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Article ; Online: Caspase-11 contributes to pulmonary host defense against

Perlee, Desiree / de Beer, Regina / Florquin, Sandrine / van der Poll, Tom / van 't Veer, Cornelis / de Vos, Alex F

American journal of physiology. Lung cellular and molecular physiology

2020 Volume 319, Issue 1, Page(s) L105–L114

Abstract: Klebsiella (K.) ... ...

Abstract	Klebsiella (K.) pneumoniae
MeSH term(s)	Animals ; Blood Coagulation/physiology ; Caspases, Initiator/deficiency ; Caspases, Initiator/metabolism ; Cell Death ; Cytokines/metabolism ; Fibrin/metabolism ; Host-Pathogen Interactions ; Inflammation Mediators/metabolism ; Klebsiella Infections/blood ; Klebsiella Infections/immunology ; Klebsiella Infections/microbiology ; Klebsiella pneumoniae/physiology ; Lung/immunology ; Lung/microbiology ; Lung/pathology ; Mice, Inbred C57BL ; Neutrophils/metabolism ; Pneumonia/blood ; Pneumonia/complications
Chemical Substances	Cytokines ; Inflammation Mediators ; Fibrin (9001-31-4) ; Casp4 protein, mouse (EC 3.4.22.-) ; Caspases, Initiator (EC 3.4.22.-)
Language	English
Publishing date	2020-05-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00422.2019
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Article ; Online: Bruton's Tyrosine Kinase in Neutrophils Is Crucial for Host Defense against Klebsiella pneumoniae.

Liu, Zhe / De Porto, Alexander P N A / De Beer, Regina / Roelofs, Joris J T H / De Boer, Onno J / Florquin, Sandrine / Van't Veer, Cornelis / Hendriks, Rudi W / Van der Poll, Tom / De Vos, Alex F

Journal of innate immunity

2022 Volume 15, Issue 1, Page(s) 1–15

Abstract: Humans with dysfunctional Bruton's tyrosine kinase (Btk) are highly susceptible to bacterial infections. Compelling evidence indicates that Btk is essential for B cell-mediated immunity, whereas its role in myeloid cell-mediated immunity against ... ...

Abstract	Humans with dysfunctional Bruton's tyrosine kinase (Btk) are highly susceptible to bacterial infections. Compelling evidence indicates that Btk is essential for B cell-mediated immunity, whereas its role in myeloid cell-mediated immunity against infections is controversial. In this study, we determined the contribution of Btk in B cells and neutrophils to host defense against the extracellular bacterial pathogen Klebsiella pneumoniae, a common cause of pulmonary infections and sepsis. Btk-/- mice were highly susceptible to Klebsiella infection, which was not reversed by Btk re-expression in B cells and restoration of natural antibody levels. Neutrophil-specific Btk deficiency impaired host defense against Klebsiella to a similar extent as complete Btk deficiency. Neutrophil-specific Btk deficiency abolished extracellular reactive oxygen species production in response to Klebsiella. These data indicate that expression of Btk in neutrophils is crucial, while in B cells, it is dispensable for in vivo host defense against K. pneumoniae.
MeSH term(s)	Animals ; Humans ; Mice ; Agammaglobulinaemia Tyrosine Kinase/metabolism ; Bacterial Infections ; Klebsiella pneumoniae ; Neutrophils/metabolism ; Sepsis
Chemical Substances	Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2) ; Btk protein, mouse (EC 2.7.10.2)
Language	English
Publishing date	2022-05-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2454158-8
ISSN	1662-8128 ; 1662-811X
ISSN (online)	1662-8128
ISSN	1662-811X
DOI	10.1159/000524583
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Article ; Online: Bruton's Tyrosine Kinase-Mediated Signaling in Myeloid Cells Is Required for Protective Innate Immunity During Pneumococcal Pneumonia.

de Porto, Alexander P / Liu, Zhe / de Beer, Regina / Florquin, Sandrine / Roelofs, Joris J T H / de Boer, Onno J / den Haan, Joke M M / Hendriks, Rudi W / van 't Veer, Cornelis / van der Poll, Tom / de Vos, Alex F

Frontiers in immunology

2021 Volume 12, Page(s) 723967

Abstract: Bruton's tyrosine kinase (Btk) is a cytoplasmic kinase expressed in B cells and myeloid cells. It is essential for B cell development and natural antibody-mediated host defense against bacteria in humans and mice, but little is known about the role of ... ...

