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Article ; Online: Novel NFKB2 Pathogenic Variants in Two Unrelated Patients with Common Variable Immunodeficiency.

Sundaram, Kruthika / Ferro, Micol / Hayman, Grant / Ibrahim, Mohammad A A

2023 Volume 43, Issue 6, Page(s) 1159–1164

MeSH term(s)	Humans ; Autoimmunity ; Common Variable Immunodeficiency/diagnosis ; Common Variable Immunodeficiency/genetics ; NF-kappa B p52 Subunit/genetics
Chemical Substances	NF-kappa B p52 Subunit ; NFKB2 protein, human
Language	English
Publishing date	2023-05-16
Publishing country	Netherlands
Document type	Case Reports ; Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-023-01491-x
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Zs.A 1640: Show issues

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Article ; Online: ARAP3 protects from excessive formylated peptide-induced microvascular leakage by acting on endothelial cells and neutrophils.

Chu, Julia Y / McCormick, Barry / Sundaram, Kruthika / Hardisty, Gareth / Karmakar, Utsa / Pumpe, Caroline / Krull, Elizabeth / Lucas, Christopher D / Amado-Azevedo, Joana / Hordijk, Peter L / Caporali, Andrea / Mellor, Harry / Baillie, J Kenneth / Rossi, Adriano G / Vermeren, Sonja

The Journal of pathology

2024

Abstract: Vascular permeability is temporarily heightened during inflammation, but excessive inflammation-associated microvascular leakage can be detrimental, as evidenced in the inflamed lung. Formylated peptides regulate vascular leakage indirectly via ... ...

Abstract	Vascular permeability is temporarily heightened during inflammation, but excessive inflammation-associated microvascular leakage can be detrimental, as evidenced in the inflamed lung. Formylated peptides regulate vascular leakage indirectly via formylated peptide receptor-1 (FPR1)-mediated recruitment and activation of neutrophils. Here we identify how the GTPase-activating protein ARAP3 protects against formylated peptide-induced microvascular permeability via endothelial cells and neutrophils. In vitro, Arap3
Language	English
Publishing date	2024-05-11
Publishing country	England
Document type	Journal Article
ZDB-ID	3119-7
ISSN	1096-9896 ; 0022-3417
ISSN (online)	1096-9896
ISSN	0022-3417
DOI	10.1002/path.6288
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Article ; Online: Immune complex-induced apoptosis and concurrent immune complex clearance are anti-inflammatory neutrophil functions.

Karmakar, Utsa / Chu, Julia Y / Sundaram, Kruthika / Astier, Anne L / Garside, Hannah / Hansen, Carsten G / Dransfield, Ian / Vermeren, Sonja

Cell death & disease

2021 Volume 12, Issue 4, Page(s) 296

Abstract: Persistent neutrophilic inflammation drives host damage in autoimmune diseases that are characterized by abundant immune complexes. Insoluble immune complexes (iICs) potently activate pro-inflammatory neutrophil effector functions. We and others have ... ...

Abstract	Persistent neutrophilic inflammation drives host damage in autoimmune diseases that are characterized by abundant immune complexes. Insoluble immune complexes (iICs) potently activate pro-inflammatory neutrophil effector functions. We and others have shown that iICs also promote resolution of inflammation via stimulation of neutrophil apoptosis. We demonstrate here that iICs trigger FcγRIIa-dependent neutrophil macropinocytosis, leading to the rapid uptake, and subsequent degradation of iICs. We provide evidence that concurrent iIC-induced neutrophil apoptosis is distinct from phagocytosis-induced cell death. First, uptake of iICs occurs by FcγRII-stimulated macropinocytosis, rather than phagocytosis. Second, production of reactive oxygen species, but not iIC-internalization is a pre-requisite for iIC-induced neutrophil apoptosis. Our findings identify a previously unknown mechanism by which neutrophils can remove pro-inflammatory iICs from the circulation. Together iIC clearance and iIC-induced neutrophil apoptosis may act to prevent the potential escalation of neutrophilic inflammation in response to iICs.
MeSH term(s)	Antigen-Antibody Complex/metabolism ; Apoptosis ; Humans ; Inflammation/immunology ; Neutrophils/immunology
Chemical Substances	Antigen-Antibody Complex
Language	English
Publishing date	2021-03-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-021-03528-8
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Article ; Online: Bioanalysis Rising Star Award 2019: announcing our finalists!

