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Article ; Online: SIRP-α instructs alveolar macrophages to stop eating after pneumonia.

de Vos, Alex F / van der Poll, Tom

2020 Volume 21, Issue 6, Page(s) 601–603

MeSH term(s)	Humans ; Inflammation ; Macrophages, Alveolar ; Pneumonia
Language	English
Publishing date	2020-05-18
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-020-0680-y
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Article ; Online: Induction of Acute or Disseminating Bacterial Pneumonia in Mice and Sampling of Infected Organs for Studying the Host Response to Bacterial Pneumonia.

Qin, Wanhai / Liu, Zhe / van der Poll, Tom / de Vos, Alex F

Bio-protocol

2022 Volume 12, Issue 1, Page(s) e4287

Abstract: Experimental pneumonia models are important tools to study the pathophysiology of lung inflammation caused by microbial infections and the efficacy of (novel) drugs. We have applied a murine model of pneumonia induced ... ...

Abstract	Experimental pneumonia models are important tools to study the pathophysiology of lung inflammation caused by microbial infections and the efficacy of (novel) drugs. We have applied a murine model of pneumonia induced by
Language	English
Publishing date	2022-01-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.4287
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Article ; Online: Post-treatment with the PPAR-γ agonist pioglitazone inhibits inflammation and bacterial growth during Klebsiella pneumonia.

Ramirez-Moral, Ivan / Ferreira, Bianca Lima / de Vos, Alex F / van der Poll, Tom

Respiratory research

2021 Volume 22, Issue 1, Page(s) 230

Abstract: Agonists of peroxisome proliferator-activated receptor (PPAR)-γ have been suggested as potential adjuvant therapy in bacterial pneumonia because of their capacity to inhibit inflammation and enhance bacterial clearance. Previous studies only assessed the ...

Abstract	Agonists of peroxisome proliferator-activated receptor (PPAR)-γ have been suggested as potential adjuvant therapy in bacterial pneumonia because of their capacity to inhibit inflammation and enhance bacterial clearance. Previous studies only assessed the effects of pretreatment with these compounds, thereby bearing less relevance for the clinical scenario. Moreover, PPAR-γ agonists have not been studied in pneumonia caused by Klebsiella pneumoniae, a common human respiratory pathogen of which antibiotic treatment is hampered by increasing antimicrobial resistance. Here we show that administration of the PPAR-γ agonist pioglitazone 6 or 8 h after infection of mice with a highly virulent strain of Klebsiella pneumoniae via the airways results in reduced cytokine and myeloperoxidase levels in the lungs at 24 h after infection, as well as reduced bacterial growth in the lungs and decreased dissemination to distant organs at 42 h post-infection. These results suggest that pioglitazone may be an interesting agent in the treatment of Klebsiella pneumonia.
MeSH term(s)	Animals ; Female ; Inflammation/drug therapy ; Inflammation/physiopathology ; Injections, Intraperitoneal ; Klebsiella Infections/drug therapy ; Klebsiella Infections/physiopathology ; Klebsiella pneumoniae/drug effects ; Klebsiella pneumoniae/growth & development ; Mice ; Mice, Inbred C57BL ; PPAR gamma/agonists ; Pioglitazone/administration & dosage
Chemical Substances	PPAR gamma ; Pioglitazone (X4OV71U42S)
Language	English
Publishing date	2021-08-19
Publishing country	England
Document type	Letter
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-9921
ISSN (online)	1465-993X
ISSN	1465-9921
DOI	10.1186/s12931-021-01823-8
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Article ; Online: CEBPD Potentiates the Macrophage Inflammatory Response but CEBPD Knock-Out Macrophages Fail to Identify CEBPD-Dependent Pro-Inflammatory Transcriptional Programs.

Spek, C Arnold / Aberson, Hella L / Butler, Joe M / de Vos, Alex F / Duitman, JanWillem

Cells

2021 Volume 10, Issue 9

Abstract: CCAAT/enhancer-binding protein delta (C/EBPδ) is a member of the C/EBP family of transcription factors. According to the current paradigm, C/EBPδ potentiates cytokine production and modulates macrophage function thereby enhancing the inflammatory ... ...

