony changes represent an inflammatory response rather than an infectious osteitis, bacteria associated with the sinonasal mucosa may induce inflammatory mediators as a mechanism of neo-osteogenesis.
Because the IKKβ-mediated signaling events in injured corneal epithelium are strikingly similar to those in TNF-α treated hTCEpi cells, we suggest that injury may induce inflammatory cytokine to activate the IKKβ signaling cascades, which in turn play a predominant role in promoting corneal re-epithelialization in vivo.
IgG from SSc patients may induce inflammatory and fibrotic conditions.
It has been known that plasmid DNA alone may induce inflammatory response.
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When a pathogen invades a joint, it may induce an inflammatory reaction via lytic effects on host tissues, immune complex formation, or the induction of inflammatory cytokines such as the well-documented effects of certain alphaviruses that target mononuclear cells within the joint [ 4].
Excessive NETs formation and poor clearance may induce severe inflammatory processes involving leukocyte accumulation, diffuse alveolar damage and epithelial injury, which result in the massive release of inflammatory cytokines both locally and in the circulation via increased alveolar permeability.
Evidence suggests that maternal infections may induce fetal inflammatory responses.
Maternal infection or inflammation may induce fetal inflammatory responses and potentially fetal brain injury.
Maternal infection or inflammation may induce fetal inflammatory responses associated with fetal injury and cerebral palsy.
More suggestions(15)
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may develop inflammatory
may elicit inflammatory
may upregulate inflammatory
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