Abstract	Bruton's tyrosine kinase (Btk) is a cytoplasmic kinase expressed in B cells and myeloid cells. It is essential for B cell development and natural antibody-mediated host defense against bacteria in humans and mice, but little is known about the role of Btk in innate host defense
MeSH term(s)	Agammaglobulinaemia Tyrosine Kinase/genetics ; Agammaglobulinaemia Tyrosine Kinase/metabolism ; Animals ; B-Lymphocytes/metabolism ; Disease Models, Animal ; Female ; Humans ; Immunity, Innate ; Lipopolysaccharides ; Lung/pathology ; Macrophages, Alveolar/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Myeloid Cells/immunology ; Phagocytosis ; Pneumonia, Pneumococcal/genetics ; Pneumonia, Pneumococcal/immunology ; Pneumonia, Pneumococcal/metabolism ; Sepsis/metabolism ; Signal Transduction ; Streptococcus pneumoniae/physiology ; Teichoic Acids
Chemical Substances	Lipopolysaccharides ; Teichoic Acids ; lipoteichoic acid (56411-57-5) ; Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2) ; Btk protein, mouse (EC 2.7.10.2)
Language	English
Publishing date	2021-09-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.723967
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Article ; Online: Btk inhibitor ibrutinib reduces inflammatory myeloid cell responses in the lung during murine pneumococcal pneumonia.

de Porto, Alexander P / Liu, Zhe / de Beer, Regina / Florquin, Sandrine / de Boer, Onno J / Hendriks, Rudi W / van der Poll, Tom / de Vos, Alex F

Molecular medicine (Cambridge, Mass.)

2019 Volume 25, Issue 1, Page(s) 3

Abstract: Background: Streptococcus pneumoniae is a major causative agent in community-acquired pneumonia and sepsis. Overwhelming lung inflammation during pneumococcal pneumonia may hamper lung function. Ibrutinib is an irreversible inhibitor of Bruton's ... ...

Abstract	Background: Streptococcus pneumoniae is a major causative agent in community-acquired pneumonia and sepsis. Overwhelming lung inflammation during pneumococcal pneumonia may hamper lung function. Ibrutinib is an irreversible inhibitor of Bruton's tyrosine kinase (Btk), a key signaling protein controlling the activation of various immune cells, including macrophages and neutrophils. The aim of this study was to determine whether ibrutinib treatment ameliorates acute lung inflammation during pneumococcal pneumonia. Methods: Mice were treated orally with ibrutinib and the effect on acute pulmonary inflammation elicited by the gram-positive bacterial cell wall component lipoteichoic acid (LTA) and during ceftriaxone-treated pneumococcal pneumonia was assessed. Results: Treatment with ibrutinib prior to and after intranasal LTA instillation reduced alveolar macrophage activation, neutrophil influx, cytokine release and plasma leakage into the lung. Postponed treatment with ibrutinib supplementing antibiotic therapy during ongoing pneumococcal pneumonia did not impair bacterial killing in lung, blood and spleen. In this setting, ibrutinib reduced alveolar macrophage and systemic neutrophil activation and substantially diminished further monocyte and neutrophil influx in the lung. In vitro, ibrutinib inhibited macrophage TNF secretion and neutrophil activation upon LTA and pneumococcal stimulation. Conclusions: Taken together, these data indicate that the Btk inhibitor ibrutinib reduces inflammatory myeloid cell responses during acute pulmonary inflammation evoked by LTA and antibiotic-treated pneumococcal pneumonia and suggest that ibrutinib has the potential to inhibit ongoing lung inflammation in an acute infectious setting.
MeSH term(s)	Agammaglobulinaemia Tyrosine Kinase/antagonists & inhibitors ; Animals ; Anti-Bacterial Agents/therapeutic use ; Anti-Inflammatory Agents/therapeutic use ; Bronchoalveolar Lavage Fluid/cytology ; Ceftriaxone/therapeutic use ; Lipopolysaccharides ; Lung/drug effects ; Lung/immunology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Cells/drug effects ; Myeloid Cells/immunology ; Pneumonia, Pneumococcal/drug therapy ; Pneumonia, Pneumococcal/immunology ; Protein Kinase Inhibitors/therapeutic use ; Pyrazoles/therapeutic use ; Pyrimidines/therapeutic use ; Teichoic Acids
Chemical Substances	Anti-Bacterial Agents ; Anti-Inflammatory Agents ; Lipopolysaccharides ; Protein Kinase Inhibitors ; Pyrazoles ; Pyrimidines ; Teichoic Acids ; ibrutinib (1X70OSD4VX) ; lipoteichoic acid (56411-57-5) ; Ceftriaxone (75J73V1629) ; Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2) ; Btk protein, mouse (EC 2.7.10.2)
Language	English
Publishing date	2019-01-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.1186/s10020-018-0069-7
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Article ; Online: Complement factor C5 inhibition reduces type 2 responses without affecting group 2 innate lymphoid cells in a house dust mite induced murine asthma model.

