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PreprintCited by 6Ferroptosis and cancer prognosisNeonatal and Maternal InfectionsIron Metabolism and Disorders

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Unveiling the Crucial Role of Ferroptosis in Host Resistance to Streptococcus agalactiae Infection

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jiang, Hua, yi, Jiaxuan, sun, zeyu, Li, Jing, Jiang, Yongqiang, Liu, Peng, Wang, Yuhang, Liu, Hui, Lv, Qingyu, Kong, Decong, Huang, Wenhua, Ren, Yuhao, Li, Qian·2024·Cell Death Discovery
DOI 10.21203/rs.3.rs-4121017/v1PMC PMC11445261

Preprint — published as 10.1038/s41420-024-02189-8

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Abstract

IL-1β represents an important inflammatory factor involved in the host response against GBS infection. Prior research has suggested a potential involvement of IL-1β in the process of ferroptosis. However, the relationship between IL-1β and ferroptosis in the context of anti-GBS infection remains uncertain. This research demonstrates that the significance of ferroptosis in the host's immune defense against GBS infection in a mouse model of abdominal infection, with peritoneal macrophages identified as the primary cells undergoing ferroptosis. Subsequent studies have shown that IL-1β promotes lipid oxidation in macrophages by upregulating pathways associated with lipid oxidation. Concurrently, IL-1β is not only involved in the initiation of ferroptosis in macrophages, but its production is intricately linked to the onset of ferroptosis. Ultimately, we posit that ferroptosis acts as a crucial initiating factor in the host response to GBS infection, with IL-1β playing a significant role in the resistance to infection by serving as a key inducer of ferroptosis.

