Tumor microenvironment-regulated drug delivery system combined with sonodynamic therapy for the synergistic treatment of breast cancer.

Co-loading of sonosensitizers and chemotherapeutic drugs into nanocarriers can improve the biocompatibilities, stabilities, and targeting of drugs and reduce the adverse reactions of drugs, providing a robust platform to orchestrate the synergistic interplay between chemotherapy and sonodynamic therapy (SDT) in cancer treatment. In this regard, biodegradable manganese dioxide (MnO) has attracted widespread attention because of its unique properties in the tumor microenvironment (TME). Accordingly, herein, MnO nanoshells with hollow mesoporous structures (H-MnO) were etched to co-load hematoporphyrin monomethyl ether (HMME) and doxorubicin (DOX), and DOX/HMME-HMnO@bovine serum albumin (BSA) obtained after simple BSA modification of DOX/HMME-HMnO exhibited excellent hydrophilicity and dispersibility.

IL-33 synergistically promotes the proliferation of lung cancer cells in vitro by inducing antibacterial peptide LL-37 and proinflammatory cytokines in macrophages.

Lung cancer is the primary cause of cancer-related deaths, and the persistent inflammation is inextricably linked with the lung cancer tumorigenesis. Pro-inflammatory cytokine interleukin-33 (IL-33) is able to serve as a potent modulator of cancer. Mounting evidence indicates IL-33 has significant effect on lung cancer progression by regulating host immune response, but the current opinions about the function and mechanism of IL-33 in lung cancer are still controversial.

Cytosolic mtDNA released from pneumolysin-damaged mitochondria triggers IFN-β production in epithelial cells.

Pneumolysin (Ply) is a major virulence factor of . Ply-induced interferon-β (IFN-β) expression in host macrophages has been shown to be due to the accumulation of mitochondrial deoxyribonucleic acid (mtDNA) in the cytoplasm during infection. Our findings extend this work to show human bronchial epithelial cells that reside at the interface of inflammatory injury, BEAS-2B, adapt to local cues by altering mitochondrial states and releasing excess mtDNA.

Type I IFN expression is stimulated by cytosolic MtDNA released from pneumolysin-damaged mitochondria via the STING signaling pathway in macrophages.

Pneumolysin (Ply), a major virulence factor of Streptococcus pneumoniae (S. pn), affects the immunity of host cells during infection. It has been reported that Ply is involved in S.

Type I interferon induced by DNA of nontypeable Haemophilus influenza modulates inflammatory cytokine profile to promote susceptibility to this bacterium.

Type I interferon (IFN) is indispensable for antiviral immunity, but its role in bacterial infections is controversial and not fully described. Nontypeable Haemophilus influenzae (NTHi) is one of the most common bacterial pathogens in patients with chronic obstructive pulmonary disease (COPD). NTHi-DNA activates type I IFN production in macrophages, but the function of type I IFN in host-pathogen interactions, in the context of NTHi infection, is still unclear.

Mitochondrial DNA Leakage Caused by Hydrogen Peroxide Promotes Type I IFN Expression in Lung Cells.

, the bacterial pathogen responsible for invasive pneumococcal diseases, is capable of producing substantial amounts of hydrogen peroxide. However, the impact of -secreted hydrogen peroxide (HO) on the host immune processes is not completely understood. Here, we demonstrated that -secreted HO caused mitochondrial damage and severe histopathological damage in mouse lung tissue.

Protective Regulatory T Cell Immune Response Induced by Intranasal Immunization With the Live-Attenuated Pneumococcal Vaccine SPY1 the Transforming Growth Factor-β1-Smad2/3 Pathway.

Vaccine effectiveness is mainly determined by the mechanism mediating protection, emphasizing the importance of unraveling the protective mechanism for novel pneumococcal vaccine development. We previously demonstrated that the regulatory T cell (Treg) immune response has a protective effect against pneumococcal infection elicited by the live-attenuated pneumococcal vaccine SPY1. However, the mechanism underlying this protective effect remains unclear.

Oxytocin Relieves Neuropathic Pain Through GABA Release and Presynaptic TRPV1 Inhibition in Spinal Cord.

Oxytocin (OT) is synthesized within the paraventricular nucleus and supraoptic nucleus of the hypothalamus. In addition to its role in uterine contraction, OT plays an important antinociceptive role; however, the underlying molecular mechanisms of antinociceptive role of OT remain elusive. We hypothesized that the antinociceptive effect of OT on neuropathic pain may occur via inhibition of TRPV1 activation in the spinal cord.