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Article ; Online: Development of an Enzyme-Linked Immunosorbent Assay for the Detection of GM Proteins in Transgenic Crops/Produce.

Kamle, Suchitra / Li, Dawei / Ojha, Abhishek / Kumar, Arvind

Methods in molecular biology (Clifton, N.J.)

2018 Volume 1902, Page(s) 159–166

Abstract: Enzyme-linked immunosorbent assays are always being used extensively for the identification of genetically modified protein in transgenic crops/produce. With the advancement in the detection strategies, competitive and sandwich immunoassays are more ... ...

Abstract	Enzyme-linked immunosorbent assays are always being used extensively for the identification of genetically modified protein in transgenic crops/produce. With the advancement in the detection strategies, competitive and sandwich immunoassays are more convenient and sensitive for the GM protein detection and its quantification in transgenic crops. This chapter is focusing on the competitive ELISA including sandwich ELISA for the detection of the GM proteins.
MeSH term(s)	Antibodies ; Antigens/immunology ; Crops, Agricultural ; Enzyme-Linked Immunosorbent Assay/methods ; Gene Expression ; Plant Leaves/metabolism ; Plant Proteins/genetics ; Plant Proteins/isolation & purification ; Plants, Genetically Modified ; Seeds/metabolism
Chemical Substances	Antibodies ; Antigens ; Plant Proteins
Language	English
Publishing date	2018-12-12
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-8952-2_12
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Article: Targeting Chitinase 1 and Chitinase 3-Like 1 as Novel Therapeutic Strategy of Pulmonary Fibrosis.

Lee, Suh-Young / Lee, Chang-Min / Ma, Bing / Kamle, Suchitra / Elias, Jack A / Zhou, Yang / Lee, Chun Geun

Frontiers in pharmacology

2022 Volume 13, Page(s) 826471

Abstract: Chitinase 1 (CHIT1) and chitinase 3-like-1 (CHI3L1), two representative members of 18-Glycosyl hydrolases family, are significantly implicated in the pathogenesis of various human diseases characterized by inflammation and remodeling. Notably, ... ...

Abstract	Chitinase 1 (CHIT1) and chitinase 3-like-1 (CHI3L1), two representative members of 18-Glycosyl hydrolases family, are significantly implicated in the pathogenesis of various human diseases characterized by inflammation and remodeling. Notably, dysregulated expression of CHIT1 and CHI3L1 was noted in the patients with pulmonary fibrosis and their levels were inversely correlated with clinical outcome of the patients. CHIT1 and CHI3L1, mainly expressed in alveolar macrophages, regulate profibrotic macrophage activation, fibroblast proliferation and myofibroblast transformation, and TGF-β signaling and effector function. Although the mechanism or the pathways that CHIT1 and CHI3L1 use to regulate pulmonary fibrosis have not been fully understood yet, these studies identify CHIT1 and CHI3L1 as significant modulators of fibroproliferative responses leading to persistent and progressive pulmonary fibrosis. These studies suggest a possibility that CHIT1 and CHI3L1 could be reasonable therapeutic targets to intervene or reverse established pulmonary fibrosis. In this review, we will discuss specific roles and regulatory mechanisms of CHIT1 and CHI3L1 in profibrotic cell and tissue responses as novel therapeutic targets of pulmonary fibrosis.
Language	English
Publishing date	2022-03-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2022.826471
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Article ; Online: CHI3L1 enhances melanoma lung metastasis

Ma, Bing / Kamle, Suchitra / Akosman, Bedia / Khan, Hina / Lee, Chang-Min / Lee, Chun Geun / Elias, Jack A

Frontiers in immunology

2022 Volume 13, Page(s) 1056397

Abstract: ICOS/ICOSL and CD28/B7-1/B7-2 are T cell co-stimulators and CTLA-4 is an immune checkpoint inhibitor that play critical roles in the pathogenesis of neoplasia. Chitinase 3-like-1 (CHI3L1) is induced in many cancers where it portends a poor prognosis and ... ...

