Interleukin-33 contributes to both M1 and M2 chemokine marker expression in human macrophages

Joshi, Amrita; Oak, Sameer R.; Hartigan, Adam J.; Finn, William G.; Kunkel, Steven L.; Duffy, Karen E.; Das, Anuk; Hogaboam, Cory M.

doi:10.1186/1471-2172-11-52

Cited by 113 publications

(92 citation statements)

References 31 publications

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“…39,40 This macrophage population represents the first line of defense against microbes breaching the intestine and ascendant gynecological infections. 22 As has been reported for other sites, 41-43 we observed that the peritoneal administration of IL-33 was able to promote an allergic like macrophage activation in the peritoneal tumor-associated macrophages. As reported previously for CD40 activated CD86 + activated macrophages in the microenvironment of pancreatic cancer, 44 or activated peritoneal macrophages were able to promote tumor cytotoxicity in vitro and delay tumor progression in vivo.…”

Section: Discusionsupporting

confidence: 80%

IL-33 delays metastatic peritoneal cancer progression inducing an allergic microenvironment

et al. 2018

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Ovarian cancer is frequently diagnosed as peritoneal carcinomatosis. Unlike other tumor locations, the peritoneal cavity is commonly exposed to gut-breaching and ascending genital microorganisms and has a unique immune environment. IL-33 is a local cytokine that can activate innate and adaptive immunity. We studied the effectiveness of local IL-33 delivery in the treatment of cancer that has metastasized to the peritoneal cavity. Direct peritoneal administration of IL-33 delayed the progression of metastatic peritoneal cancer. Prolongation in survival was not associated with a direct effect of IL-33 on tumor cells, but with major changes in the immune microenvironment of the tumor. IL-33 promoted a significant increase in the leukocyte compartment of the tumor immunoenvironment and an allergic cytokine profile. We observed a substantial increase in the number of activated CD4+ T-cells accompanied by peritoneal eosinophil infiltration, B-cell activation and activation of peritoneal macrophages which displayed tumoricidal capacity. Depletion of CD4+ cells, eosinophils or macrophages reduced the anti-tumor effects of IL-33 but none of these alone were sufficient to completely abrogate its positive benefit. In conclusion, local administration of IL-33 generates an allergic tumor environment resulting in a novel approach for treatment of metastatic peritoneal malignancies, such as advanced ovarian cancer.

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Section: Discusionsupporting

confidence: 80%

IL-33 delays metastatic peritoneal cancer progression inducing an allergic microenvironment

et al. 2018

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“…The reduced levels of IRF4 protein observed are not reflected in the mRNA levels, suggesting that IRF4 may be posttranslationally regulated in RMs. IL-33 is a proinflammatory cytokine, alarmin, and amplifier of LPS activation (50)(51)(52)(53)(54). The lack of IL-33 expression in RMs may be important in limiting the amplification of LPS responses and M2 polarization through paracrine signaling.…”

Section: Discussionmentioning

confidence: 99%

Identification of a Unique Hybrid Macrophage-Polarization State following Recovery from Lipopolysaccharide Tolerance

O’Carroll

Fagan

Shanahan

et al. 2014

The Journal of Immunology

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LPS tolerance is an essential immune-homeostatic response to repeated exposure to LPS that prevents excessive inflammatory responses. LPS tolerance induces a state of altered responsiveness in macrophages, resulting in repression of proinflammatory gene expression and increased expression of factors that mediate the resolution of inflammation. In this study, we analyzed the transcriptional plasticity of macrophages following LPS tolerance using genome-wide transcriptional profiling. We demonstrate that LPS tolerance is a transient state and that the expression of proinflammatory genes is restored to levels comparable to the acute response to LPS. However, following recovery from LPS tolerance a number of genes remained locked in a tolerizable state, including IL-33, CD86, IL-10, and NFIL3. Furthermore, we identified of a number of genes uniquely induced following recovery from LPS tolerance. Thus, macrophages adopt a unique transcriptional profile following recovery from LPS tolerance and have a distinct expression pattern of regulators of Ag presentation, antiviral responses, and transcription factors. Our data suggest that recovery from LPS tolerance leads to a hybrid macrophage activation state that is proinflammatory and microbicidal in nature but that possesses a regulatory anti-inflammatory profile distinct from that of LPS-tolerant and LPS-activated macrophages.

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“…Кроме того, выделяют популяцию атипичных Мф (табл. 1), которые демонстриру-ют характерный как для М1, так и М2 характер транскрипции генов [47]. Тканевые и опухоле-вые Мф также экспрессируют М2-маркеры [58].…”

Section: м1-и м2-макрофаги характеристика про-исхождение и роль в пunclassified

Characteristics and Role of Macrophages in Pathogenesis of Acute and Chronic Lung Diseases

Nikonova¹,

Khaitov²,

Хаитов³

2017

Med. immunol.

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Interleukin-33 contributes to both M1 and M2 chemokine marker expression in human macrophages

Cited by 113 publications

References 31 publications

IL-33 delays metastatic peritoneal cancer progression inducing an allergic microenvironment

IL-33 delays metastatic peritoneal cancer progression inducing an allergic microenvironment

Identification of a Unique Hybrid Macrophage-Polarization State following Recovery from Lipopolysaccharide Tolerance

Characteristics and Role of Macrophages in Pathogenesis of Acute and Chronic Lung Diseases

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