Mak, Justin / Sundaram, Kruthika / Andrews, Lee / Boridy, Sebastien / Wang, Xiaoyu / Li, Zhiyu

Bioanalysis

2019 Volume 11, Issue 14, Page(s) 1315–1319

MeSH term(s)	Awards and Prizes ; Clinical Chemistry Tests
Language	English
Publishing date	2019-12-15
Publishing country	England
Document type	Journal Article ; Portrait
ISSN	1757-6199
ISSN (online)	1757-6199
DOI	10.4155/bio-2019-0173
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Article ; Online: House Dust Mite Allergens and the Induction of Monocyte Interleukin 1β Production That Triggers an IκBζ-Dependent Granulocyte Macrophage Colony-Stimulating Factor Release from Human Lung Epithelial Cells.

Sundaram, Kruthika / Mitra, Srabani / Gavrilin, Mikhail A / Wewers, Mark D

American journal of respiratory cell and molecular biology

2015 Volume 53, Issue 3, Page(s) 400–411

Abstract: Asthma is a chronic lung disease characterized by inflammation centered upon bronchial epithelium. House dust mite is one of the most common respiratory allergens that trigger exacerbations of asthma. IκBζ (gene NFKBIZ) is a recently recognized member of ...

Abstract	Asthma is a chronic lung disease characterized by inflammation centered upon bronchial epithelium. House dust mite is one of the most common respiratory allergens that trigger exacerbations of asthma. IκBζ (gene NFKBIZ) is a recently recognized member of the NF-κB family that can be induced in mononuclear phagocytes and lung epithelial cells and has been shown to play a prominent role in epithelial cell function. We therefore analyzed the role of IκBζ in regulating lung epithelial cell cytokine responses to house dust mite mix (HDM). We found that human bronchial epithelial cells express IκBζ and release IL-6 and granulocyte macrophage colony-stimulating factor (GMCSF) when cocultured with human monocytes and HDM. This response is blocked in the presence of IL-1 receptor antagonist (IL-1Ra), indicating that it is IL-1 mediated. Neither HDM-stimulated macrophages nor dendritic cells release IL-1β and subsequently induce cytokine release from the bronchial epithelial cells. Rhodobacter sphaeroides LPS (RS-LPS), a TLR4 antagonist, blocks the ability of HDM to induce IκBζ and release GMCSF from epithelial cells cocultured with monocytes. Additionally, human bronchial epithelial cells show no induction of IκBζ or cytokine responses to direct HDM stimulation. Finally, NFKBIZ small interfering RNA-mediated knockdown in the bronchial epithelial cells suppresses the release of IL-1-induced IL-6 and GMCSF. Our findings indicate a possible role for monocyte recruitment and lung epithelial cell IκBζ in mediating asthma associated inflammation. Thus, IκBζ, IL-1Ra, and RS-LPS deserve future study as potential modulators of house dust mite-induced asthma.
MeSH term(s)	Allergens/immunology ; Alveolar Epithelial Cells/immunology ; Alveolar Epithelial Cells/metabolism ; Animals ; Asthma/immunology ; Asthma/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Coculture Techniques ; Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Granulocyte-Macrophage Colony-Stimulating Factor/secretion ; Humans ; I-kappa B Proteins/physiology ; Interleukin-1beta/biosynthesis ; Lipopolysaccharides/pharmacology ; Monocytes/metabolism ; Nuclear Proteins/physiology ; Pyroglyphidae/immunology ; Respiratory Mucosa/immunology ; Respiratory Mucosa/metabolism
Chemical Substances	Allergens ; I-kappa B Proteins ; Interleukin-1beta ; Lipopolysaccharides ; NFKBIZ protein, human ; Nuclear Proteins ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2014-0370OC
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Article ; Online: Receptor interacting protein-2 plays a critical role in human lung epithelial cells survival in response to Fas-induced cell-death.