Abstract	ICOS/ICOSL and CD28/B7-1/B7-2 are T cell co-stimulators and CTLA-4 is an immune checkpoint inhibitor that play critical roles in the pathogenesis of neoplasia. Chitinase 3-like-1 (CHI3L1) is induced in many cancers where it portends a poor prognosis and contributes to tumor metastasis. Here we demonstrate that CHI3L1 inhibits the expression of ICOS, ICOSL and CD28 while stimulating CTLA-4 and the B7 moieties in melanoma lung metastasis. We also demonstrate that RIG-like helicase innate immune activation augments T cell co-stimulation, inhibits CTLA-4 and suppresses pulmonary metastasis. At least additive antitumor responses were seen in melanoma lung metastasis treated with anti-CTLA-4 and anti-CHI3L1 antibodies in combination. Synergistic cytotoxic T cell-induced tumor cell death and the heightened induction of the tumor suppressor PTEN were seen in co-cultures of T and tumor cells treated with bispecific antibodies that target both CHI3L1 and CTLA-4. Thus, CHI3L1 contributes to pulmonary metastasis by inhibiting T cell co-stimulation and stimulating CTLA-4. The simultaneous targeting of CHI3L1 and the CTLA-4 axis with individual and, more powerfully with bispecific antibodies, represent promising therapeutic strategies for pulmonary metastasis.
MeSH term(s)	Humans ; CD28 Antigens ; Antigens, CD ; Antibodies, Bispecific ; Melanoma/metabolism ; Lung Neoplasms ; Chitinase-3-Like Protein 1
Chemical Substances	CD28 Antigens ; Antigens, CD ; Antibodies, Bispecific ; CHI3L1 protein, human ; Chitinase-3-Like Protein 1
Language	English
Publishing date	2022-12-21
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1056397
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Article ; Online: Host chitinase 3-like-1 is a universal therapeutic target for SARS-CoV-2 viral variants in COVID-19.

Kamle, Suchitra / Ma, Bing / Lee, Chang Min / Schor, Gail / Zhou, Yang / Lee, Chun Geun / Elias, Jack A

eLife

2022 Volume 11

Abstract: Coronavirus disease 2019 (COVID-19) is the disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2; SC2), which has caused a worldwide pandemic with striking morbidity and mortality. Evaluation of SC2 strains demonstrated impressive ...

Abstract	Coronavirus disease 2019 (COVID-19) is the disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2; SC2), which has caused a worldwide pandemic with striking morbidity and mortality. Evaluation of SC2 strains demonstrated impressive genetic variability, and many of these viral variants are now defined as variants of concern (VOC) that cause enhanced transmissibility, decreased susceptibility to antibody neutralization or therapeutics, and/or the ability to induce severe disease. Currently, the delta (δ) and omicron (ο) variants are particularly problematic based on their impressive and unprecedented transmissibility and ability to cause breakthrough infections. The delta variant also accumulates at high concentrations in host tissues and has caused waves of lethal disease. Because studies from our laboratory have demonstrated that chitinase 3-like-1 (CHI3L1) stimulates ACE2 and Spike (S) priming proteases that mediate SC2 infection, studies were undertaken to determine if interventions that target CHI3L1 are effective inhibitors of SC2 viral variant infection. Here, we demonstrate that CHI3L1 augments epithelial cell infection by pseudoviruses that express the alpha, beta, gamma, delta, or omicron S proteins and that the CHI3L1 inhibitors anti-CHI3L1 and kasugamycin inhibit epithelial cell infection by these VOC pseudovirus moieties. Thus, CHI3L1 is a universal, VOC-independent therapeutic target in COVID-19.
MeSH term(s)	Angiotensin-Converting Enzyme 2 ; COVID-19/drug therapy ; Chitinases/genetics ; Humans ; Peptidyl-Dipeptidase A/metabolism ; SARS-CoV-2/genetics ; Virus Internalization
Chemical Substances	Chitinases (EC 3.2.1.14) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2022-06-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.78273
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Article: Host Chitinase 3-like-1 is a Universal Therapeutic Target for SARS-CoV-2 Viral Variants in COVID 19.

Kamle, Suchitra / Ma, Bing / Lee, Chang Min / Schor, Gail / Zhou, Yang / Lee, Chun Geun / Elias, Jack A

bioRxiv : the preprint server for biology

2022

Abstract: COVID 19 is the disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2; SC2) which has caused a world-wide pandemic with striking morbidity and mortality. Evaluation of SC2 strains demonstrated impressive genetic variability and ... ...

Abstract	COVID 19 is the disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2; SC2) which has caused a world-wide pandemic with striking morbidity and mortality. Evaluation of SC2 strains demonstrated impressive genetic variability and many of these viral variants are now defined as variants of concern (VOC) that cause enhanced transmissibility, decreased susceptibility to antibody neutralization or therapeutics and or the ability to induce severe disease. Currently, the delta (δ) and omicron (o) variants are particularly problematic based on their impressive and unprecedented transmissibility and ability to cause break through infections. The delta variant also accumulates at high concentrations in host tissues and has caused waves of lethal disease. Because studies from our laboratory have demonstrated that chitinase 3-like-1 (CHI3L1) stimulates ACE2 and Spike (S) priming proteases that mediate SC2 infection, studies were undertaken to determine if interventions that target CHI3L1 are effective inhibitors of SC2 viral variant infection. Here we demonstrate that CHI3L1 augments epithelial cell infection by pseudoviruses that express the alpha, beta, gamma, delta or omicron S proteins and that the CHI3L1 inhibitors anti-CHI3L1 and kasugamycin inhibit epithelial cell infection by these VOC pseudovirus moieties. Thus, CHI3L1 is a universal, VOC-independent therapeutic target in COVID 19.
Language	English
Publishing date	2022-02-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2022.01.21.477274
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Article ; Online: Chi3l1 Is a Modulator of Glioma Stem Cell States and a Therapeutic Target in Glioblastoma.