Abstract	CCAAT/enhancer-binding protein delta (C/EBPδ) is a member of the C/EBP family of transcription factors. According to the current paradigm, C/EBPδ potentiates cytokine production and modulates macrophage function thereby enhancing the inflammatory response. Remarkably, however, C/EBPδ deficiency does not consistently lead to a reduction in Lipopolysaccharide (LPS)-induced cytokine production by macrophages. Here, we address this apparent discrepancy and show that the effect of C/EBPδ on cytokine production and macrophage function depends on both the macrophage subtype and the LPS concentration used. Using CRISPR-Cas generated macrophages in which the transactivation domain of C/EBPδ was deleted from the endogenous locus (ΔTAD macrophages), we next show that the context-dependent role of C/EBPδ in macrophage biology relies on compensatory transcriptional activity in the absence of C/EBPδ. We extend these findings by revealing a large discrepancy between transcriptional programs in C/EBPδ knock-out and C/EBPδ transactivation dead (ΔTAD) macrophages implying that compensatory mechanisms do not specifically modify C/EBPδ-dependent inflammatory responses but affect overall macrophage biology. Overall, these data imply that knock-out approaches are not suited for identifying the genuine transcriptional program regulated by C/EBPδ, and we suggest that this phenomenon applies for transcription factor families in general.
MeSH term(s)	Animals ; CCAAT-Enhancer-Binding Protein-delta/deficiency ; CCAAT-Enhancer-Binding Protein-delta/genetics ; CCAAT-Enhancer-Binding Protein-delta/metabolism ; CRISPR-Cas Systems/genetics ; Cell Differentiation ; Cells, Cultured ; Gene Editing ; Gene Expression Regulation/drug effects ; Interleukin-6/metabolism ; Lipopolysaccharides/pharmacology ; Macrophage Colony-Stimulating Factor/pharmacology ; Macrophages/cytology ; Macrophages/drug effects ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutagenesis ; Transcriptional Activation ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Interleukin-6 ; Lipopolysaccharides ; Tumor Necrosis Factor-alpha ; CCAAT-Enhancer-Binding Protein-delta (142662-43-9) ; Macrophage Colony-Stimulating Factor (81627-83-0)
Language	English
Publishing date	2021-08-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10092233
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Article ; Online: DNA Methyltransferase 3b in Myeloid Cells Does Not Affect the Acute Immune Response in the Airways during

Qin, Wanhai / Brands, Xanthe / Van't Veer, Cornelis / de Vos, Alex F / Scicluna, Brendon P / van der Poll, Tom

Cells

2022 Volume 11, Issue 5

Abstract: DNA methyltransferase 3b (Dnmt3b) has been suggested to play a role in the host immune response during bacterial infection. Neutrophils and other myeloid cells are crucial for lung defense ... ...

Abstract	DNA methyltransferase 3b (Dnmt3b) has been suggested to play a role in the host immune response during bacterial infection. Neutrophils and other myeloid cells are crucial for lung defense against
MeSH term(s)	Animals ; DNA (Cytosine-5-)-Methyltransferases ; Immunity ; Interleukin-6/metabolism ; Mice ; Neutrophils/metabolism ; Pneumonia/pathology ; Pseudomonas ; Pseudomonas Infections ; Pseudomonas aeruginosa/physiology ; DNA Methyltransferase 3B
Chemical Substances	Interleukin-6 ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37)
Language	English
Publishing date	2022-02-24
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11050787
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Article ; Online: Myeloid liver kinase B1 contributes to lung inflammation induced by lipoteichoic acid but not by viable Streptococcus pneumoniae.

Pereverzeva, Liza / Otto, Natasja A / Roelofs, Joris J T H / de Vos, Alex F / van der Poll, Tom

Respiratory research

2022 Volume 23, Issue 1, Page(s) 241

Abstract: Background: Liver kinase B1 (Lkb1, gene name Stk11) functions as a tumor suppressor in cancer. Myeloid cell Lkb1 potentiates lung inflammation induced by the Gram-negative bacterial cell wall component lipopolysaccharide and in host defense during Gram- ... ...