Rahman, Mohd Akhlakur / Sundaram, Kruthika / Mitra, Srabani / Gavrilin, Mikhail A / Wewers, Mark D

PloS one

2014 Volume 9, Issue 3, Page(s) e92731

Abstract: Lung epithelial cell death is critical to the lung injury that occurs in the acute respiratory distress syndrome. It is known that FasL plays a prominent role in this lung cell death pathway and may work in part through activation of the receptor ... ...

Abstract	Lung epithelial cell death is critical to the lung injury that occurs in the acute respiratory distress syndrome. It is known that FasL plays a prominent role in this lung cell death pathway and may work in part through activation of the receptor interacting protein-2 (RIP2). RIP2 is serine/threonine kinase with a C-terminal caspase activation and recruitment domain (CARD). This CARD contains a highly conserved, predicted tyrosine phosphorylation site. Thus, involvement of tyrosine phosphorylation in the CARD domain of RIP2 may play a critical role in Fas-mediated apoptosis in the human lung immune system. To test this hypothesis, human lung epithelial cells (BEAS-2B) were induced to undergo cell death in response to the Fas agonist antibody CH11 with and without manipulation of endogenous RIP2 concentrations. We show that CH11 increases lung epithelial cell death in a dose-dependent manner as determined by LDH release and nuclear condensation. Fas-induced LDH release was inhibited by RIP2 knock-down. Reduced levels of RIP2 in BEAS-2B cells after treatment with RIP2 siRNA were confirmed by immunoblot. Overexpression of RIP2 in BEAS-2B cells synergized with Fas ligand-induced LDH release in a dose-dependent manner. Finally, mutation of the tyrosine phosphorylation site in CARD of RIP2 protected BEAS-2B cells from Fas ligand induced cell death. Thus RIP2's CARD tyrosine phosphorylation may represent a new therapeutic target to promote the survival of human lung epithelial cells in disorders that lead to acute lung injury and ARDS.
MeSH term(s)	Alveolar Epithelial Cells/metabolism ; Apoptosis ; Cell Death ; Cell Line ; Cell Nucleus/metabolism ; Cell Survival ; Fas Ligand Protein/metabolism ; Gene Expression ; Gene Knockdown Techniques ; Humans ; Lactate Dehydrogenases/biosynthesis ; Mutation ; Phosphorylation ; Protein Stability ; Receptor-Interacting Protein Serine-Threonine Kinase 2/genetics ; Receptor-Interacting Protein Serine-Threonine Kinase 2/metabolism ; Respiratory Mucosa/metabolism ; fas Receptor/metabolism
Chemical Substances	Fas Ligand Protein ; fas Receptor ; Lactate Dehydrogenases (EC 1.1.-) ; RIPK2 protein, human (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinase 2 (EC 2.7.11.1)
Language	English
Publishing date	2014-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0092731
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Article ; Online: Novel ADA2 mutation presenting with neutropenia, lymphopenia and bone marrow failure in patients with deficiency in adenosine deaminase 2 (DADA2).

Ghurye, Rohit R / Sundaram, Kruthika / Smith, Frances / Clark, Barnaby / Simpson, Michael A / Fairbanks, Lynette / Adhya, Zoe / Mufti, Ghulam J / Marsh, Judith C W / Ibrahim, Mohammad A A

