Demonstration of IL-1α and IL-1β secretion by the monocytic leukemia cell line, THP-1

Gaffney, Edwin V.; Stoner, Cheryl R.; Lingenfelter, Susan E.; Wagner, Lisa A.

doi:10.1016/0022-1759(89)90266-4

Cited by 9 publications

(2 citation statements)

References 13 publications

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“…28,34,35,[37][38][39][40][41] IL-1A gene expression and release by macrophages/monocytes and THP-1 cells has been demonstrated in several studies. [42][43][44][45][46] In complete accordance with these findings, we observed a TNF-a dependent upregulation of IL-1A in THP-1, but not in CaCo-2 microarray experiments. Our findings indicate an IBD-specific gene expression regulation for IL-1A.…”

Section: Discussionsupporting

confidence: 86%

From model cell line to in vivo gene expression: disease-related intestinal gene expression in IBD

et al. 2008

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Crohn's disease (CD) and ulcerative colitis (UC) are subforms of inflammatory bowel diseases (IBD). Genetic and environmental factors influencing the onset and course of the diseases have been recently identified. This study uses a twostep approach to detect genes involved in the pathogenesis of IBD by microarray analysis and real-time PCR (RT-PCR). In a first step, microarray expression screening was used to obtain tumour necrosis factor-a (TNF-a) induction profiles of two human cell lines to represent the tissue cell types involved in IBD. In a second step, a subset of differentially expressed genes was examined by real-time PCR in intestinal biopsy samples of normal controls (NC) compared with UC and CD patients, as well as to a cohort of patients suffering from intestinal diseases other than IBD. Data were obtained from 88 CD, 88 UC, 53 non-IBD patients (inflammatory control), DC and 45 NC individuals. The experimental design enabled the identification of disease-specific expressed genes. DnaJ (Hsp40) homologue, subfamily B, member 5 (DNAJB5) was downregulated in intestinal biopsy samples of the UC cohort compared with NC. A difference in JUNB expression levels was observed by comparing biopsy samples from inflamed and non-inflamed areas of UC patients. Transcript expression differences between IBD and control cohorts were found by examining histamine N-methyltransferase (HNMT), interleukin-1A (IL-1A) and proplatelet basic protein (PPBP) expression. The experimental procedure represents an approach to identify disease-relevant genes, which is applicable to any disease where appropriate model systems are available.

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Section: Discussionsupporting

confidence: 86%

From model cell line to in vivo gene expression: disease-related intestinal gene expression in IBD

et al. 2008

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“…In transfected THP‐1 cells, IL‐1β was the only cytokine, among an array of cytokines studied, that was significantly associated with the expression of the mutated NLRP3. This latter observation, which is not surprising given the existing differences between THP‐1 cells and human primary monocytes , underlines the importance of using both cell models in order to better understand the functional consequences of the identified mutation.…”

Section: Discussionmentioning

confidence: 73%

The NLRP3 p.A441V Mutation in NLRP3‐AID Pathogenesis: Functional Consequences, Phenotype‐Genotype Correlations and Evidence for a Recurrent Mutational Event

Awad

Assrawi

Jumeau

et al. 2019

ACR Open Rheumatology

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ObjectiveTo determine the molecular and cellular bases of autoinflammatory syndromes in a multigenerational French family with Muckle‐Wells syndrome and in a patient originating from Portugal with familial cold autoinflammatory syndrome.MethodsSequencing of NLRP3 exon 3 was performed in all accessible patients. Microsatellite and whole‐genome single nucleotide polymorphism genotyping was used i) to test the intrafamilial segregation of the identified variant and ii) to look for a founder effect. Functional analyses included the study of i) apoptosis‐associated speck‐like protein containing a CARD (ASC) speck formation in HEK293T cells (stably expressing ASC–green fluorescent protein and pro‐caspase 1‐FLAG) transiently expressing the wild‐type or mutated NLRP3 protein, ii) levels of IL‐1β secreted from transfected THP‐1 cells, and iii) inflammasome‐related gene expression and cytokine secretion from monocytes isolated from patients in crisis (probands from the two families), related patients out of crisis, and from controls.ResultsThe same heterozygous mutation (c.1322C>T, p.A441V) located in the NACHT domain, segregating with the disease within the first family, was identified in the two families. This mutation was found to be associated with different core haplotypes. NLRP3‐A441V led to increased ASC speck formation and high levels of secreted IL‐1β. Monocyte inflammasome‐related gene expression and cytokine secretion, which were within the normal range in patients out of crisis, were found to be differentially regulated between the two probands, correlating with their phenotypic status.ConclusionThese molecular and cellular findings, which indicate a recurrent mutational event, clearly demonstrate the pathogenicity of the p.A441V missense mutation in NLRP3‐associated autoinflammatory disease and point to the interest of studying patients’ primary cells to assess disease activity.

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Detecting cytokine production at the single-cell level

Lewis

1991

Cytokine

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Demonstration of IL-1α and IL-1β secretion by the monocytic leukemia cell line, THP-1

Cited by 9 publications

References 13 publications

From model cell line to in vivo gene expression: disease-related intestinal gene expression in IBD

From model cell line to in vivo gene expression: disease-related intestinal gene expression in IBD

The NLRP3 p.A441V Mutation in NLRP3‐AID Pathogenesis: Functional Consequences, Phenotype‐Genotype Correlations and Evidence for a Recurrent Mutational Event

Detecting cytokine production at the single-cell level

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