Abstract	Background: Liver kinase B1 (Lkb1, gene name Stk11) functions as a tumor suppressor in cancer. Myeloid cell Lkb1 potentiates lung inflammation induced by the Gram-negative bacterial cell wall component lipopolysaccharide and in host defense during Gram-negative pneumonia. Here, we sought to investigate the role of myeloid Lkb1 in lung inflammation elicited by the Gram-positive bacterial cell wall component lipoteichoic acid (LTA) and during pneumonia caused by the Gram-positive respiratory pathogen Streptococcus pneumoniae (Spneu). Methods: Alveolar and bone marrow derived macrophages (AMs, BMDMs) harvested from myeloid-specific Lkb1 deficient (Stk11-ΔM) and littermate control mice were stimulated with LTA or Spneu in vitro. Stk11-ΔM and control mice were challenged via the airways with LTA or infected with Spneu in vivo. Results: Lkb1 deficient AMs and BMDMs produced less tumor necrosis factor (TNF)α upon activation by LTA or Spneu. During LTA-induced lung inflammation, Stk11-ΔM mice had reduced numbers of AMs in the lungs, as well as diminished cytokine release and neutrophil recruitment into the airways. During pneumonia induced by either encapsulated or non-encapsulated Spneu, Stk11-ΔM and control mice had comparable bacterial loads and inflammatory responses in the lung, with the exception of lower TNFα levels in Stk11-ΔM mice after infection with the non-encapsulated strain. Conclusion: Myeloid Lkb1 contributes to LTA-induced lung inflammation, but is not important for host defense during pneumococcal pneumonia.
MeSH term(s)	AMP-Activated Protein Kinases ; Animals ; Lipopolysaccharides/immunology ; Liver ; Mice ; Pneumonia, Bacterial/chemically induced ; Pneumonia, Pneumococcal ; Streptococcus pneumoniae/pathogenicity ; Teichoic Acids ; Tumor Necrosis Factor-alpha
Chemical Substances	Lipopolysaccharides ; Teichoic Acids ; Tumor Necrosis Factor-alpha ; lipoteichoic acid (56411-57-5) ; Stk11 protein, mouse (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2022-09-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-993X
ISSN (online)	1465-993X
ISSN	1465-993X
DOI	10.1186/s12931-022-02168-6
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Article ; Online: The PPAR-γ agonist pioglitazone exerts proinflammatory effects in bronchial epithelial cells during acute Pseudomonas aeruginosa pneumonia.

Ferreira, Bianca L / Ramirez-Moral, Ivan / Otto, Natasja A / Salomão, Reinaldo / de Vos, Alex F / van der Poll, Tom

Clinical and experimental immunology

2022 Volume 207, Issue 3, Page(s) 370–377

Abstract: Pseudomonas aeruginosa is a common respiratory pathogen that causes injurious airway inflammation during acute pneumonia. Peroxisome proliferator-activated receptor (PPAR)-γ is involved in the regulation of metabolic and inflammatory responses in ... ...

Abstract	Pseudomonas aeruginosa is a common respiratory pathogen that causes injurious airway inflammation during acute pneumonia. Peroxisome proliferator-activated receptor (PPAR)-γ is involved in the regulation of metabolic and inflammatory responses in different cell types and synthetic agonists of PPAR-γ exert anti-inflammatory effects on myeloid cells in vitro and in models of inflammation in vivo. We sought to determine the effect of the PPAR-γ agonist pioglitazone on airway inflammation induced by acute P. aeruginosa pneumonia, focusing on bronchial epithelial cells. Mice pretreated with pioglitazone or vehicle (24 and 1 h) were infected with P. aeruginosa via the airways. Pioglitazone treatment was associated with increased expression of chemokine (Cxcl1, Cxcl2, and Ccl20) and cytokine genes (Tnfa, Il6, and Cfs3) in bronchial brushes obtained 6 h after infection. This pro-inflammatory effect was accompanied by increased expression of Hk2 and Pfkfb3 genes encoding rate-limiting enzymes of glycolysis; concurrently, the expression of Sdha, important for maintaining metabolite flux in the tricarboxylic acid cycle, was reduced in bronchial epithelial cells of pioglitazone treated-mice. Pioglitazone inhibited bronchoalveolar inflammatory responses measured in lavage fluid. These results suggest that pioglitazone exerts a selective proinflammatory effect on bronchial epithelial cells during acute P. aeruginosa pneumonia, possibly by enhancing intracellular glycolysis.
MeSH term(s)	Animals ; Epithelial Cells/metabolism ; Hypoglycemic Agents ; Inflammation ; Mice ; PPAR gamma/agonists ; PPAR gamma/genetics ; Pioglitazone/pharmacology ; Pneumonia ; Pseudomonas aeruginosa ; Thiazolidinediones/pharmacology
Chemical Substances	Hypoglycemic Agents ; PPAR gamma ; Thiazolidinediones ; Pioglitazone (X4OV71U42S)
Language	English
Publishing date	2022-04-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218531-3
ISSN	1365-2249 ; 0009-9104 ; 0964-2536
ISSN (online)	1365-2249
ISSN	0009-9104 ; 0964-2536
DOI	10.1093/cei/uxab036
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Article ; Online: Bruton's Tyrosine Kinase Deficiency Ameliorates Antimicrobial Host Defense during Peritonitis Induced by Pathogenic Escherichia coli.

