Mice with targeted deletion of p50 (p50−/−) are more sensitive to cigarette smoke induced emphysema, demonstrating enhanced lung inflammation, and enhanced DNA binding and activity of the transcriptionally active p65/p50 dimers in association with alterations in chromatin remodeling (Rajendrasozhan et al., 2010).
Enhanced lung epithelial specification of human induced pluripotent stem cells on decellularized lung matrix.
Increasing the Ab density enhanced lung accumulation with minimally reduced liver and spleen uptake.
This study was designed to investigate whether absence of TNF receptor enhanced lung damage and mortality through toll-like receptors (TLRs) and inducible nitric oxide synthase (iNOS).
Although MV-O2 induced larger and fewer alveoli in both, TNF-α and TNF-α mice, it caused enhanced lung apoptosis (TUNEL, caspase-3/-6/-8), infiltration of macrophages and neutrophils, and proinflammatory mediator expression (IL-1β, CXCL-1, MCP-1) in TNF-α mice.
Moreover, treatment of mice immunized with ΔclpB with anti-IL-17 antibodies post-challenge enhanced lung infection.
Further, mice exposed to nicotine showed significantly enhanced lung metastasis as well as tumor recurrence post surgical removal of the primary tumor.
Surprisingly, adoptive transfer of syngeneic HDM-pulsed bone marrow derived mDCs (BMDCs) to the lungs of C3H mice markedly enhanced lung IL-17A production, and rendered them susceptible to allergen-driven airway hyperresponsiveness.
Whereas C57BL/6J mice could control virus replication and clear the infection, DBA/2J mice exhibited higher viral loads, higher levels of cytokines and chemokines, enhanced lung pathology, and were not able to clear the viral infection.
During sepsis there is enhanced lung NO production that is associated with ICU mortality.
