Phagocytic and signaling innate immune receptors: are they dysregulated in cystic fibrosis in the fight against Pseudomonas aeruginosa?

Sallenave, Jean–Michel

doi:10.1016/j.biocel.2014.01.013

Cited by 14 publications

(15 citation statements)

References 83 publications

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“…In general, pattern recognition receptors (PRR), including TLRs representing the prototypic PRR, are traditionally considered as 'signaling receptors' that, upon recognition of a variety of microbial components, induce the synthesis of pro-inflammatory cytokines [53]. In addition, recognition of pathogens may occur through dependent or independent receptors on serum opsonins including scavenger receptors, C-type lectins complement receptors and Fcγ receptors [54].…”

Section: Alteration Of Pattern Recognition Receptors In Cf Macrophagesmentioning

confidence: 99%

The impact of impaired macrophage functions in cystic fibrosis disease progression

Lévêque

Trionnaire

Porto³

et al. 2017

Journal of Cystic Fibrosis

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The underlying cause of morbidity in cystic fibrosis (CF) is the decline in lung function, which results in part from chronic inflammation. Inflammation and infection occur early in infancy in CF and the role of innate immune defense in CF has been highlighted in the last years. Once thought simply to be consumers of bacteria, macrophages have emerged as highly sensitive immune cells that are located at the balance point between inflammation and resolution of this inflammation in CF pathophysiology. In order to assess the potential role of macrophage in CF, we review the evidence that: (1) CF macrophage has a dysregulated inflammatory phenotype; (2) CF macrophage presents altered phagocytosis capacity and bacterial killing; and (3) lipid disorders in CF macrophage affect its function. These alterations of macrophage weaken innate defense of CF patients and may be involved in CF disease progression and lung damage.

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Section: Alteration Of Pattern Recognition Receptors In Cf Macrophagesmentioning

confidence: 99%

The impact of impaired macrophage functions in cystic fibrosis disease progression

Lévêque

Trionnaire

Porto³

et al. 2017

Journal of Cystic Fibrosis

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“…CF is the most commonly inherited genetic disease in persons of European descent affecting 1 in 2500 newborns (Sallenave, 2014). The major symptoms are observed in the lungs and digestive tract where cycles of exocrine gland obstruction, infection and inflammation lead to destruction of the mucosal tissue (Rowe et al, 2005;Sallenave, 2014).…”

Section: Salsa and Complement In Cystic Fibrosismentioning

confidence: 99%

SALSA—A dance on a slippery floor with changing partners

Reichhardt

Holmskov

Meri

2017

Molecular Immunology

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It is becoming increasingly clear that the connections between our immune system and the microbiota colonizing us have a tremendous impact on human health. A number of innate molecular defence mechanisms cooperate to selectively target unwanted microorganisms at the mucosal surfaces. Amongst others these include the complement system, IgA and the SALSA molecule. The salivary scavenger and agglutinin (SALSA), also known as deleted in malignant brain tumors 1 (DMBT1), salivary agglutinin (SAG) or gp340 is a multifunctional molecule with important functions in innate immunity, inflammation and epithelial homeostasis. The SALSA protein is expressed at most mucosal surfaces, where it is one of the most abundant proteins. In the fetal meconium and infant intestine it may constitute even up to 10% of the total protein amount. SALSA is found either directly associated with the epithelial surface or secreted into the lining fluids. In the fluid-phase SALSA interacts with a number of bacterial and viral organisms, as well as with endogenous ligands, including IgA, lactoferrin, surfactant proteins and complement components. While complement has been shown to impact the mucosal environment, this remains an area of limited research. The multiple interactions of the SALSA molecule provide a scaffold, where this potent defence system may engage in cooperative microbial clearance together with corresponding mucosal host ligands. With its high abundance, and multiple effects on both host and microbes, the SALSA molecule is a key player in maintaining the immunological balance at the mucosal surfaces. This is further supported by observations linking the expression of different SALSA isoforms to the development of chronic inflammatory conditions, such as Crohn's disease and ulcerative colitis. This review describes the latest advances in understanding functions of SALSA and its different isoforms. Recently recognized functions are related to complement activation and regulation, endothelial development and epithelial homeostasis. In addition, we suggest mechanisms how SALSA regulates inflammation at the mucosal surfaces.

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“…Moreover, host defenses include complex mechanisms of the innate immune system, such as phagocytosis by macrophages, dendritic cells, and neutrophils. These cells are attracted to the infection site by chemokines and play an important role in removing pathogens (Janeway and Medzhitov, 2002 ; Gellatly and Hancock, 2013 ; Sallenave, 2014 ). The Gram-negative bacterium Pseudomonas aeruginosa is a major opportunistic pathogen that causes severe infections, such as pneumonia and bacteremia, in immunocompromised patients.…”

Section: Introductionmentioning

confidence: 99%

Extracellular Signals of a Human Epithelial Colorectal Adenocarcinoma (Caco-2) Cell Line Facilitate the Penetration of Pseudomonas aeruginosa PAO1 Strain through the Mucin Layer

Hayashi

Yokotani

Yamamoto

et al. 2017

Front. Cell. Infect. Microbiol.

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Pseudomonas aeruginosa can penetrate the layer of mucus formed by host intestinal epithelial cells, often resulting in sepsis in immunocompromised patients. We have previously demonstrated that P. aeruginosa can penetrate the mucin layer by flagellar motility and the degradation of the mucin layer. However, it remains unclear how P. aeruginosa initially recognizes epithelial cells. Using the human epithelial colorectal adenocarcinoma (Caco-2) cell line, we investigated extracellular signaling that could facilitate the penetration of P. aeruginosa through the mucin layer. The supernatant from Caco-2 cell cultures increased penetration of P. aeruginosa through an artificial mucin layer. The Caco-2 cell supernatant increased bacterial flagella-dependent swarming motility, but it did not influence P. aeruginosa growth or protease activity. Filtering of the Caco-2 cell supernatant indicated that proteins weighing <10 kDa increased mucin penetration, swarming motility, and, based on a tethered cell assay, induced acceleration of the flagellar filament rotational rate. Furthermore, a capillary assay showed that <10 kDa proteins in the Caco-2 cell supernatant attracted P. aeruginosa cells. Finally, we identified that growth-regulated oncogene-α (GRO-α) secreted by Caco-2 cells was a factor facilitating flagellar filament rotation and swarming motility, although it did not attract the bacteria. We conclude that penetration of the mucin layer by P. aeruginosa is facilitated by small proteins (<10 kDa) secreted by Caco-2 cells, both by inducing acceleration of flagellar motility and increasing chemotaxis.

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Phagocytic and signaling innate immune receptors: are they dysregulated in cystic fibrosis in the fight against Pseudomonas aeruginosa?

Cited by 14 publications

References 83 publications

The impact of impaired macrophage functions in cystic fibrosis disease progression

The impact of impaired macrophage functions in cystic fibrosis disease progression

SALSA—A dance on a slippery floor with changing partners

Extracellular Signals of a Human Epithelial Colorectal Adenocarcinoma (Caco-2) Cell Line Facilitate the Penetration of Pseudomonas aeruginosa PAO1 Strain through the Mucin Layer

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