Macrophage-polarizing stimuli differentially modulate the inflammatory profile induced by the secreted phospholipase A2 group IA in human lung macrophages

Ferrara, Anne Lise; Galdiero, Maria Rosaria; Fiorelli, Alfonso; Cristinziano, Leonardo; Granata, Francescopaolo; Marone, Giancarlo; Crescenzo, Rosa Maria Di; Braile, Mariantonia; Marcella, Simone; Modestino, Luca; Varricchi, Gilda; Spadaro, Giuseppe; Santini, Mario; Loffredo, Stefania

doi:10.1016/j.cyto.2020.155378

Cited by 15 publications

(17 citation statements)

References 26 publications

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“…Besides, tumor cells, HIF-1, IL-10, lactic acid, and pyruvate in the hypoxic environment are thought to activate the pro-angiogenesis process in TAMs. 50 Moreover, the number of TAMs in colon cancer is positively correlated with the number of blood vessels. 49 Treatment regimens for TAMs are mainly divided into four directions: 49 removal of macrophages, restriction of TAMs recruitment, inhibition of TAMs activation, and increase of M1 and decrease of M2.…”

Section: Tamsmentioning

confidence: 99%

“…58 Due to the secretion of bFGF by tumor cells themselves, TAMs, and cancer associated fibroblasts (CAFs), the carrying of exosomes, and the promoting effect of COX-2/ mPGES-1, FGF is highly expressed in the microenvironment of various tumors. 6,31,32,38,50,60 However, in diabetes, different experiments have drawn different conclusions: some believe that the expression of FGF is increased, while others believe that there is no abnormality. 35 This may be related to different measurement methods and specific microenvironment differences in different patients and in different parts of the same patient.…”

Section: Fgfmentioning

confidence: 99%

“…As the long-term stimulation of diabetes itself, the activation of PKC and other factors, promote the synthesis of PDGF is promoted to, increases the level of PDGF in the retina and kidney of diabetic patients, further advance the formation of new blood vessels by stimulating intercellular adhesion molecule -1 (IGAM-1) and other ways, and aggravate microvascular-related lesions. The tumor microenvironment also contains abundant PDGF, possibly for the following reasons: TAMs 32,49,50,63 and CAFs 31,46 can secrete PDGF, and on the other hand, active HIF-1 can increase the release of PDGF under hypoxia conditions. 35 PDGF promotes tumor angiogenesis through its effects and co-action with other factors, 8 but overexpression of PDGF-B significantly inhibits tumor growth in vivo.…”

Section: Pdgfmentioning

confidence: 99%

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Differences of Angiogenesis Factors in Tumor and Diabetes Mellitus

Tan¹,

Zang²,

Wang³

et al. 2021

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Angiogenesis, as a process occurring under the regulation of a variety of factors, is one of the important ways of vascular development. It coexists in a variety of pathological and physiological processes. Now a large number of studies have proved that tumor growth, metastasis, and various vascular complications of diabetes are closely related to angiogenesis, and an increasing number of studies have shown that there are many common factors between the two. But angiogenesis is the opposite of the two: it is enhanced in tumors and suppressed in diabetes. Therefore, this review discusses the causes of the phenomenon from the expression of various factors affecting angiogenesis in these two diseases and their effects on angiogenesis in the relevant microenvironment, as well as the application status of these factors or cells as therapeutic targets in the treatment of these two diseases.

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Section: Tamsmentioning

confidence: 99%

Section: Fgfmentioning

confidence: 99%

Section: Pdgfmentioning

confidence: 99%

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Differences of Angiogenesis Factors in Tumor and Diabetes Mellitus

Tan¹,

Zang²,

Wang³

et al. 2021

DMSO

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“…7/19), and informed consent was obtained from donors. Macrophages were purified from macroscopically normal lung tissue obtained from 39 patients [hepatitis C virus (HCV−), hepatitis B surface Ag (HBsAg−), HIV−] (age 62.4 ± 1.7 years) affected by lung adenocarcinoma undergoing thoracic surgery [59,75]. Freshly resected lung tissue was obtained intraoperatively and was minced finally with scissors and washed extensively with PIPES buffer over Nytex cloth (120-µm pore size (Tetko Elmsford, NY, USA).…”

Section: Isolation and Purification Of Human Lung Macrophages (Hlms)mentioning

confidence: 99%

“…We have previously shown that LPS can activate HLMs to release several proinflammatory and immunomodulatory mediators [59,75]. T H 2-like cytokines, IL-4 and IL-13, can synergize with LPS in several systems [16].…”

Section: Effects Of Il-4 Il-13 and Lps On Tslp System In Hlmsmentioning

confidence: 99%

Human Lung-Resident Macrophages Express and Are Targets of Thymic Stromal Lymphopoietin in the Tumor Microenvironment

Braile

Fiorelli

Sorriento

et al. 2021

Cells

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Thymic stromal lymphopoietin (TSLP) is a pleiotropic cytokine highly expressed by epithelial cells and several innate and adaptive immune cells. TSLP exerts its biological effects by binding to a heterodimeric complex composed of TSLP receptor (TSLPR) and IL-7Rα. In humans, there are two TSLP isoforms: the short form (sfTSLP), constitutively expressed, and the long form (lfTSLP), which is upregulated in inflammation. TSLP has been implicated in the induction and progression of several experimental and human cancers. Primary human lung macrophages (HLMs), monocyte-derived macrophages (MDMs), and peripheral blood monocytes consitutively expressed sfTSLP mRNA. Incubation of HLMs, MDMs, and monocytes with lipopolysaccharide (LPS) or IL-4, but not with IL-13, induced TSLP release from HLMs. LPS, but not IL-4 or IL-13, induced CXCL8 release from HLMs. LPS, IL-4 alone or in combination with IL-13, induced the expression of lfTSLP, but not of sfTSLP from HLMs. Preincubation of HLMs with IL-4, alone or in combination with IL-13, but not IL-13 alone, synergistically enhanced TSLP release from LPS-activated macrophages. By contrast, IL-4, alone or in combination with IL-13, inhibited LPS-induced CXCL8 release from HLMs. Immunoreactive TSLP was detected in lysates of HLMs, MDMs, and monocytes. Incubation of HLMs with TSLP induced the release of proinflammatory (TNF-α), angiogenic (VEGF-A, angiopoietin 2), and lymphangiogenic (VEGF-C) factors. TSLP, TSLPR, and IL-7Rα were expressed in intratumoral and peritumoral areas of human lung cancer. sfTSLP and lfTSLP mRNAs were differentially expressed in peritumoral and intratumoral lung cancer tissues. The TSLP system, expressed in HLMs, MDMs, and monocytes, could play a role in chronic inflammatory disorders including lung cancer.

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