Yang, Jack / Ramirez Moral, Ivan / van 't Veer, Cornelis / de Vos, Alex F / de Beer, Regina / Roelofs, Joris J T H / Morgan, B Paul / van der Poll, Tom

Respiratory research

2019 Volume 20, Issue 1, Page(s) 165

Abstract: Background: Complement factor C5 can either aggravate or attenuate the T-helper type 2 (T: Objectives: We aimed to determine the effect of C5 blockade during the effector phase on the pulmonary T: Methods: BALB/c mice were sensitized and ... ...

Abstract	Background: Complement factor C5 can either aggravate or attenuate the T-helper type 2 (T Objectives: We aimed to determine the effect of C5 blockade during the effector phase on the pulmonary T Methods: BALB/c mice were sensitized and challenged repeatedly with HDM via the airways to induce allergic lung inflammation. Sensitized mice received twice weekly injections with a blocking anti-C5 or control antibody 24 h before the first challenge. Results: HDM challenge in sensitized mice resulted in elevated C5a levels in bronchoalveolar lavage fluid. Anti-C5 administered to sensitized mice prior to the first HDM challenge prevented this rise in C5a, but did not influence the influx of eosinophils or neutrophils. While anti-C5 did not impact the recruitment of CD4 T cells upon HDM challenge, it reduced the proportion of T Conclusions: Generation of C5a during the effector phase of HDM induced allergic lung inflammation contributes to T
MeSH term(s)	Animals ; Asthma/chemically induced ; Asthma/immunology ; Asthma/prevention & control ; Complement C5a/antagonists & inhibitors ; Complement C5a/immunology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Female ; Immunity, Innate/drug effects ; Immunity, Innate/immunology ; Lymphocytes/drug effects ; Lymphocytes/immunology ; Methacholine Chloride/pharmacology ; Mice ; Mice, Inbred BALB C ; Pyroglyphidae/immunology ; Th2 Cells/drug effects ; Th2 Cells/immunology
Chemical Substances	Methacholine Chloride (0W5ETF9M2K) ; Complement C5a (80295-54-1)
Language	English
Publishing date	2019-07-24
Publishing country	England
Document type	Journal Article
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-9921
ISSN (online)	1465-993X
ISSN	1465-9921
DOI	10.1186/s12931-019-1136-5
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Article ; Online: Platelet Btk is Required for Maintaining Lung Vascular Integrity during Murine Pneumococcal Pneumosepsis.

de Porto, Alexander P N A / Claushuis, Theodora A M / van der Donk, Lieve E H / de Beer, Regina / de Boer, Onno J / Florquin, Sandrine / Roelofs, Joris J T H / Hendriks, Rudi W / van der Poll, Tom / Van't Veer, Cornelis / de Vos, Alex F

Thrombosis and haemostasis

2019 Volume 119, Issue 6, Page(s) 930–940

Abstract: Platelet Bruton's tyrosine kinase (Btk) is an essential signalling protein for the collagen receptor glycoprotein VI (GPVI) and podoplanin receptor C-type-lectin-like receptor-2, which are platelet receptors implicated in the maintenance of vascular ... ...

