Scavenger receptor A is expressed by macrophages in response to <i>Porphyromonas gingivalis</i>, and participates in TNF‐α expression

Baer, Michael T.; Huang, Nasi; Gibson, Frank C.

doi:10.1111/j.1399-302x.2009.00538.x

Cited by 16 publications

(20 citation statements)

References 77 publications

(97 reference statements)

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“…[68] reported that mice deficient in SR-A had greater levels of bone mineral density than WT mice. Our studies support that P. gingivalis stimulates SR-A ( msr 1) gene and surface protein expression and that the presence of SR-A in part limits host TNF-α production to this organism [69]. Triantafilou et al .…”

Section: Innate Sensing Of Periodontal Pathogenssupporting

confidence: 79%

Immuno-Pathogenesis of Periodontal Disease: Current and Emerging Paradigms

Huang

Gibson

2014

Curr Oral Health Rep

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Periodontal disease (PD) is a highly complex disease involving many factors; however, two principal facets central to initiation and progression of the majority of PD are the composition of the microbes in the sub-gingival plaque, and the host immune response to these organisms. Numerous studies point to the complexity of PD, and to the fact that despite innate and adaptive immune activation, and resultant inflammation, our immune response fails to cure disease. Stunning new findings have begun to clarify several complexities of the host-pathogen interaction of PD pointing to key roles for microbial dysboisis and immune imbalance in the pathogenesis of disease. Furthermore, these investigations have identified novel translational opportunities to intercede in PD treatment. In this review we will highlight a select few recent findings in innate and adaptive immunity, and host pathogen interactions of PD at a micro-environmental level that may have profound impact on PD progression.

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Section: Innate Sensing Of Periodontal Pathogenssupporting

confidence: 79%

Immuno-Pathogenesis of Periodontal Disease: Current and Emerging Paradigms

Huang

Gibson

2014

Curr Oral Health Rep

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“…SRs also bind bacterial ligands and have been shown to mediate phagocytosis 29 , 35 , 36 . MARCO, SR-A and SR-B1 (CD36) can internalize oxLDL in macrophages 37 , 38 . To confirm that SRs were functional in MSCs, we examined endocytosis of lipids by using a fluorescent ligand, Dil-labeled oxidized low-density lipoprotein (Dil-oxLDL), a known endocytic marker for SRs in human macrophages 34 .…”

Section: Resultsmentioning

confidence: 99%

Mesenchymal stem cells internalize Mycobacterium tuberculosis through scavenger receptors and restrict bacterial growth through autophagy

Khan

Mann

Papanna

et al. 2017

Sci Rep

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Human mesenchymal stem cells (MSCs) express scavenger receptors that internalize lipids, including oxidized low-density lipoprotein (oxLDL). We report that MSCs phagocytose Mycobacterium tuberculosis (Mtb) through two types of scavenger receptors (SRs; MARCO and SR-B1), as blockade of the receptors with antibodies or siRNA knockdown decreased the uptake of Mtb. MSCs also expressed mannose receptor (MR) that was found to endocytose rhodamine-labeled mannosylated BSA (rMBSA), though the receptor was not involved in the uptake of Mtb. Dil-oxLDL and rMBSA taken up into MSC endosomes colocalized with Mtb phagosomes, thus suggesting that the latter were fusion competent. Phagocytosed Mtb did not replicate within MSCs, thus suggesting an intrinsic control of bacterial growth. Indeed, MSCs exhibited intrinsic autophagy, which was up-regulated after activation with rapamycin. SiRNA knockdown of autophagy initiator beclin-1 enhanced Mtb survival, whereas rapamycin-induced autophagy increased intracellular killing of Mtb. In addition, MSCs secreted nitric oxide after Mtb infection, and inhibition of NO by N(G)-monomethyl-L-arginine enhanced intracellular survival of Mtb. MSCs can be grown in large numbers in vitro, and autologous MSCs transfused into tuberculosis patients have been found to be safe and improve lung immunity. Thus, MSCs are novel phagocytic cells with a potential for immunotherapy in treating multidrug-resistant tuberculosis.

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“…This increase is partially dependent on the major fimbriae of P. gingivalis FimA and promotes TNF-α, thus suggesting a role for SR-A in inflammation ( Fig. 2) (Baer et al 2009).…”

Section: Sp-a Increases Cell Surface Localization Of Sr-a and Potentimentioning

confidence: 94%

Scavenger Receptors: Promiscuous Players during Microbial Pathogenesis

Pombinho

Sousa

Cabanes

2018

Critical Reviews in Microbiology

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Innate immunity is the most broadly effective host defense, being essential to clear the majority of microbial infections. Scavenger Receptors comprise a family of sensors expressed in a multitude of host cells, whose dual role during microbial pathogenesis gained importance over recent years. SRs regulate the recruitment of immune cells and control both host inflammatory response and bacterial load. In turn, pathogens have evolved different strategies to overcome immune response, avoid recognition by SRs and exploit them to favor infection. Here, we discuss the most relevant findings regarding the interplay between SRs and pathogens, discussing how these multifunctional proteins recognize a panoply of ligands and act as bacterial phagocytic receptors.

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Scavenger receptor A is expressed by macrophages in response to Porphyromonas gingivalis, and participates in TNF‐α expression

Cited by 16 publications

References 77 publications

Immuno-Pathogenesis of Periodontal Disease: Current and Emerging Paradigms

Immuno-Pathogenesis of Periodontal Disease: Current and Emerging Paradigms

Mesenchymal stem cells internalize Mycobacterium tuberculosis through scavenger receptors and restrict bacterial growth through autophagy

Scavenger Receptors: Promiscuous Players during Microbial Pathogenesis

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