Liu, Zhe / van 't Veer, Cornelis / Hendriks, Rudi W / Roelofs, Joris J T H / van der Poll, Tom / de Vos, Alex F

Infection and immunity

2022 Volume 90, Issue 6, Page(s) e0067421

Abstract: Peritonitis and abdominal sepsis remain major health problems and challenge for clinicians. Bruton's tyrosine kinase (Btk) is a versatile signaling protein involved in the regulation of B cell development and function, as well as innate host defense. In ... ...

Abstract	Peritonitis and abdominal sepsis remain major health problems and challenge for clinicians. Bruton's tyrosine kinase (Btk) is a versatile signaling protein involved in the regulation of B cell development and function, as well as innate host defense. In the current study, we aimed to explore the role of Btk in the host response during peritonitis and sepsis in mice induced by a gradually growing pathogenic strain of Escherichia coli bacteria. We found that Btk deficiency ameliorated antibacterial host defense during the late stage of E. coli-induced peritonitis. Btk was not required for cytokine and chemokine release in response to either E. coli or lipopolysaccharide and did not impact organ damage evoked by E. coli. Btk deficiency also did not alter neutrophil influx to the primary site of infection. However, the absence of Btk modestly enhanced phagocytosis of E. coli by neutrophils. These results indicate that Btk-mediated signaling is superfluous for inflammatory responses and remarkably detrimental for antibacterial defense during E. coli-induced peritonitis.
MeSH term(s)	Agammaglobulinaemia Tyrosine Kinase/metabolism ; Animals ; Anti-Bacterial Agents ; Anti-Infective Agents ; Escherichia coli/metabolism ; Escherichia coli Infections ; Mice ; Peritonitis ; Sepsis
Chemical Substances	Anti-Bacterial Agents ; Anti-Infective Agents ; Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2)
Language	English
Publishing date	2022-05-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/iai.00674-21
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Article ; Online: Role of Hypoxia-inducible factor 1α in host defense during pneumococcal pneumonia.

Pereverzeva, Liza / Otto, Natasja A / Peters-Sengers, Hessel / Roelofs, Joris J T H / de Vos, Alex F / van der Poll, Tom

Pathogens and disease

2022 Volume 81

Abstract: Hypoxia-inducible factor (HIF)1α is a transcription factor involved in cellular metabolism and regulation of immune cell effector functions. Here, we studied the role of HIF1α in myeloid cells during pneumonia caused by the major causative pathogen, ... ...

