Increased association of Trypanosoma cruzi with sialoadhesin positive mice macrophages

Monteiro, V.G; Lobato, Caroliny Samary Silva; Silva, Alexandre Rodrigues; Medina, Diego V.; Oliveira, Marco Antônio de; Seabra, Sérgio Henrique; Souza, Wanderley de; DaMatta, Renato Augusto

doi:10.1007/s00436-005-1460-1

Cited by 53 publications

(37 citation statements)

References 28 publications

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“…As shown in this report, Siglec-F can also mediate uptake of Neisseria meningitidis expressing sialylated lipooligosaccharides containing the NeuAc␣2-3Gal linkage recognized as a ligand by Siglec-F (3,71). Sn was also found to mediate association of macrophages with Trypanosoma cruzi, a parasite expressing cell surface sialic acids (45), and porcine Sn was shown to mediate the entry of porcine reproductive and respiratory viruses into porcine alveolar macrophages (30,77). Thus, bacteria, parasites, and viruses expressing sialic acids on their cell surfaces are likely to be natural trans ligands of siglec proteins (20,79).…”

Section: Discussionsupporting

confidence: 54%

“…Thus, bacteria, parasites, and viruses expressing sialic acids on their cell surfaces are likely to be natural trans ligands of siglec proteins (20,79). The diversity of interactions of siglec proteins with sialylated pathogens suggests that they may play multiple roles in their interactions with immune cells (8,18,30,38,45).…”

Section: Discussionmentioning

confidence: 99%

“…Over 20 pathogenic microorganisms express sialic acid-containing glycans on their surface (25). Recent demonstration of the binding or uptake of several sialylated pathogens, including Neisseria meningitidis, Trypanosoma cruzi, Campylobacter jejuni, and group B Streptococcus, by Sn and Siglec-5, -7, and -9 has suggested various roles of these siglec proteins in the immune responses to these organisms (8,18,25,30,38,45). Since mechanisms of pathogen entry and engulfment are increasingly recognized to involve the host cells' endocytic machinery (12), the endocytic functions of the siglec proteins are also relevant to their roles in pathogen recognition and uptake.…”

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confidence: 99%

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Distinct Endocytic Mechanisms of CD22 (Siglec-2) and Siglec-F Reflect Roles in Cell Signaling and Innate Immunity

Tateno

Schur

et al. 2007

Molecular and Cellular Biology

116

109

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Sialic acid-binding immunoglobulin-like lectins (siglecs) are predominately expressed on immune cells. They are best known as regulators of cell signaling mediated by cytoplasmic tyrosine motifs and are increasingly recognized as receptors for pathogens that bear sialic acid-containing glycans. Most siglec proteins undergo endocytosis, an activity tied to their roles in cell signaling and innate immunity. Here, we investigate the endocytic pathways of two siglec proteins, CD22 (Siglec-2), a regulator of B-cell signaling, and mouse eosinophil Siglec-F, a member of the rapidly evolving CD33-related siglec subfamily that are expressed on cells of the innate immune system. CD22 exhibits hallmarks of clathrin-mediated endocytosis and traffics to recycling compartments, consistent with previous reports demonstrating its localization to clathrin domains. Like CD22, Siglec-F mediates endocytosis of anti-Siglec-F and sialoside ligands, a function requiring intact tyrosinebased motifs. In contrast, however, we find that Siglec-F endocytosis is clathrin and dynamin independent, requires ADP ribosylation factor 6, and traffics to lysosomes. The results suggest that these two siglec proteins have evolved distinct endocytic mechanisms consistent with roles in cell signaling and innate immunity.The siglec (sialic-acid binding immunoglobulin [Ig]-like lectins) proteins are subset of the Ig superfamily of cell recognition molecules that bind to sialic acid-containing glycans of cell surface glycoconjugates as ligands (27,78). Of the 13 human and 9 murine siglec proteins, 4 are highly conserved in mammalian species: sialoadhesin (Sn)/Siglec-1, CD22/Siglec-2, myelin-associated glycoprotein (MAG)/Siglec-4, and Siglec-15. The others comprise a rapidly evolving subfamily homologous to CD33/Siglec-4, known as the CD33-related siglec proteins. With two exceptions (MAG and Siglec-6) the siglec proteins are predominantly expressed in various white blood cells of the immune system (25,43,78,85). All contain a N-terminal V-set sugar-binding Ig domain, a variable number of additional C-set Ig domains, a transmembrane domain, and a cytoplasmic domain that typically contains tyrosine-based motifs implicated in regulation of cell signaling and endocytosis.Many of the siglec proteins contain one or more immunoreceptor tyrosine-based inhibitory motifs (ITIMs), (I/L/V)XYXX (L/V), suggesting that they play important roles as inhibitory receptors of cell signaling (25, 78), as exemplified by CD22, which is well documented as a regulator of B-cell receptor (BCR) signaling. Upon antigen binding to the BCR, the ITIMs of CD22 are quickly tyrosine phosphorylated and recruit protein tyrosine phosphatase SHP-1, which dephosphorylates the BCR and dampens the B-cell response, setting a threshold for B-cell activation (27,73).CD22 is also known to undergo endocytosis following ligation by anti-CD22 antibody (38, 64) or high-affinity multivalent-sialoside ligands (22). The tyrosine-based ITIMs of CD22 also fit the sorting signal YXXØ (where Ø is a hydrophobic...

