Transcellular delivery of vesicular SOCS proteins from macrophages to epithelial cells blunts inflammatory signaling

Bourdonnay, Emilie; Zasłona, Zbigniew; Penke, L.R.K.; Speth, John D.; Schneider, Daniel J.; Przybranowski, Sally; Swanson, Joel A.; Mancuso, Peter; Freeman, Christine M.; Curtis, Jeffrey L.; Peters‐Golden, Marc

doi:10.1084/jem.20141675

Cited by 180 publications

(189 citation statements)

References 52 publications

Supporting

Mentioning

182

Contrasting

Order By: Relevance

Section: Interference With Anti-inflammatory Signalingmentioning

confidence: 99%

“…EV from alveolar macrophages contribute to this anti-inflammatory state by delivering suppressor of cytokine signaling (SOCS) 1 and 3 to epithelial cells (Bourdonnay et al 2015). Importantly, CS-exposed mice and human smokers exhibited decreased SOCS concentrations in BALF compared to nonsmoking controls, suggesting a loss of EV-dependent antiinflammatory state in smokers (Bourdonnay et al 2015). In addition, the anti-inflammatory effect of alveolar macrophage-derived EV depends upon their internalization by target cells, which is inhibited by the presence of CS extract (CSE) (Schneider et al 2017).…”

Section: Interference With Anti-inflammatory Signalingmentioning

confidence: 99%

See 1 more Smart Citation

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Benedikter

Wouters

Savelkoul

et al. 2018

Journal of Toxicology and Environmental Health, Part B

View full text Add to dashboard Cite

Extracellular vesicles (EV) are secreted signaling entities that enhance various pathological processes when released in response to cellular stresses. Respiratory exposures such as cigarette smoke and air pollution exert cellular stresses and are associated with an increased risk of several chronic diseases. The aim of this review was to examine the evidence that modifications in EV contribute to respiratory exposure-associated diseases. Publications were searched using PubMed and Google Scholar with the search terms (cigarette smoke OR tobacco smoke OR air pollution OR particulate matter) AND (extracellular vesicles OR exosomes OR microvesicles OR microparticles OR ectosomes). All original research articles were included and reviewed. Fifty articles were identified, most of which investigated the effect of respiratory exposures on EV release in vitro (25) and/or on circulating EV in human plasma (24). The majority of studies based their main observations on the relatively insensitive scatter-based flow cytometry of EV (29). EV induced by respiratory exposures were found to modulate inflammation (19), thrombosis (13), endothelial dysfunction (11), tissue remodeling (6), and angiogenesis (3). By influencing these processes, EV may play a key role in the development of cardiovascular diseases and chronic obstructive pulmonary disease and possibly lung cancer and allergic asthma. The current findings warrant additional research with improved methodologies to evaluate the contribution of respiratory exposure-induced EV to disease etiology, as well as their potential as biomarkers of exposure or risk and as novel targets for preventive or therapeutic strategies.

show abstract

Section: Interference With Anti-inflammatory Signalingmentioning

confidence: 99%

Section: Interference With Anti-inflammatory Signalingmentioning

confidence: 99%

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Benedikter

Wouters

Savelkoul

et al. 2018

Journal of Toxicology and Environmental Health, Part B

View full text Add to dashboard Cite

show abstract

“…SOCS1 and SOCS3 are released from alveolar macrophages in exosomes and microparticles, respectively. These are then internalised by alveolar epithelial 7 cells, resulting in attenuation of cytokine signalling, a previously unrecognised mechanism of smoking-mediated inflammatory activity [61].…”

