Innate lymphoid cells (ILCs) function in producing effector cytokines in response to pathogenic infections. However, the roles and related mechanisms of the ILC subpopulations, ILC1 and ILC2, which mirror Th1 and Th2 in adaptive immunity, remain unclear. In this study, we found the markedly elevated levels of the ILC1 transcription factor T-bet, the effector cytokine IFN-γ and the IL/receptor signaling molecules IL-12/IL-12R, which are indispensable for ILC1 differentiation, in the helper ILCs of chronic hepatitis B (CHB) patients. The elevated level of the ILC1 population was significantly associated with hepatic damage in CHB patients, and was not related to telbivudine treatment. In contrast, although we also observed elevated levels of ILC2-related factors, including IL-33, ST2, GATA3 and IL-13 in helper ILCs, the extent of elevation shown by each was lower than that shown by the ILC1-related factors. Furthermore, the activity of the ILC2s did not correlate with either HBV copies or liver damage. The findings of this study suggest potential pro-inflammatory roles for ILC1s in CHB pathogenesis, potentiating these cells and their related molecules as targets of diagnostic, prognostic and/or therapeutic strategies for hepatitis B.

The NALP3 inflammasome interacts with various immune and cell metabolic pathways and may participate in pulmonary fibrosis. However, little is known on its regulatory mechanism with respect to collagen synthesis. The objective of the present study was to investigate whether NALP3 inflammasome activation is involved in H2O2‑mediated collagen synthesis, in addition to examining the possible cell signaling mechanisms underlying this effect. It was demonstrated that the NF‑κB signaling pathway was activated under conditions of H2O2‑mediated oxidative stress in NIH‑3T3 mouse embryonic fibroblasts. H2O2‑exposed fibroblasts exhibited activated NALP3 inflammasomes via increased NALP3, apoptosis‑associated Speck‑like protein and caspase‑1 expression and the secretion of interleukin‑1β. H2O2 also elevated α‑SMA and type I collagen expression. In vitro silencing of NALP3 attenuated the degradation of IκBα and decreased the synthesis of type I collagen. Furthermore, the NALP3 inflammasome was found to be activated in bleomycin‑induced pulmonary fibrosis in mice, and this activation was relieved by a nuclear factor (NF)‑κB inhibitor. Taken together, these findings indicate that the NALP3 inflammasome is involved in H2O2‑induced type I collagen synthesis, which is mediated by the NF‑κB signaling pathway. Additionally, the NALP3 inflammasome contributes to the development of bleomycin‑induced pulmonary fibrosis.