Abstract	Platelet Bruton's tyrosine kinase (Btk) is an essential signalling protein for the collagen receptor glycoprotein VI (GPVI) and podoplanin receptor C-type-lectin-like receptor-2, which are platelet receptors implicated in the maintenance of vascular integrity during inflammation. Moreover, platelets, platelet GPVI and Btk are important for host defence during murine bacterial pneumosepsis. The aim of this study was to determine the role of platelet Btk in vascular integrity and host defence during murine pneumosepsis caused by the common human pathogens
MeSH term(s)	Agammaglobulinaemia Tyrosine Kinase/genetics ; Agammaglobulinaemia Tyrosine Kinase/metabolism ; Animals ; Blood Platelets/physiology ; Disease Models, Animal ; Hemorrhage ; Humans ; Immunity ; Klebsiella pneumoniae/physiology ; Lung/blood supply ; Lung/pathology ; Male ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Knockout ; Platelet Aggregation/genetics ; Platelet Membrane Glycoproteins/metabolism ; Pneumonia, Pneumococcal/genetics ; Pneumonia, Pneumococcal/metabolism ; Regional Blood Flow ; Sepsis/metabolism ; Signal Transduction ; Streptococcus pneumoniae/physiology
Chemical Substances	Gp38 protein, mouse ; Membrane Glycoproteins ; Platelet Membrane Glycoproteins ; platelet membrane glycoprotein VI ; Agammaglobulinaemia Tyrosine Kinase (EC 2.7.10.2)
Language	English
Publishing date	2019-03-14
Publishing country	Germany
Document type	Journal Article
ZDB-ID	518294-3
ISSN	2567-689X ; 0340-6245
ISSN (online)	2567-689X
ISSN	0340-6245
DOI	10.1055/s-0039-1681046
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Article ; Online: Limited role of the receptor for advanced glycation end products during Streptococcus pneumoniae bacteremia.

Achouiti, Ahmed / de Vos, Alex F / de Beer, Regina / Florquin, Sandrine / van 't Veer, Cornelis / van der Poll, Tom

Journal of innate immunity

2013 Volume 5, Issue 6, Page(s) 603–612

Abstract: Streptococcus pneumoniae is one of the most common causes of sepsis. Sepsis is associated with the release of 'damage-associated molecular patterns' (DAMPs). The receptor for advanced glycation end products (RAGE) is a multiligand receptor, abundantly ... ...

Abstract	Streptococcus pneumoniae is one of the most common causes of sepsis. Sepsis is associated with the release of 'damage-associated molecular patterns' (DAMPs). The receptor for advanced glycation end products (RAGE) is a multiligand receptor, abundantly expressed in the lungs, that recognizes several of these DAMPs. Triggering of RAGE leads to activation of the NF-κB pathway and perpetuation of inflammation. Earlier investigations have shown that the absence of RAGE reduces inflammation and bacterial dissemination and increases survival in sepsis caused by S. pneumoniae pneumonia. We hypothesized that the detrimental role of RAGE depends on the level of RAGE expression in the primary organ of infection. By directly injecting S. pneumoniae intravenously, thereby circumventing the extensive RAGE-expressing lung, we here determined whether RAGE contributes to an adverse outcome of bacteremia or whether its role is restricted to primary lung infection. During late-stage infection (48 h), rage(-/-) mice had an attenuated systemic inflammatory response, as reflected by lower plasma levels of proinflammatory cytokines, reduced endothelial cell activation (as measured by E-selectin levels) and less neutrophil accumulation in lung tissue. However, RAGE deficiency did not influence bacterial loads or survival in this model. In accordance, plasma markers for cell injury were similar in both mouse strains. These results demonstrate that while RAGE plays a harmful part in S. pneumoniae sepsis originating from the respiratory tract, this receptor has a limited role in the outcome of primary bloodstream infection by this pathogen.
MeSH term(s)	Animals ; Bacteremia/genetics ; Bacteremia/immunology ; Bacteremia/microbiology ; Cytokines/blood ; Cytokines/immunology ; E-Selectin/immunology ; E-Selectin/metabolism ; Endothelial Cells/immunology ; Endothelial Cells/metabolism ; Host-Pathogen Interactions/immunology ; Immunohistochemistry ; Lung/immunology ; Lung/metabolism ; Lung/microbiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neutrophil Infiltration/genetics ; Neutrophil Infiltration/immunology ; Pneumococcal Infections/genetics ; Pneumococcal Infections/immunology ; Pneumococcal Infections/microbiology ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic/genetics ; Receptors, Immunologic/immunology ; Receptors, Immunologic/metabolism ; Sepsis/genetics ; Sepsis/immunology ; Sepsis/microbiology ; Streptococcus pneumoniae/immunology ; Streptococcus pneumoniae/physiology ; Survival Analysis ; Time Factors
Chemical Substances	Cytokines ; E-Selectin ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic
Language	English
Publishing date	2013-06-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454158-8
ISSN	1662-8128 ; 1662-811X
ISSN (online)	1662-8128
ISSN	1662-811X
DOI	10.1159/000348739
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Article ; Online: ASC and NLRP3 impair host defense during lethal pneumonia caused by serotype 3 Streptococcus pneumoniae in mice.

