Mouse LIMR3/CD300f is a negative regulator of the antimicrobial activity of neutrophils

Ueno, Keigo; Urai, Makoto; Izawa, Kumi; Otani, Yoshiko; Yanagihara, Nao; Kataoka, Michiyo; Takatsuka, Shogo; Abe, Masahiro; Hasegawa, Hideki; Shimizu, Kiminori; Kitamura, Toshio; Kitaura, Jiro; Miyazaki, Yoshitsugu; Kinjo, Yuki

doi:10.1038/s41598-018-35699-4

Cited by 11 publications

(8 citation statements)

References 48 publications

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“…All procedures were performed as described previously [6,41]. In brief, BMDCs (1 × 10 6 cells) and heat-inactivated fungal cells (2 × 10 6 cells) were placed in 96-well round bottom plates containing 200 μL of the complete RPMI1640 medium supplemented with mGM-CSF.…”

Section: Methodsmentioning

confidence: 99%

Cryptococcus gattii alters immunostimulatory potential in response to the environment

et al. 2019

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Cryptococcus gattii is a capsular fungal pathogen, which causes life-threatening cryptococcosis in immunocompetent individuals. This emerging pathogen is less likely to be recognized by innate immunity compared to traditional Cryptococcus neoformans strains. Previous studies indicate that C-type lectin receptors (CLRs), including dectin-1 and dectin-2, play a role in recognizing cryptococcal cells; however, it remains to be elucidated whether the receptors physically associate with C . gattii yeast cell surfaces. Based on the previous findings, we hypothesized that culture conditions influence the expression or exposure of CLR ligands on C . gattii . Therefore, in the present study, we first investigated the culture conditions that induce exposure of CLR ligands on C . gattii yeast cells via the binding assay using recombinant fusion proteins of mouse CLR and IgG Fc, Fc dectin-1 and Fc dectin-2. Common fungal culture media, such as yeast extract–peptone–dextrose (YPD) broth, Sabouraud broth, and potato dextrose agar, did not induce the exposure of dectin-1 ligands, including β-1,3-glucan, on both capsular and acapsular C . gattii strains, in contrast to Fc dectin-1 and Fc dectin-2 bound to C . gattii cells growing in the conventional synthetic dextrose (SD) medium [may also be referred to as a yeast nitrogen base with glucose medium]. The medium also induced the exposure of dectin-1 ligands on C . neoformans , whereas all tested media induced dectin-1 and dectin-2 ligands in a control fungus Candida albicans . Notably, C . gattii did not expose dectin-1 ligands in SD medium supplemented with yeast extract or neutral buffer. In addition, compared to YPD medium-induced C . gattii , SD medium-induced C . gattii more efficiently induced the phosphorylation of Syk, Akt, and Erk1/2 in murine dendritic cells (DCs). Afterwards, the cells were considerably engulfed by DCs and remarkably induced DCs to secrete the inflammatory cytokines. Overall, the findings suggest that C . gattii alters its immunostimulatory potential in response to the environment.

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Section: Methodsmentioning

confidence: 99%

Cryptococcus gattii alters immunostimulatory potential in response to the environment

et al. 2019

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“…CD300f has been shown to suppress the antimicrobial activity of neutrophils against Pseudomonas aeruginosa and Candida albicans infection (37). However, infection studies using pathogenic rickettsiae suggest that neutrophils do not alter the course of rickettsiosis or contribute to the restriction of bacterial growth (35).…”

Section: Discussionmentioning

confidence: 99%

Pathogenic rickettsiae utilize the phosphatidylserine binding receptor CD300f on macrophages for host invasion and pathogenesis