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Fig. 1 Ferroptosis promotes host resistance to GBS infection. A Mice were injected with 100 μL 0.2 mg/mL Fer-1 i.p. followed with infecting with 500 μL of 8×107CFU/mL GBS i.p. Survival rate was observed (n = 10 per group). B, C Bacterial load was quantified in abdominal cavity and peripheral blood at 3, 6, and 15 hours post-infection. Each group included 6 animals. D, E Lipid oxidation levels were detected via flow cytometry after staining with Lipoflu at 3 hours postinfection (n = 3 per group). F–H The expression of PTGS2 was detected by qPCR(F), and Western blot and grayscale value analysis(G,H), at 3 hours post-infection(n = 4 per group). Data were shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ns means not significant.
Fig. 1 Ferroptosis promotes host resistance to GBS infection. A Mice were injected with 100 μL 0.2 mg/mL Fer-1 i.p. followed with infecting with 500 μL of 8×107CFU/mL GBS i.p. Survival rate was observed (n = 10 per group). B, C Bacterial load was quantified in abdominal cavity and peripheral blood at 3, 6, and 15 hours post-infection. Each group included 6 animals. D, E Lipid oxidation levels were detected via flow cytometry after staining with Lipoflu at 3 hours postinfection (n = 3 per group). F–H The expression of PTGS2 was detected by qPCR(F), and Western blot and grayscale value analysis(G,H), at 3 hours post-infection(n = 4 per group). Data were shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ns means not significant.CC BY · PubMed Central
Fig. 2 The ferroptosis of macrophages plays an important role for the host resistance to GBS infection. Mice were infected with 500 μL 8×107 CFU/mL GBS i.p. Ratio of macrophages and neutrophils (A, B) and proportion of M1 and M2 macrophages (C,D) in peritoneal lavage fluid at 3 hours postinfection were assayed by flow cytometry. E Mice were treated with 200 μL clodronate lipome and control i.p. 24 hours before GBS infection and simultaneously Fer-1 treatment. The survival rates were compared. F –J Peritoneal macrophages from C57BL/6 mice were incubated with GBS at MOI of 1:30. The levels of lipid oxidation and Fe2+ were assessed using 100 μL of 2 μM C11-BODIPY581/591 and 200 μL of 1 μmol/L FerroOrange, respectively (F, G). The expression of PTGS2 was detected by qPCR (n = 4 per group) (H) and Western blot and grayscale value analysis (n = 3 per group) (I, J). Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ns means not significant.
Fig. 2 The ferroptosis of macrophages plays an important role for the host resistance to GBS infection. Mice were infected with 500 μL 8×107 CFU/mL GBS i.p. Ratio of macrophages and neutrophils (A, B) and proportion of M1 and M2 macrophages (C,D) in peritoneal lavage fluid at 3 hours postinfection were assayed by flow cytometry. E Mice were treated with 200 μL clodronate lipome and control i.p. 24 hours before GBS infection and simultaneously Fer-1 treatment. The survival rates were compared. F –J Peritoneal macrophages from C57BL/6 mice were incubated with GBS at MOI of 1:30. The levels of lipid oxidation and Fe2+ were assessed using 100 μL of 2 μM C11-BODIPY581/591 and 200 μL of 1 μmol/L FerroOrange, respectively (F, G). The expression of PTGS2 was detected by qPCR (n = 4 per group) (H) and Western blot and grayscale value analysis (n = 3 per group) (I, J). Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ns means not significant.CC BY · PubMed Central
Fig. 3 Association between IL-1β and ferroptosis macrophages. A–D Mice were infected with 500 μL 8 × 107CFU/mL GBS i.p. Cytokines in peritoneal lavage fluid postinfection for 3 and 6 hours were detected by Luminex. E The level of IL-1β postinfection for 3 hours was detected by ELISA. F Mice were treated with 100 μL of 50 μg/mL mouse IL-1β/IL-1F2 antibody and homotypic control i.p. 0.5 hours before GBS infection and simultaneously Fer-1 treatment. The survival rate of mice was observed and compared by log-rank test (n = 10 per group). G Mice were injected with 500 μL of 100 pg/mL recombinant mouse IL-1β/IL-1F2(IL-1β) i.p. followed with GBS infection. The survival rate of mice was observed and compared by log-rank test (n = 10 per group). H IL-1β was blocked for 0.5 h followed by GBS infection for 0.5 h. Lipid oxidation level of peritoneal macrophages was detected by flow cytometry. I Mice were injected with 500 μL of 100 pg/mL IL-1β i.p.. Lipid oxidation levels of peritoneal macrophages were detected by flow cytometry. Data were shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ns means not significant.
Fig. 3 Association between IL-1β and ferroptosis macrophages. A–D Mice were infected with 500 μL 8 × 107CFU/mL GBS i.p. Cytokines in peritoneal lavage fluid postinfection for 3 and 6 hours were detected by Luminex. E The level of IL-1β postinfection for 3 hours was detected by ELISA. F Mice were treated with 100 μL of 50 μg/mL mouse IL-1β/IL-1F2 antibody and homotypic control i.p. 0.5 hours before GBS infection and simultaneously Fer-1 treatment. The survival rate of mice was observed and compared by log-rank test (n = 10 per group). G Mice were injected with 500 μL of 100 pg/mL recombinant mouse IL-1β/IL-1F2(IL-1β) i.p. followed with GBS infection. The survival rate of mice was observed and compared by log-rank test (n = 10 per group). H IL-1β was blocked for 0.5 h followed by GBS infection for 0.5 h. Lipid oxidation level of peritoneal macrophages was detected by flow cytometry. I Mice were injected with 500 μL of 100 pg/mL IL-1β i.p.. Lipid oxidation levels of peritoneal macrophages were detected by flow cytometry. Data were shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ns means not significant.CC BY · PubMed Central
Fig. 4 IL-1β caused ferroptosis of macrophages by direct lipid oxidation. A–C Macrophages were stimulated with 200 μL IL-1β at different concentrations (10 pg/mL, 100 pg/mL, and 1000 pg/mL) and different times (0.5 h, 1 h, 3 h). Lipid oxidation levels were analysed by flow cytometry. D–G Macrophages were stimulated with 200 μL of 100 pg/mL IL-1β for 0.5 hours. Expression of PTGS2 was evaluated by qPCR (D) and Western blot and grayscale value analysis (E, F). The mitochondrial morphology was observed by transmission electron microscopy (G). H Macrophages were stimulated with 200 μL IL-1β at different concentrations (10 pg/mL, 100 pg/mL, and 1000 pg/mL) for 0.5 hours and Fe2+ levels were detected via laser confocal fluorescence microscopy after staining with FerroOrange. I, J Macrophages were stimulated with 200 μL of 100 pg/mL IL-1β for 0.5 hours. Intracellular Fe2+ levels were evaluated by Iron Assay Kit (I) and the relative expression of Fth, Ftl and Fpn was evaluated by qPCR (J). Each group included 3-5 animals. Data were shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ns means not significant.
Fig. 4 IL-1β caused ferroptosis of macrophages by direct lipid oxidation. A–C Macrophages were stimulated with 200 μL IL-1β at different concentrations (10 pg/mL, 100 pg/mL, and 1000 pg/mL) and different times (0.5 h, 1 h, 3 h). Lipid oxidation levels were analysed by flow cytometry. D–G Macrophages were stimulated with 200 μL of 100 pg/mL IL-1β for 0.5 hours. Expression of PTGS2 was evaluated by qPCR (D) and Western blot and grayscale value analysis (E, F). The mitochondrial morphology was observed by transmission electron microscopy (G). H Macrophages were stimulated with 200 μL IL-1β at different concentrations (10 pg/mL, 100 pg/mL, and 1000 pg/mL) for 0.5 hours and Fe2+ levels were detected via laser confocal fluorescence microscopy after staining with FerroOrange. I, J Macrophages were stimulated with 200 μL of 100 pg/mL IL-1β for 0.5 hours. Intracellular Fe2+ levels were evaluated by Iron Assay Kit (I) and the relative expression of Fth, Ftl and Fpn was evaluated by qPCR (J). Each group included 3-5 animals. Data were shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ns means not significant.CC BY · PubMed Central
Fig. 5 IL-1β induced lipid oxidation in macrophages through the upregulation of ALOX15 expression. A–C Macrophages were stimulated with 200 μL of 100 pg/mL IL-1β for 0.5 hours, and the expression levels of SLC7A11, GPX4, ACSL4, ALOX15, and LPCAT3 were detected by qPCR(A) and Western blot and grayscale value analysis (B,C). D, E Macrophages were treated with 100 μL of 1,000 μM PD146176 for 0.5 h, followed by IL-1β for 0.5 h, and flow cytometry was used to detect macrophage lipid oxidation levels. F Macropahges were incubated with 1000 μM PD146176 and 1 µg/mL mouse IL-1 β/IL-1F2 antibody for 0.5 hours, and then stimulated with 100 pg/mL IL-1 β for 0.5 hours. MDA levels were detected. Macropahges used here is RAW264.7, and RAW264.7 transfected with ALOX15(ALOX15 + ) or empty vector (Mock + ). The results were shown for three repetitions as the mean ± SD. Statistical significance: *P < 0.05, **P < 0.01, *P < 0.05. ns means not significant.
Fig. 5 IL-1β induced lipid oxidation in macrophages through the upregulation of ALOX15 expression. A–C Macrophages were stimulated with 200 μL of 100 pg/mL IL-1β for 0.5 hours, and the expression levels of SLC7A11, GPX4, ACSL4, ALOX15, and LPCAT3 were detected by qPCR(A) and Western blot and grayscale value analysis (B,C). D, E Macrophages were treated with 100 μL of 1,000 μM PD146176 for 0.5 h, followed by IL-1β for 0.5 h, and flow cytometry was used to detect macrophage lipid oxidation levels. F Macropahges were incubated with 1000 μM PD146176 and 1 µg/mL mouse IL-1 β/IL-1F2 antibody for 0.5 hours, and then stimulated with 100 pg/mL IL-1 β for 0.5 hours. MDA levels were detected. Macropahges used here is RAW264.7, and RAW264.7 transfected with ALOX15(ALOX15 + ) or empty vector (Mock + ). The results were shown for three repetitions as the mean ± SD. Statistical significance: *P < 0.05, **P < 0.01, *P < 0.05. ns means not significant.CC BY · PubMed Central
Fig. 6 Diagram of a proposed model depicting the mechanism through which ferroptosis enhances host immunity against GBS infection. GBS infection induces macrophage ferroptosis involving iron accumulation and the release of inflammatory cytokines, including IL-1β. IL-1β is subsequently released into the extracellular space where it binds to its receptor, upregulating ACSL4, LPCAT3, and ALOX15. This process affected polyunsaturated fatty acid (PUFA) metabolism, ultimately leading to lipid oxidation and ferroptosis.
Fig. 6 Diagram of a proposed model depicting the mechanism through which ferroptosis enhances host immunity against GBS infection. GBS infection induces macrophage ferroptosis involving iron accumulation and the release of inflammatory cytokines, including IL-1β. IL-1β is subsequently released into the extracellular space where it binds to its receptor, upregulating ACSL4, LPCAT3, and ALOX15. This process affected polyunsaturated fatty acid (PUFA) metabolism, ultimately leading to lipid oxidation and ferroptosis.CC BY · PubMed Central