van Lieshout, Miriam H P / de Vos, Alex F / Dessing, Mark C / de Porto, Alexander P N A / de Boer, Onno J / de Beer, Regina / Terpstra, Sanne / Florquin, Sandrine / Van't Veer, Cornelis / van der Poll, Tom

European journal of immunology

2017 Volume 48, Issue 1, Page(s) 66–79

Abstract: Streptococcus (S.) pneumoniae is the most common cause of community-acquired pneumonia. The Nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, consisting of NLRP3, ASC (the adaptor apoptosis-associated speck-like protein containing ... ...

Abstract	Streptococcus (S.) pneumoniae is the most common cause of community-acquired pneumonia. The Nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, consisting of NLRP3, ASC (the adaptor apoptosis-associated speck-like protein containing a CARD) and caspase-1, has been implicated in protective immunity during pneumonia induced by high doses of S. pneumoniae serotype 2. Here we investigated the role of the NLRP3 inflammasome in the host response during lethal airway infection with a low dose of serotype 3 S. pneumoniae. Mice were euthanized at predefined endpoints for analysis or observed in survival studies. In additional studies, Tlr2
MeSH term(s)	Animals ; CARD Signaling Adaptor Proteins/genetics ; CARD Signaling Adaptor Proteins/immunology ; Caspase 1/immunology ; Community-Acquired Infections/immunology ; Community-Acquired Infections/microbiology ; Immunity, Innate/genetics ; Immunity, Innate/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Differentiation Factor 88/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/immunology ; Pneumonia, Pneumococcal/immunology ; Pneumonia, Pneumococcal/pathology ; Signal Transduction/immunology ; Streptococcus pneumoniae/classification ; Streptococcus pneumoniae/immunology ; Toll-Like Receptor 2/genetics ; Toll-Like Receptor 4/genetics
Chemical Substances	CARD Signaling Adaptor Proteins ; Myd88 protein, mouse ; Myeloid Differentiation Factor 88 ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Pycard protein, mouse ; Tlr2 protein, mouse ; Tlr4 protein, mouse ; Toll-Like Receptor 2 ; Toll-Like Receptor 4 ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	2017-11-03
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201646554
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Article: Platelet Btk is Required for Maintaining Lung Vascular Integrity during Murine Pneumococcal Pneumosepsis

de Porto, Alexander P. N. A. / Claushuis, Theodora A. M. / van der Donk, Lieve E. H. / de Beer, Regina / de Boer, Onno J. / Florquin, Sandrine / Roelofs, Joris J. T. H. / Hendriks, Rudi W. / van der Poll, Tom / van't Veer, Cornelis / de Vos, Alex F.