Voss,

Moin,

Gaytan

et al. 2024

Preprint

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Some arthropod-borne obligate intracellular rickettsiae are among the most virulent human pathogens. Upon entry, Rickettsia species modulate immune (e.g., macrophages; MΦ) and non-immune cell (e.g., endothelial cells) responses to create a habitable environment for host colonization. In particular, MΦ play a crucial role in either terminating an infection at an early stage or succumbing to bacterial replication and colonization. However, our understanding on how Rickettsia species modulate crucial cellular processes within MΦ, including phagocytosis, and host cell defenses, to establish an intracytosolic replication niche, remain poorly defined. In this study, we describe a previously unappreciated mechanism, in which pathogenic rickettsiae infection is mediated by the phosphatidylserine (PS)-binding receptor, CD300f. We found that CD300f-/- mice but not wild-type (WT) C57BL/6J mice were protected against R. typhi- or R. rickettsii [Shelia Smith]-induced fatal rickettsiosis. Adoptative transfer studies further revealed that CD300f-expressing bone marrow-derived macrophages (BMDMΦ) are important mediators to control rickettsiosis in WT mice. Mechanistical analysis, using WT or CD300f-/- BMDMΦ, showed that CD300f facilitates the engulfment of both pathogenic R. typhi and R. rickettsii species, likely via a PS-mediated mechanism. Furthermore, CD300f was involved in the intracytosolic replication of both pathogenic rickettsiae by differentially modulating the anti-inflammatory Interleukin (IL)-10 and anti-rickettsial IL-1alpha and IL-1beta cytokine responses. Collectively, our findings describe a previously unappreciated role for the efferocytic receptor, CD300f, to facilitate engulfment and the intracellular survival of pathogenic rickettsiae within the host.

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“…CD300f modulates the macrophage inflammatory phenotype and contributes to peripheral nerve regeneration (Peluffo et al, 2015) and the expression of CD300f in microglial cells, as expected, but also in oligodendrocytes and neurons, which demonstrates its neuroprotective role in acute brain injury (Peluffo et al, 2012). In addition, in bacterial infections, the inhibition of CD300f could enhance neutrophil antibacterial activity and could be exploited to treat bacterial infectious diseases (Ueno et al, 2018). The regulation of CD300f has been suggested to play a significant role in MC activation.…”

Section: Discussionmentioning

confidence: 99%

Dehydroandrographolide targets CD300f and negatively regulated MRGPRX2‐induced pseudo‐allergic reaction

Che

Zheng

Hou³

et al. 2022

Phytotherapy Research

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Mas-related G protein-coupled receptor X2 (MRGPRX2) mediates mast cells (MCs) activation, which is a key target for the treatment of allergic diseases. However, there are few drugs targeting MRGPRX2. Leukocyte mono-immunoglobulin-like receptor 3 (CD300f) is a negative regulator of FcεRΙ-mediated MC activation. However, the regulatory effect of CD300f on MRGPRX2 remains unclear. Dehydroandrographolide (DA) is a main contributor of Andrographis paniculata (Burm.f.) Nees (family: Acanthaceae) have been shown to inhibit type I hypersensitivity. The aim of this study was to determine whether DA negatively regulated MRGPRX2-mediated MC activation via CD300f and showed therapeutic effect on pseudo-allergic reactions. Mouse allergic models and MC degranulation were detected in vivo and in vitro, and inflammatory mediators were detected. siRNA interference and Biacore were used to verify the target. DA inhibited pseudo-allergic reactions by reducing vasodilation and serum cytokine levels in mice and inhibited MRGPRX2-mediated MC activation. The regulatory effect of DA was significantly decreased after the knockdown of CD300f expression. Moreover, DA upregulated the phosphorylation level of Src homology region 2 domain-containing phosphatase (SHP)-1 and SHP-2, which are key kinases in the negative regulatory signaling pathways associated with CD300f. In conclusion, DA negatively regulates MRGPRX2-mediated MC activation via CD300f to inhibit pseudo-allergic reactions.

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Mouse LIMR3/CD300f is a negative regulator of the antimicrobial activity of neutrophils

Cited by 11 publications

References 48 publications

Cryptococcus gattii alters immunostimulatory potential in response to the environment

Cryptococcus gattii alters immunostimulatory potential in response to the environment

Pathogenic rickettsiae utilize the phosphatidylserine binding receptor CD300f on macrophages for host invasion and pathogenesis

Dehydroandrographolide targets CD300f and negatively regulated MRGPRX2‐induced pseudo‐allergic reaction

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