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NLRP3 inflammasome signal pathway involves in Vibrio harveyi-induced inflammatory response in murine peritoneal
Guili Yu1, Jinxin Wang1, Wei Zhang1
1Jiangsu Key Laboratory of Marine Biological Resources and Environment, Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, Co-Innovation Center of Jiangsu Marine Bio-industry Technology, School of Pharmacy, Jiangsu Ocean University, Lianyungang 222005, China.
Abstract:
Vibrio harveyi, an important zoonotic pathogen, can infect wounds and cause inflammatory response. Understanding the inflammatory response pathways could facilitate the exploration of molecular mechanisms for treating V. harveyi infection. NLR family pyrin domain-containing 3 (NLRP3) inflammasome is involved in the interaction between hosts and pathogenic microorganisms and could be sensed by various pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). Nonetheless, the function of NLRP3 inflammasome in V. harveyi infection remains unclear. In the present study, we established a V. harveyi infection model using murine peritoneal macrophages (PMs). Various techniques, including western blot analysis, enzyme-linked immunosorbent assay (ELISA), RT-qPCR, immunofluorescence, and inhibition assays, were used to explore the molecular mechanism of V. harveyi-induced inflammation. The results showed that many inflammatory cytokines participated in V. harveyi infection, with interleukin (IL)-1β being the most abundant. Pan-caspase inhibitor pretreatment significantly decreased the secretion of IL-1β in murine PMs. Moreover, the identification of V. harveyi involved a large number of NLR molecules, especially the NLRP3 receptor, and further studies revealed that NLPR3 inflammasome was activated by V. harveyi infection, as evidenced by puncta-like NLRP3 surrounding cell nuclear, ASC specks in the nucleus and cytoplasm, and ASC oligomerization. Inhibition of NLRP3 inflammasome impaired the release of mature IL-1β in V. harveyi-infected murine PMs. Furthermore, blocking the secretion of mature IL-1β could markedly decrease the release of other proinflammatory cytokines, including IL-6, IL-12, and tumor necrosis factor-α. Overall, these data indicated that NLRP3 inflammasome was activated in response to V. harveyi infection and enhanced inflammatory response by promoting IL-1β secretion in murine PMs.
Insights
Vibrio harveyi infection activates the NLRP3 inflammasome in macrophages, leading to increased interleukin-1 beta (IL-1β) secretion and amplified inflammatory responses. This study clarifies the role of NLRP3 inflammasome in V. harveyi-induced inflammation.
Area of Science:
- Immunology
- Microbiology
- Molecular Biology
Background:
- Vibrio harveyi is a zoonotic pathogen causing inflammatory responses.
- The NLR family pyrin domain-containing 3 (NLRP3) inflammasome plays a role in host-pathogen interactions.
- The function of NLRP3 inflammasome in V. harveyi infection is not well understood.
Purpose of the Study:
- To investigate the role of NLRP3 inflammasome activation in V. harveyi infection.
- To elucidate the molecular mechanisms of V. harveyi-induced inflammation in murine peritoneal macrophages (PMs).
Main Methods:
- Murine peritoneal macrophages (PMs) were infected with V. harveyi.
- Western blot, ELISA, RT-qPCR, immunofluorescence, and inhibition assays were employed.
- NLRP3 inflammasome activation was assessed through cellular localization and oligomerization studies.
Main Results:
- V. harveyi infection induced significant inflammatory cytokine production, particularly IL-1β.
- NLRP3 inflammasome activation was confirmed by NLRP3 puncta, ASC speck formation, and oligomerization.
- Inhibition of NLRP3 inflammasome or IL-1β secretion reduced the release of other pro-inflammatory cytokines (IL-6, IL-12, TNF-α).
Conclusions:
- NLRP3 inflammasome is activated during V. harveyi infection in murine PMs.
- Activated NLRP3 inflammasome promotes IL-1β secretion, enhancing the inflammatory response.
- Targeting NLRP3 inflammasome or IL-1β may offer therapeutic strategies for V. harveyi infections.