Section: Pro-inflammatory Effects Of Smokingmentioning

confidence: 99%

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

Anderson

Meyer

Ally

et al. 2016

NICTOB

View full text Add to dashboard Cite

Smoking is now well recognised not only as a risk factor for rheumatoid arthritis (RA), but also as a determinant of disease activity, severity, response to therapy, and possibly mortality. Recent studies have provided significant insights into the molecular and cellular mechanisms which underpin the pathogenesis of smokingrelated RA. These involve release of the enzymes, peptidylarginine deiminases (PADs) 2 and 4 from smoke-activated, resident and infiltrating pulmonary phagocytes. PADs, in turn, mediate the conversion of various endogenous proteins to putative citrullinated autoantigens. In genetically susceptible individuals, these autoantigens trigger the production of anti-citrullinated peptide/protein pathogenic autoantibodies (ACPA), an event which precedes the development of RA. This review is focused primarily on smoking-mediated harmful chronic inflammatory responses, both local and systemic, which promote the formation of ACPA, as well as the possible involvement of other types of outdoor and indoor pollution in the pathogenesis of RA. This is preceded by a brief overview of the evidence implicating smoking as a risk factor for development of ACPA-positive RA.Keywords: Anti-citrullinated peptide/protein antibodies; airway microbiota; atmospheric pollution; heavy metals; peptidylarginine deiminases; smoking cessation strategies. ImplicationsChronic inflammatory mechanisms operative in the lungs of smokers lead to the production of anti-citrullinated protein antibodies which, in turn, drive the development of rheumatoid arthritis. These mechanistic insights not only reinforce the association between smoking and risk for rheumatoid arthritis, but also the necessity to increase the level of awareness in those at highest risk.

show abstract

“…The preferential uptake of microvesicles over apoptotic cells serves to suppress epithelial cell inflammatory responses, and accordingly the deletion of IGF1R in airway epithelial cells exacerbates airway inflammation (284). Macrophage-derived microvesicles may contain anti-inflammatory mediators such as SOCS1 and SOCS3 proteins that were reported to be present within microvesicles released by alveolar macrophages (285). These proteins attenuated JAK-STAT signaling in alveolar epithelial cells during smoking-induced lung inflammation (285).…”

Section: In Conclusion – One More Aspect Of the Biology Of Apoptoticmentioning

confidence: 99%

“…Macrophage-derived microvesicles may contain anti-inflammatory mediators such as SOCS1 and SOCS3 proteins that were reported to be present within microvesicles released by alveolar macrophages (285). These proteins attenuated JAK-STAT signaling in alveolar epithelial cells during smoking-induced lung inflammation (285). There are undoubtedly many more ways in which phagocytes suppress inflammation, mediate immune tolerance, and orchestrate tissue homeostasis.…”

Section: In Conclusion – One More Aspect Of the Biology Of Apoptoticmentioning

confidence: 99%

The many ways tissue phagocytes respond to dying cells

Blander

2017

Immunological Reviews

View full text Add to dashboard Cite

Summary Apoptosis is an important component of normal tissue physiology, and the prompt removal of apoptotic cells is equally essential to avoid the undesirable consequences of their accumulation and disintegration. Professional phagocytes are highly specialized for engulfing apoptotic cells. The recent ability to track cells that have undergone apoptosis in situ has revealed a division of labor among the tissue resident phagocytes that sample them. Macrophages are uniquely programmed to process internalized apoptotic cell-derived fatty acids, cholesterol and nucleotides, as a reflection of their dominant role in clearing the bulk of apoptotic cells. Dendritic cells carry apoptotic cells to lymph nodes where they signal the emergence and expansion of highly suppressive regulatory CD4 T cells. A broad suppression of inflammation is executed through distinct phagocyte-specific mechanisms. A clever induction of negative regulatory nodes is notable in dendritic cells serving to simultaneously shut down multiple pathways of inflammation. Several of the genes and pathways modulated in phagocytes in response to apoptotic cells have been linked to chronic inflammatory and autoimmune diseases such as atherosclerosis, inflammatory bowel disease and systemic lupus erythematosus. Our collective understanding of old and new phagocyte functions after apoptotic cell phagocytosis demonstrates the enormity of ways to mediate immune suppression and enforce tissue homeostasis.

show abstract

Transcellular delivery of vesicular SOCS proteins from macrophages to epithelial cells blunts inflammatory signaling

Cited by 180 publications

References 52 publications

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

The many ways tissue phagocytes respond to dying cells

Contact Info

Product

Resources

About