Role of macrophage sialoadhesin in host defense against the sialylated pathogen group B Streptococcus.
Role of macrophage sialoadhesin in host defense against the sialylated pathogen group B Streptococcus.
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DOI:
10.1007/s00109-014-1157-y
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发表时间:
2014-09
影响因子:
4.7
通讯作者:
Nizet, Victor
中科院分区:
文献类型:
--
作者:
Chang, Yung-Chi;Olson, Joshua;Louie, Aaron;Crocker, Paul R.;Varki, Ajit;Nizet, Victor
Several bacterial pathogens decorate their surfaces with sialic acid (Sia) residues within cell wall components or capsular exopolysaccharides. Sialic acid expression can promote bacterial virulence by blocking complement activation or by engagement of inhibitory sialic acid-binding immunoglobulin-like lectins (Siglecs) on host leukocytes. Expressed at high levels on splenic and lymph node macrophages, sialoadhesin (Sn) is a unique Siglec with an elongated structure that lacks intracellular signaling motifs. Sialoadhesin allows macrophage to engage certain sialylated pathogens and stimulate inflammatory responses, but the in vivo significance of sialoadhesin in infection has not been shown. We demonstrate that macrophages phagocytose the sialylated pathogen group B Streptococcus (GBS) and increase bactericidal activity via sialoadhesin-sialic-acid-mediated recognition. Sialoadhesin expression on marginal zone metallophillic macrophages in the spleen trapped circulating GBS and restricted the spread of the GBS to distant organs, reducing mortality. Specific IgM antibody responses to GBS challenge were also impaired in sialoadhesin-deficient mice. Thus, sialoadhesin represents a key bridge to orchestrate innate and adaptive immune defenses against invasive sialylated bacterial pathogens. Sialoadhesin is critical for macrophages to phagocytose and clear GBS. Increased GBS organ dissemination in the sialoadhesin-deficient mice. Reduced anti-GBS IgM production in the sialoadhesin-deficient mice. The online version of this article (doi:10.1007/s00109-014-1157-y) contains supplementary material, which is available to authorized users.
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DOI:
10.4049/jimmunol.1200776
发表时间:
2012-09-01
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Klaas M;Oetke C;Lewis LE;Erwig LP;Heikema AP;Easton A;Willison HJ;Crocker PR
通讯作者:
Crocker PR
影响因子:
3.7
作者:
Rempel H;Calosing C;Sun B;Pulliam L
通讯作者:
Pulliam L
影响因子:
5.3
作者:
Oetke, C;Vinson, MC;Crocker, PR
通讯作者:
Crocker, PR
影响因子:
3.6
作者:
Jones, C;Virji, M;Crocker, PR
通讯作者:
Crocker, PR
DOI:
10.1016/s0074-7696(06)50005-1
发表时间:
2006
期刊:
International review of cytology
影响因子:
--
作者:
Kraal G;Mebius R
通讯作者:
Mebius R