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Metadata

Authors
jiang, H., yi, J., sun, Z., Li, J., Jiang, Y., Liu, P., Wang, Y., Liu, H., Lv, Q., Kong, D., Huang, W., Ren, Y., & Li, Q.
Affiliations
  • Academy of Military Medical Sciences (CN)
  • Life Science College, Southwest Forestry University
  • Southwest Forestry University (CN)
Corresponding author
  • jiang, Hua
  • Li, Jing
  • Jiang, Yongqiang
ORCID
Venue
Cell Death Discovery
Publisher
Springer Science and Business Media LLC
Published
2024-04-18
Volume
10
Issue
1
Pages
423-423
ISSN
2058-7716 (ISSN-L)
DOI
10.21203/rs.3.rs-4121017/v1
PMC
PMC11445261
OpenAlex
W4403032921
Cited by
6
References
1
Citations by year
2026: 3 · 2025: 3
FWCI
1.73
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Death Discovery (publishedVersion, cc-by)
  • Research Square (acceptedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
State Key Laboratory of Pathogen and Biosecurity
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Ferroptosis and cancer prognosis
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and Maternal Infections
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
Keywords
ferroptosis, Streptococcus agalactiae, IL-1β, peritoneal macrophages, lipid peroxidation, host resistance to infection, intra-abdominal infection, innate immunity

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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