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Distinct Endocytic Mechanisms of CD22 (Siglec-2) and Siglec-F Reflect Roles in Cell Signaling and Innate Immunity

Tateno

Schur

et al. 2007

Molecular and Cellular Biology

116

109

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“…Siglecs which lack an ITIM domain (such as Siglec-14, 15, and 16) associate with DAP12 via a positively charged amino acid in their transmembrane region to activate receptors through the recruitment of Syk (15,40). Siglec-1, the first discovered member of Siglecs, has been shown to play an important role in sialylated pathogen uptake (17,19,(53)(54)(55), antigen presentation (56,57), lymphocyte proliferation (58), self-tolerance (59,60) and antiviral immune response (47). However, the biological function of Siglec-1 in endotoxin tolerance is unknown.…”

Section: Discussionmentioning

confidence: 99%

Induction of Siglec-1 by Endotoxin Tolerance Suppresses the Innate Immune Response by Promoting TGF-β1 Production

Lan

Ren

et al. 2016

Journal of Biological Chemistry

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Sepsis is one of the leading causes of death worldwide. Although the prevailing theory for the sepsis syndrome is a condition of uncontrolled inflammation in response to infection, sepsis is increasingly being recognized as an immunosuppressive state known as endotoxin tolerance. We found sialylation of cell surface was significantly increased on LPS-induced tolerant cells; knockdown of Neu1 in macrophage cell line RAW 264.7 cells resulted in enhanced LPS-induced tolerance, whereas overexpression of Neu1 or treatment with sialidase abrogated LPS-induced tolerance, as defined by measuring TNF-␣ levels in the culture supernatants. We also found that the expression of Siglec-1 (a member of sialic acid-binding Ig (I)-like lectin family members, the predominant sialic acid-binding proteins on cell surface) was specifically up-regulated in endotoxin tolerant cells and the induction of Siglec-1 suppresses the innate immune response by promoting TGF-␤1 production. The enhanced TGF-␤1 production by Siglec-1 was significantly attenuated by spleen tyrosine kinase (Syk) inhibitor. Knockdown of siglec-1 in RAW 264.7 cells resulted in inhibiting the production of TGF-␤1 by ubiquitin-dependent degradation of Syk. Mechanistically, Siglec-1 associates with adaptor protein DNAX-activation protein of 12 kDa (DAP12) and transduces a signal to Syk to control the production of TGF-␤1 in endotoxin tolerance. Thus, Siglec-1 plays an important role in the development of endotoxin tolerance and targeted manipulation of this process could lead to a new therapeutic opportunity for patients with sepsis.Sepsis is generally defined as a systemic inflammatory response syndrome in response to infection. Sepsis can be potentially life threatening; of more than 1 million Americans who are diagnosed with severe sepsis every year, between 28 and 50% will die from this disease (1, 2). It is well-recognized that patients with sepsis are often immune suppressed, a state of reduced responsiveness to endotoxin known as endotoxin tolerance, deaths in this immunosuppressive phase are typically due to failure to control the secondary infections (3-5). The molecular mechanisms underlying this endotoxin tolerance phenomenon is poorly understood.Sialic acids are a family of nine-carbon acidic monosaccharides and are involved in immune response, such as host-pathogen recognition, migration, and antigen presentation. Mounting experimental evidence suggests that the presence of sialic acid residue act as a marker of self in the immune system, as such residues are absent from most microbes (6). Indeed, host cells can be lysed by immune cytotoxic effector mechanisms after extensive desialylation, an observation that demonstrates the significant role played by cell surface sialic acids in the selfrecognition process (7). In addition, normal human serum contains natural antibodies to sialidase-treated red blood cells (7-9), lymphocytes (10), and thymocytes (7). Recently, Meesmann et al. showed that desialylation acted as an "eat me" signal and caused an enhanced upt...