British journal of haematology

2019 Volume 186, Issue 3, Page(s) e60–e64

MeSH term(s)	Adenosine Deaminase/blood ; Adenosine Deaminase/deficiency ; Adenosine Deaminase/genetics ; Adult ; Amino Acid Sequence ; Bone Marrow Failure Disorders/blood ; Bone Marrow Failure Disorders/enzymology ; Bone Marrow Failure Disorders/genetics ; Bone Marrow Failure Disorders/pathology ; Female ; Humans ; Intercellular Signaling Peptides and Proteins/blood ; Intercellular Signaling Peptides and Proteins/deficiency ; Intercellular Signaling Peptides and Proteins/genetics ; Lymphopenia/blood ; Lymphopenia/enzymology ; Lymphopenia/genetics ; Middle Aged ; Mutation ; Neutropenia/blood ; Neutropenia/enzymology ; Neutropenia/genetics ; Pedigree
Chemical Substances	Intercellular Signaling Peptides and Proteins ; ADA2 protein, human (EC 3.5.4.4) ; Adenosine Deaminase (EC 3.5.4.4)
Language	English
Publishing date	2019-03-28
Publishing country	England
Document type	Case Reports ; Letter
ZDB-ID	80077-6
ISSN	1365-2141 ; 0007-1048
ISSN (online)	1365-2141
ISSN	0007-1048
DOI	10.1111/bjh.15896
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Article ; Online: IκBζ Regulates Human Monocyte Pro-Inflammatory Responses Induced by Streptococcus pneumoniae.

Sundaram, Kruthika / Rahman, Mohd Akhlakur / Mitra, Srabani / Knoell, Daren L / Woodiga, Shireen A / King, Samantha J / Wewers, Mark D

PloS one

2016 Volume 11, Issue 9, Page(s) e0161931

Abstract: Pneumococcal lung infections represent a major cause of death worldwide. Single nucleotide polymorphisms (SNPs) in the NFKBIZ gene, encoding the transcription factor IκBζ, are associated with increased susceptibility to invasive pneumococcal disease. We ... ...

Abstract	Pneumococcal lung infections represent a major cause of death worldwide. Single nucleotide polymorphisms (SNPs) in the NFKBIZ gene, encoding the transcription factor IκBζ, are associated with increased susceptibility to invasive pneumococcal disease. We hence analyzed how IκBζ might regulate inflammatory responses to pneumococcal infection. We first demonstrate that IκBζ is expressed in human blood monocytes but not in bronchial epithelial cells, in response to wild type pneumococcal strain D39. D39 transiently induced IκBζ in a dose dependent manner, with subsequent induction of downstream molecules involved in host defense. Of these molecules, IκBζ knockdown reduced the expression of IL-6 and GMCSF. Furthermore, IκBζ overexpression increased the activity of IL-6 and GMCSF promoters, supporting the knockdown findings. Pneumococci lacking either pneumolysin or capsule still induced IκBζ. While inhibition of TLR1/TLR2 blocked D39 induced IκBζ expression, TLR4 inhibition did not. Blockade of p38 MAP kinase and NFκB suppressed D39 induced IκBζ. Overall, our data demonstrates that IκBζ regulates monocyte inflammatory responses to Streptococcus pneumoniae by promoting the production of IL-6 and GMCSF.
MeSH term(s)	Adaptor Proteins, Signal Transducing ; Benzocycloheptenes/pharmacology ; Bronchi/drug effects ; Bronchi/immunology ; Bronchi/microbiology ; Epithelial Cells/drug effects ; Epithelial Cells/immunology ; Epithelial Cells/microbiology ; Gene Expression Regulation ; Granulocyte-Macrophage Colony-Stimulating Factor/genetics ; Granulocyte-Macrophage Colony-Stimulating Factor/immunology ; Host-Pathogen Interactions ; Humans ; I-kappa B Proteins/antagonists & inhibitors ; I-kappa B Proteins/genetics ; I-kappa B Proteins/immunology ; Interleukin-6/genetics ; Interleukin-6/immunology ; Lipopolysaccharides/pharmacology ; Monocytes/drug effects ; Monocytes/immunology ; Monocytes/microbiology ; NF-kappa B/genetics ; NF-kappa B/immunology ; Nuclear Proteins/antagonists & inhibitors ; Nuclear Proteins/genetics ; Nuclear Proteins/immunology ; Primary Cell Culture ; RNA, Small Interfering/genetics ; RNA, Small Interfering/immunology ; Signal Transduction ; Streptococcus pneumoniae/drug effects ; Streptococcus pneumoniae/physiology ; Toll-Like Receptor 1/antagonists & inhibitors ; Toll-Like Receptor 1/genetics ; Toll-Like Receptor 1/immunology ; Toll-Like Receptor 2/antagonists & inhibitors ; Toll-Like Receptor 2/genetics ; Toll-Like Receptor 2/immunology ; Toll-Like Receptor 4/antagonists & inhibitors ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/immunology ; p38 Mitogen-Activated Protein Kinases/genetics ; p38 Mitogen-Activated Protein Kinases/immunology
Chemical Substances	Adaptor Proteins, Signal Transducing ; Benzocycloheptenes ; I-kappa B Proteins ; IL6 protein, human ; Interleukin-6 ; Lipopolysaccharides ; NF-kappa B ; NFKBIZ protein, human ; Nuclear Proteins ; RNA, Small Interfering ; TLR2 protein, human ; TLR4 protein, human ; Toll-Like Receptor 1 ; Toll-Like Receptor 2 ; Toll-Like Receptor 4 ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2016-09-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0161931
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Article ; Online: Oxidatively modified low density lipoprotein (LDL) inhibits TLR2 and TLR4 cytokine responses in human monocytes but not in macrophages.

