ArticlePLoS pathogens2015
Production of anti-LPS IgM by B1a B cells depends on IL-1β and is protective against lung infection with Francisella tularensis LVS.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Modulatory Role of ATG5 Protein in Immune Modulation During Experimental Tularemia.Microorganisms · 2026Article
- Immunoglobulin M regulates airway hyperresponsiveness independent of T helper 2 allergic inflammation.eLife · 2025Article
- Activation of B1 B cells by F. tularensis atypical LPS depends on classical complement and C3a.PLoS pathogens · 2025Article
- An examination of the LPS-TLR4 immune response through the analysis of molecular structures and protein-protein interactions.Cell communication and signaling : CCS · 2025Review
- The immune response toFrontiers in microbiology · 2025Review
- Loss of TET2 increases B-1 cell number and IgM production while limiting CDR3 diversity.Frontiers in immunology · 2024Article
- Pathogenicity and virulence ofVirulence · 2023Review
- B Cells Induce Early-Onset Maternal Inflammation to Protect against LPS-Induced Fetal Rejection.International journal of molecular sciences · 2023Article
- Review
- Critical role of IL-25-ILC2-IL-5 axis in the production of anti-Francisella LPS IgM by B1 B cells.PLoS pathogens · 2021Article
- Deletion Mutants ofPathogens (Basel, Switzerland) · 2021Article
- Stochastic dynamics of Francisella tularensis infection and replication.PLoS computational biology · 2020Article
- Host defense mechanisms against Mycobacterium tuberculosis.Cellular and molecular life sciences : CMLS · 2020Review
- Immunoglobulin M in Health and Diseases: How Far Have We Come and What Next?Frontiers in immunology · 2020Review
- Interleukin-1 receptor antagonist treatment in acute ischaemic stroke does not alter systemic markers of anti-microbial defence.F1000Research · 2019Article
- Fishing for vaccines againstPeerJ · 2019Article
- Gasdermin D Promotes AIM2 Inflammasome Activation and Is Required for Host Protection againstJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- Interleukin 1α (IL-1α) Promotes Pathogenic Immature Myeloid Cells and IL-1β Favors Protective Mature Myeloid Cells During Acute Lung Infection.The Journal of infectious diseases · 2018Article
- Detrimental Influence of Alveolar Macrophages on Protective Humoral Immunity during Francisella tularensis SchuS4 Pulmonary Infection.Infection and immunity · 2018Article
- Deletion of the Major Facilitator Superfamily TransporterInfection and immunity · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The role of IL-1β and IL-18 during lung infection with the gram-negative bacterium Francisella tularensis LVS has not been characterized in detail. Here, using a mouse model of pneumonic tularemia, we show that both cytokines are protective, but through different mechanisms. Il-18-/- mice quickly succumb to the infection and showed higher bacterial burden in organs and lower level of IFNγ in BALF and serum compared to wild type C57BL/6J mice. Administration of IFNγ rescued the survival of Il-18-/- mice, suggesting that their decreased resistance to tularemia is due to inability to produce IFNγ. In contrast, mice lacking IL-1 receptor or IL-1β, but not IL-1α, appeared to control the infection in its early stages, but eventually succumbed. IFNγ administration had no effect on Il-1r1-/- mice survival. Rather, Il-1r1-/- mice were found to have significantly reduced titer of Ft LPS-specific IgM. The anti-Ft LPS IgM was generated in a IL-1β-, TLR2-, and ASC-dependent fashion, promoted bacteria agglutination and phagocytosis, and was protective in passive immunization experiments. B1a B cells produced the anti-Ft LPS IgM and these cells were significantly decreased in the spleen and peritoneal cavity of infected Il-1b-/- mice, compared to C57BL/6J mice. Collectively, our results show that IL-1β and IL-18 activate non-redundant protective responses against tularemia and identify an essential role for IL-1β in the rapid generation of pathogen-specific IgM by B1a B cells.
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