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“…Depletion experiments have demonstrated that MZMs are crucial for the entrapment of blood-borne pathogens such as lymphocytic choriomeningitis virus (LCMV) (6), Streptococcus pneumoniae (3), and Listeria monocytogenes (7). MMMs display CD169 (also known as Siglec-1 and recognized by MOMA-1 MAb [8,9]) that recognizes sialylated lipopolysaccharides from Neisseria meningitidis (10) and Campylobacter jejuni (11) and binds to Trypanosoma cruzi (12). MZM populations also play a key role in antigen delivery to B cells (13) and CD4 ϩ T cells (14) and regulate tolerance to apoptotic cells (15,16).…”

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confidence: 99%

Chronic Brucella Infection Induces Selective and Persistent Interferon Gamma-Dependent Alterations of Marginal Zone Macrophages in the Spleen

et al. 2017

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The spleen is known as an important filter for blood-borne pathogens that are trapped by specialized macrophages in the marginal zone (MZ): the CD209 ϩ MZ macrophages (MZMs) and the CD169 ϩ marginal metallophilic macrophages (MMMs). Acute systemic infection strongly impacts MZ populations and the location of T and B lymphocytes. This phenomenon has been linked to reduced chemokine secretion by stromal cells. Brucella spp. are the causative agent of brucellosis, a widespread zoonotic disease. Here, we used Brucella melitensis infection as a model to investigate the impact of chronic stealth infection on splenic MZ macrophage populations. During the late phase of Brucella infection, we observed a loss of both MZMs and MMMs, with a durable disappearance of MZMs, leading to a reduction of the ability of the spleen to take up soluble antigens, beads, and unrelated bacteria. This effect appears to be selective as every other lymphoid and myeloid population analyzed increased during infection, which was also observed following Brucella abortus and Brucella suis infection. Comparison of wild-type and deficient mice suggested that MZ macrophage population loss is dependent on interferon gamma (IFN-␥) receptor but independent of T cells or tumor necrosis factor alpha receptor 1 (TNF-␣R1) signaling pathways and is not correlated to an alteration of CCL19, CCL21, and CXCL13 chemokine mRNA expression. Our results suggest that MZ macrophage populations are particularly sensitive to persistent low-level IFN-␥-mediated inflammation and that Brucella infection could reduce the ability of the spleen to perform certain MZM-and MMM-dependent tasks, such as antigen delivery to lymphocytes and control of systemic infection.KEYWORDS Brucella melitensis, marginal zone macrophages, low-grade Th1 inflammation, brucellosis, infection, spleen T he spleen is both the largest secondary lymphoid organ and the main filter of blood (for a general review, see reference 1). The white pulp, which contains T and B cell populations, is surrounded by the red pulp, a network of reticular fibers and fibroblasts rich in macrophages, where blood is filtered and old erythrocytes are removed. The marginal zone (MZ) located between the white pulp and the red pulp constitutes a specialized filtering area for blood content. The MZ contains specialized macrophage populations, various dendritic cell (DC) subsets, and MZ B cells. The marginal metallophilic macrophages (MMMs) form an inner ring between the MZ and white pulp, whereas MZ macrophages (MZMs) are situated at the outer boundary of the MZ,

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Increased association of Trypanosoma cruzi with sialoadhesin positive mice macrophages

Cited by 53 publications

References 28 publications

Distinct Endocytic Mechanisms of CD22 (Siglec-2) and Siglec-F Reflect Roles in Cell Signaling and Innate Immunity

Distinct Endocytic Mechanisms of CD22 (Siglec-2) and Siglec-F Reflect Roles in Cell Signaling and Innate Immunity

Induction of Siglec-1 by Endotoxin Tolerance Suppresses the Innate Immune Response by Promoting TGF-β1 Production

Chronic Brucella Infection Induces Selective and Persistent Interferon Gamma-Dependent Alterations of Marginal Zone Macrophages in the Spleen

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