ArticleInfection and immunity2008
Evasion of innate immune responses: evidence for mannose binding lectin inhibition of tumor necrosis factor alpha production by macrophages in response to Blastomyces dermatitidis.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 31 citations in OpenAlex.
- Collectins: Innate Immune Pattern Recognition Molecules.Advances in experimental medicine and biology · 2020Review
- Turning on virulence: Mechanisms that underpin the morphologic transition and pathogenicity ofVirulence · 2019Review
- How Environmental Fungi Cause a Range of Clinical Outcomes in Susceptible Hosts.Journal of molecular biology · 2019Review
- The Fungal Cell Wall:Frontiers in microbiology · 2019Review
- Evasion Mechanisms Used by Pathogens to Escape the Lectin Complement Pathway.Frontiers in microbiology · 2017Review
- Fungal Dimorphism and Virulence: Molecular Mechanisms for Temperature Adaptation, Immune Evasion, and In Vivo Survival.Mediators of inflammation · 2017Review
- Surfactant protein D facilitates Cryptococcus neoformans infection.Infection and immunity · 2012Article
- Toll-like receptors (TLRs) and mannan-binding lectin (MBL): on constant alert in a hostile environment.Upsala journal of medical sciences · 2011Review
- Heterocomplexes of mannose-binding lectin and the pentraxins PTX3 or serum amyloid P component trigger cross-activation of the complement system.The Journal of biological chemistry · 2011Article
- Insights into Fungal Morphogenesis and Immune Evasion: Fungal conidia, when situated in mammalian lungs, may switch from mold to pathogenic yeasts or spore-forming spherules.Microbe (Washington, D.C.) · 2008Article
- Fungal killing by mammalian phagocytic cells.Current opinion in microbiology · 2008Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serum factors, including mannose binding lectins (MBL), influence innate responses to microbes. Little is known about the effects of serum factors or MBL on the interaction of Blastomyces dermatitidis, a pulmonary fungal pathogen, with macrophages or on tumor necrosis factor alpha (TNF-alpha) production. Since macrophage production of TNF-alpha is an important innate immune response, we examined a mouse peritoneal macrophage (PM) cell line (RAW) and resident PM from CD-1 mice to study TNF-alpha production by PM stimulated with heat-killed (HK) or live B. dermatitidis yeast cells. Mouse serum and heat-inactivated mouse serum inhibited TNF-alpha production 94% when macrophages were stimulated by B. dermatitidis, whereas mouse immunoglobulin G (IgG) did not have this effect. HK B. dermatitidis incubated with serum and then washed also failed to stimulate significant TNF-alpha production by PM. By the sandwich immunofluorescent antibody (IFA) method with anti-mouse MBL (MBL-A or -C), we showed that serum MBL bound to B. dermatitidis. When serum was absorbed with HK B. dermatitidis or live B. dermatitidis, absorbed serum failed to significantly inhibit TNF-alpha production by RAW cells plus B. dermatitidis, and immunoblotting showed that absorbed serum was depleted of MBL-C. If serum was absorbed with live B. dermatitidis, unbound serum was eluted, and bound serum factor(s) (BS) was released with guanidine buffer, BS inhibited TNF-alpha production by PM plus B. dermatitidis in a concentration-dependent manner. BS contained MBL-C, which bound B. dermatitidis, as shown by IFA assay. 1,3-beta-Glucan stimulated TNF-alpha production by PM, and this was inhibited by mouse serum. Treatment of B. dermatitidis with anti-1,3-beta-glucan antibody inhibited TNF-alpha production by PM. With anti-1,3-beta-glucan antibody, we showed by IFA assay that B. dermatitidis contained 1,3-beta-glucan. In an IFA study with B. dermatitidis, serum with an anti-mouse IgG conjugate did not result in fluorescence, yet serum blocked IFA staining of B. dermatitidis by anti-1,3-beta-glucan IgG antibody. This indicated that non-IgG serum factors binding to B. dermatitidis prevented access to 1,3-beta-glucan by anti-1,3-beta-glucan antibody. These results suggest that the mechanism of inhibition of the innate proinflammatory immune response of PM to B. dermatitidis is mediated by serum MBL binding to B. dermatitidis at 1,3-beta-glucan sites or sterically masking 1,3-beta-glucan sites, thus preventing 1,3-beta-glucan stimulation of PM for TNF-alpha production.
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