Kannan, Yashaswini / Sundaram, Kruthika / Aluganti Narasimhulu, Chandrakala / Parthasarathy, Sampath / Wewers, Mark D

The Journal of biological chemistry

2012 Volume 287, Issue 28, Page(s) 23479–23488

Abstract: Inflammation characterized by the expression and release of cytokines and chemokines is implicated in the development and progression of atherosclerosis. Oxidatively modified low density lipoproteins, central to the formation of atherosclerotic plaques, ... ...

Abstract	Inflammation characterized by the expression and release of cytokines and chemokines is implicated in the development and progression of atherosclerosis. Oxidatively modified low density lipoproteins, central to the formation of atherosclerotic plaques, have been reported to signal through Toll-like receptors (TLRs), TLR4 and TLR2, in concert with scavenger receptors to regulate the inflammatory microenvironment in atherosclerosis. This study evaluates the role of low density lipoproteins (LDL) and oxidatively modified LDL (oxmLDL) in the expression and release of proinflammatory mediators IκBζ, IL-6, IL-1β, TNFα, and IL-8 in human monocytes and macrophages. Although standard LDL preparations induced IκBζ along with IL-6 and IL-8 production, this inflammatory effect was eliminated when LDL was isolated under endotoxin-restricted conditions. However, when added with TLR4 and TLR2 ligands, this low endotoxin preparation of oxmLDL suppressed the expression and release of IL-1β, IL-6, and TNFα but surprisingly spared IL-8 production. The suppressive effect of oxmLDL was specific to monocytes as it did not inhibit LPS-induced proinflammatory cytokines in human macrophages. Thus, TLR ligand contamination of LDL/oxmLDL preparations can complicate interpretations of inflammatory responses to these modified lipoproteins. In contrast to providing a proinflammatory function, oxmLDL suppresses the expression and release of selected proinflammatory mediators.
MeSH term(s)	Adaptor Proteins, Signal Transducing ; CD36 Antigens/metabolism ; Cells, Cultured ; Cytokines/genetics ; Cytokines/metabolism ; Dose-Response Relationship, Drug ; Flow Cytometry ; Gene Expression/drug effects ; Humans ; I-kappa B Proteins ; Immunoblotting ; Interleukin-1beta/genetics ; Interleukin-1beta/metabolism ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Lipopeptides/pharmacology ; Lipopolysaccharides/pharmacology ; Lipoproteins, LDL/pharmacology ; Macrophages/cytology ; Macrophages/drug effects ; Macrophages/metabolism ; Monocytes/cytology ; Monocytes/drug effects ; Monocytes/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/drug effects ; Time Factors ; Toll-Like Receptor 2/metabolism ; Toll-Like Receptor 4/metabolism ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; CD36 Antigens ; Cytokines ; I-kappa B Proteins ; Interleukin-1beta ; Interleukin-6 ; Lipopeptides ; Lipopolysaccharides ; Lipoproteins, LDL ; NFKBIZ protein, human ; Nuclear Proteins ; Pam(3)CSK(4) peptide ; Toll-Like Receptor 2 ; Toll-Like Receptor 4 ; Tumor Necrosis Factor-alpha ; oxidized low density lipoprotein
Language	English
Publishing date	2012-05-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M111.320960
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