Thrombosis and Haemostasis

2019 Volume 119, Issue 06, Page(s) 930–940

Abstract	Platelet Bruton's tyrosine kinase (Btk) is an essential signalling protein for the collagen receptor glycoprotein VI (GPVI) and podoplanin receptor C-type-lectin-like receptor-2, which are platelet receptors implicated in the maintenance of vascular integrity during inflammation. Moreover, platelets, platelet GPVI and Btk are important for host defence during murine bacterial pneumosepsis. The aim of this study was to determine the role of platelet Btk in vascular integrity and host defence during murine pneumosepsis caused by the common human pathogens Streptococcus pneumoniae and Klebsiella pneumoniae. Using the Cre-loxP system, male platelet-specific Btk-deficient mice (PF4creBtk fl /Y) were created. Similar to platelets from total Btk-deficient mice, platelets from PF4creBtk fl /Y mice showed abrogated aggregation and P-selectin expression when stimulated with the GPVI ligand cross-linked collagen-related peptide. Upon infection with S. pneumoniae, PF4creBtk fl /Y mice showed increased lung bleeding, but unimpaired anti-bacterial defence. During pneumosepsis evoked by K. pneumoniae, platelet Btk deficiency was not associated with lung bleeding and did not impact on host defence, even when platelet function was further compromised by blocking secondary platelet activation by the P2Y 12 receptor antagonist clopidogrel. Together, these data indicate that, while platelet Btk is not important for anti-bacterial defence in pneumosepsis, its role in maintaining vascular integrity in the lung depends on the causative pathogen.
Keywords	Bruton's tyrosine kinase ; blood platelets ; haemostasis ; infection ; innate immunity
Language	English
Publishing date	2019-03-14
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	518294-3
ISSN	2567-689X ; 0340-6245
ISSN (online)	2567-689X
ISSN	0340-6245
DOI	10.1055/s-0039-1681046
Database	Thieme publisher's database

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Article ; Online: Mast cells impair host defense during murine Streptococcus pneumoniae pneumonia.

van den Boogaard, Florry E / Brands, Xanthe / Roelofs, Joris J T H / de Beer, Regina / de Boer, Onno J / van 't Veer, Cornelis / van der Poll, Tom

The Journal of infectious diseases

2014 Volume 210, Issue 9, Page(s) 1376–1384

Abstract: Background: Streptococcus pneumoniae is the most common causative pathogen in community-acquired pneumonia. Mast cells (MCs) are located mainly at the host-environment interface where they function as sentinels.: Objective: Our goal was to study the ... ...

Abstract	Background: Streptococcus pneumoniae is the most common causative pathogen in community-acquired pneumonia. Mast cells (MCs) are located mainly at the host-environment interface where they function as sentinels. Objective: Our goal was to study the role of MCs during pneumonia caused by S. pneumoniae. Methods: Lung tissue of patients who had died from pneumococcal pneumonia or a nonpulmonary cause was stained for MCs and tryptase. Wild-type (WT) and MC-deficient (Kit(W-sh/W-sh)) mice were observed or sacrificed after induction of pneumonia by intranasal inoculation of S. pneumoniae. In separate experiments, WT mice were treated with doxantrazole or cromoglycate, which are MC stabilizing agents. Results: The constitutive presence of tryptase-positive MCs was reduced in affected lungs from pneumonia patients. Kit(W-sh/W-sh) mice showed a prolonged survival during the first few days after median lethal dose (LD)100 and LD50 infection, while overall mortality did not differ from that in WT mice. Relative to WT mice, Kit(W-sh/W-sh) mice showed reduced bacterial counts with less bacterial dissemination to distant organs and less inflammation. Neither doxantrazole nor cromoglycate influenced antibacterial defense or inflammatory responses after airway infection with S. pneumoniae. Conclusions: MCs exhibit an unfavorable role in host defense during pneumococcal pneumonia by a mechanism independent of degranulation.
MeSH term(s)	Animals ; Bacterial Load ; Female ; Host-Pathogen Interactions/immunology ; Humans ; Lung/microbiology ; Lung/pathology ; Male ; Mast Cells/physiology ; Mice ; Mice, Inbred C57BL ; Pneumonia, Pneumococcal/immunology ; Pneumonia, Pneumococcal/microbiology ; Pneumonia, Pneumococcal/pathology ; Streptococcus pneumoniae/immunology
Language	English
Publishing date	2014-11-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	3019-3
ISSN	1537-6613 ; 0022-1899
ISSN (online)	1537-6613
ISSN	0022-1899
DOI	10.1093/infdis/jiu285
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

Order via subito