Abstract	Hypoxia-inducible factor (HIF)1α is a transcription factor involved in cellular metabolism and regulation of immune cell effector functions. Here, we studied the role of HIF1α in myeloid cells during pneumonia caused by the major causative pathogen, Streptococcus pneumoniae (Spneu). Mice deficient for HIF1α in myeloid cells (LysMcreHif1αfl/fl) were generated to study the in vitro responsiveness of bone marrow-derived macrophages (BMDMs) and alveolar macrophages (AMs) to the Gram-positive bacterial wall component lipoteichoic acid (LTA) and heat-killed Spneu, and the in vivo host response after infection with Spneu via the airways. Both BMDMs and AMs released more lactate upon stimulation with LTA or Spneu, indicative of enhanced glycolysis; HIF1α-deficiency in these cells was associated with diminished lactate release. In BMDMs, HIF1α-deficiency resulted in reduced secretion of tumor necrosis factor (TNF)α and interleukin (IL)-6 upon activation with Spneu but not LTA, while HIF1α-deficient AMs secreted less TNFα and IL-6 in response to LTA, and TNFα after Spneu stimulation. However, no difference was found in the host response of LysMcreHif1αfl/fl mice after Spneu infection as compared to controls. Similar in vivo findings were obtained in neutrophil (Mrp8creHif1αfl/fl) HIF1α-deficient mice. These data suggest that myeloid HIF1α is dispensable for the host defense during pneumococcal pneumonia.
MeSH term(s)	Animals ; Mice ; Hypoxia ; Macrophages, Alveolar ; Mice, Inbred C57BL ; Pneumonia, Pneumococcal/pathology ; Streptococcus pneumoniae ; Tumor Necrosis Factor-alpha
Chemical Substances	Tumor Necrosis Factor-alpha ; Hif1a protein, mouse
Language	English
Publishing date	2022-12-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2049-632X
ISSN (online)	2049-632X
DOI	10.1093/femspd/ftac047
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Article ; Online: Myeloid cell tet methylcytosine dioxygenase 2 does not affect the host response during gram-negative bacterial pneumonia and sepsis.

Qin, Wanhai / Brands, Xanthe / van 't Veer, Cornelis / de Vos, Alex F / Scicluna, Brendon P / van der Poll, Tom

Cytokine

2022 Volume 154, Page(s) 155876

Abstract: Tet methylcytosine dioxygenase 2 (Tet2) is an important enzyme in the demethylation of DNA. Recent evidence has indicated a role for Tet2 in the regulation of macrophage activation by lipopolysaccharide (LPS) and mice with a myeloid cell Tet2 deficiency ... ...

Abstract	Tet methylcytosine dioxygenase 2 (Tet2) is an important enzyme in the demethylation of DNA. Recent evidence has indicated a role for Tet2 in the regulation of macrophage activation by lipopolysaccharide (LPS) and mice with a myeloid cell Tet2 deficiency showed enhanced lung inflammation upon local LPS administration. However, mice with a global Tet2 deficiency showed reduced systemic inflammation during abdominal sepsis. Here, we sought to determine the role of myeloid cell Tet2 in the host response during gram-negative bacterial pneumonia. To this end we infected myeloid cell specific Tet2 deficient and control mice with two common gram-negative respiratory pathogens via the airways: Pseudomonas aeruginosa (PAK, causing acute infection that remains confined in the lungs) or Klebsiella pneumoniae (causing a gradually evolving pneumonia with subsequent dissemination and sepsis) and compared bacterial loads and host response parameters between mouse strains. Bone marrow derived macrophages from myeloid Tet2 deficient mice released more interleukin-6 than control macrophages upon stimulation with PAK or K. pneumoniae. However, bacterial loads did not differ between mouse strains upon infection with viable PAK or K. pneumoniae, and neither did cytokine levels or neutrophil recruitment. In addition, in the K. pneumoniae pneumosepsis model myeloid Tet2 deficiency did not affect systemic inflammation or organ injury. Together these data strongly argue against a role for myeloid cell Tet2 in the host response during gram-negative bacterial pneumonia and pneumosepsis.
MeSH term(s)	Animals ; DNA-Binding Proteins/genetics ; Dioxygenases/genetics ; Inflammation ; Klebsiella pneumoniae ; Lipopolysaccharides ; Lung/microbiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Cells ; Pneumonia, Bacterial/microbiology ; Sepsis/microbiology
Chemical Substances	DNA-Binding Proteins ; Lipopolysaccharides ; Dioxygenases (EC 1.13.11.-) ; Tet2 protein, mouse (EC 1.13.11.-)
Language	English
Publishing date	2022-04-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1018055-2
ISSN	1096-0023 ; 1043-4666
ISSN (online)	1096-0023
ISSN	1043-4666
DOI	10.1016/j.cyto.2022.155876
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