Diversity and environmental adaptation of phagocytic cell metabolism

Rice, Christopher M.; McVicar, Daniel W.; Weiss, Jonathan M.

doi:10.1002/jlb.4ri0518-195r

Cited by 44 publications

(38 citation statements)

References 143 publications

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“…The different phagocytes share receptor profiles, pathogen engulfing ability, and also some intracellular processes (such as phagolysosome formation or respiratory burst) maintain subset-specific roles ( 32 , 33 ). During sepsis, the presence of pathogens and high levels of inflammatory cytokines results in a dynamic change in the proportion of leukocytes in the blood ( 34 ).…”

Section: Sepsis-associated Changes To Phagocyte Subsetsmentioning

confidence: 99%

Phagocytosis–Inflammation Crosstalk in Sepsis: New Avenues for Therapeutic Intervention

Hortová-Kohoutková

Tidu

Zuani

et al. 2020

Shock

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Phagocytosis is a complex process by which cells within most organ systems remove pathogens and cell debris. Phagocytosis is usually followed by inflammatory pathway activation, which promotes pathogen elimination and inhibits pathogen growth. Delayed pathogen elimination is the first step in sepsis development and a key factor in sepsis resolution. Phagocytosis thus has an important role during sepsis and likely contributes to all of its clinical stages. However, only a few studies have specifically explored and characterized phagocytic activity during sepsis. Here, we describe the phagocytic processes that occur as part of the immune response preceding sepsis onset and identify the elements of phagocytosis that might constitute a predictive marker of sepsis outcomes. First, we detail the key features of phagocytosis, including the main receptors and signaling hallmarks associated with different phagocytic processes. We then discuss how the initial events of phagosome formation and cytoskeletal remodeling might be associated with known sepsis features, such as a cytokine-driven hyperinflammatory response and immunosuppression. Finally, we highlight the unresolved mechanisms of sepsis development and progression and the need for cross-disciplinary approaches to link the clinical complexity of the disease with basic cellular and molecular mechanisms.

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Section: Sepsis-associated Changes To Phagocyte Subsetsmentioning

confidence: 99%

Phagocytosis–Inflammation Crosstalk in Sepsis: New Avenues for Therapeutic Intervention

Hortová-Kohoutková

Tidu

Zuani

et al. 2020

Shock

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“…26,[55][56][57] Neutrophils and other immune cells can also release protons from their exocytic granules and lysosomes into the microenvironment [58][59][60] and this inflammation-induced microenvironment acidification conceivably could activate TRPV1 even in the absence of reflux episodes. [61][62][63] TRPV1 expression has been demonstrated to be increased in biopsies taken from GERD patients compared to controls. 64 Acidactivation of TRPV1 in cat esophageal mucosa has been shown to result in release of substance P and CGRP, strongly implicating a nociceptive role.…”

Section: Acid -S En S Ing Recep Tor S and Mucosal Innervati Onmentioning

confidence: 99%

Mucosal pathogenesis in gastro‐esophageal reflux disease

Ustaoglu

Nguyen

Spechler

et al. 2020

Neurogastroenterology Motil

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Gastro-esophageal reflux disease (GERD) is a spectrum of disorders that occur when reflux of gastric contents into the esophagus causes symptoms and/or complications. 1,2 The most typical symptoms of GERD are heartburn and regurgitation. Symptoms and complications occur due to contact of noxious components of the refluxate with the esophageal mucosa. There is heterogeneity of GERD characteristics between patients with apparently similar amount of reflux. First, while 30% of patients with pathological esophageal acid exposure have visible esophageal mucosal injury at endoscopy (erosive esophagitis, EE) and up to 10% have Barrett's esophagus, 60%-70% of patients with GERD have no visible macroscopic injury (non-erosive reflux disease, NERD). 3 Second, symptoms do not accurately predict the severity of GERD and do not correlate well to endoscopic findings. 5 Functional

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“…Taking into consideration an anti-inflammatory potential of KYNA, this compound may be considered as a potent anticancer agent since continuous inflammation is one of the factors which may induce process of carcinogenesis [103,104]. On the other hand, the proper immune response may inhibit the early stages of carcinogenesis or prevent spreading of cancer cells into the whole body [105,106].…”

Section: Signalling Pathwaysmentioning

confidence: 99%

Kynurenic acid and cancer: facts and controversies

Walczak

Wnorowski

Turski

et al. 2019

Cell. Mol. Life Sci.

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Kynurenic acid (KYNA) is an endogenous tryptophan metabolite exerting neuroprotective and anticonvulsant properties in the brain. However, its importance on the periphery is still not fully elucidated. KYNA is produced endogenously in various types of peripheral cells, tissues and by gastrointestinal microbiota. Furthermore, it was found in several products of daily human diet and its absorption in the digestive tract was evidenced. More recent studies were focused on the potential role of KYNA in carcinogenesis and cancer therapy; however, the results were ambiguous and the biological activity of KYNA in these processes has not been unequivocally established. This review aims to summarize the current views on the relationship between KYNA and cancer. The differences in KYNA concentration between physiological conditions and cancer, as well as KYNA production by both normal and cancer cells, will be discussed. The review also describes the effect of KYNA on cancer cell proliferation and the known potential molecular mechanisms of this activity. Keywords Cancer therapy • Proliferation • Cell cycle • GPR35 • AhR Abbreviations 3-HAA 3-Hydroxyanthranilic acid AFMID Kynurenine formamidase (arylformamidase) AhR Aryl hydrocarbon receptor alpha7 nAChR α-7 nicotinic acetylcholine receptor BCRP Breast cancer resistance protein BMSCs Bone marrow stromal cells BRAF B-Raf proto-oncogene, serine/threonine kinase ERK Extracellular signal-regulated kinases GPR35 G protein-coupled receptor 35 HAAO 3-Hydroxyanthranilate 3,4-dioxygenase hOAT Human organic anion transporter IDO Indoleamine 2,3-dioxygenase KAT Kynurenine aminotransferase KMO Kynurenine 3-monooxygenase KRAS KRAS proto-oncogene KYN Kynurenine KYNA Kynurenic acid KYNU Kynureninase MAPK Mitogen-activated protein kinase MDS Myelodysplastic syndrome MGUS Monoclonal gammopathy of undetermined significance MM Multiple myeloma MRP Multidrug resistance protein NMDA N-Methyl-d-aspartate NSCLC Non-small cell lung carcinoma PI3K/Akt Phosphoinositide 3-kinase/protein kinase B PIK3CA Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha PTEN Phosphatase and tensin homolog QPRT Quinolinate phosphoribosyl transferase QUIN Quinolinic acid RCC Renal cell carcinoma SCC Squamous cell carcinoma TDO Tryptophan 2,3-dioxygenase TP53 Tumour protein p53 Cellular and Molecular Life Sciences

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Diversity and environmental adaptation of phagocytic cell metabolism

Cited by 44 publications

References 143 publications

Phagocytosis–Inflammation Crosstalk in Sepsis: New Avenues for Therapeutic Intervention

Phagocytosis–Inflammation Crosstalk in Sepsis: New Avenues for Therapeutic Intervention

Mucosal pathogenesis in gastro‐esophageal reflux disease

Kynurenic acid and cancer: facts and controversies

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