Guetta-Terrier, Charlotte / Karambizi, David / Akosman, Bedia / Zepecki, John P / Chen, Jia-Shu / Kamle, Suchitra / Fajardo, J Eduardo / Fiser, Andras / Singh, Ritambhara / Toms, Steven A / Lee, Chun Geun / Elias, Jack A / Tapinos, Nikos

Cancer research

2023 Volume 83, Issue 12, Page(s) 1984–1999

Abstract: Chitinase 3-like 1 (Chi3l1) is a secreted protein that is highly expressed in glioblastoma. Here, we show that Chi3l1 alters the state of glioma stem cells (GSC) to support tumor growth. Exposure of patient-derived GSCs to Chi3l1 reduced the frequency of ...

Abstract	Chitinase 3-like 1 (Chi3l1) is a secreted protein that is highly expressed in glioblastoma. Here, we show that Chi3l1 alters the state of glioma stem cells (GSC) to support tumor growth. Exposure of patient-derived GSCs to Chi3l1 reduced the frequency of CD133+SOX2+ cells and increased the CD44+Chi3l1+ cells. Chi3l1 bound to CD44 and induced phosphorylation and nuclear translocation of β-catenin, Akt, and STAT3. Single-cell RNA sequencing and RNA velocity following incubation of GSCs with Chi3l1 showed significant changes in GSC state dynamics driving GSCs towards a mesenchymal expression profile and reducing transition probabilities towards terminal cellular states. ATAC-seq revealed that Chi3l1 increases accessibility of promoters containing a Myc-associated zinc finger protein (MAZ) transcription factor footprint. Inhibition of MAZ downregulated a set of genes with high expression in cellular clusters that exhibit significant cell state transitions after treatment with Chi3l1, and MAZ deficiency rescued the Chi3L-induced increase of GSC self-renewal. Finally, targeting Chi3l1 in vivo with a blocking antibody inhibited tumor growth and increased the probability of survival. Overall, this work suggests that Chi3l1 interacts with CD44 on the surface of GSCs to induce Akt/β-catenin signaling and MAZ transcriptional activity, which in turn upregulates CD44 expression in a pro-mesenchymal feed-forward loop. The role of Chi3l1 in regulating cellular plasticity confers a targetable vulnerability to glioblastoma. Significance: Chi3l1 is a modulator of glioma stem cell states that can be targeted to promote differentiation and suppress growth of glioblastoma.
MeSH term(s)	Humans ; Glioblastoma/pathology ; beta Catenin/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Neoplastic Stem Cells/pathology ; Glioma/metabolism ; Brain Neoplasms/pathology ; Cell Line, Tumor ; Cell Proliferation
Chemical Substances	beta Catenin ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2023-04-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-21-3629
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Article ; Online: The tumor-derived cytokine Chi3l1 induces neutrophil extracellular traps that promote T cell exclusion in triple-negative breast cancer.

Taifour, Tarek / Attalla, Sherif Samer / Zuo, Dongmei / Gu, Yu / Sanguin-Gendreau, Virginie / Proud, Hailey / Solymoss, Emilie / Bui, Tung / Kuasne, Hellen / Papavasiliou, Vasilios / Lee, Chun Geun / Kamle, Suchitra / Siegel, Peter M / Elias, Jack A / Park, Morag / Muller, William J

Immunity

2023 Volume 56, Issue 12, Page(s) 2755–2772.e8

Abstract: In triple-negative breast cancer (TNBC), stromal restriction of ... ...

Abstract	In triple-negative breast cancer (TNBC), stromal restriction of CD8
MeSH term(s)	Animals ; Humans ; Mice ; CD8-Positive T-Lymphocytes ; Cell Line, Tumor ; Cytokines ; Extracellular Traps/metabolism ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology ; Tumor Microenvironment
Chemical Substances	Cytokines ; CHI3L1 protein, human ; Chil1 protein, mouse
Language	English
Publishing date	2023-11-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2023.11.002
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Article ; Online: Host Chitinase 3-like-1 is a Universal Therapeutic Target for the Delta, Omicron and Other SARS-CoV-2 Viral Variants in COVID 19

Kamle, Suchitra / Ma, Bing / Lee, Chang Min / Schor, Gail / Lee, Chun Geun / Elias, Jack A.

bioRxiv

Abstract: COVID 19 is the disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2; SC2) which has caused a world-wide pandemic with striking morbidity and mortality. Evaluation of early SC2 strains suggested limited viral genetic diversity. ... ...

Abstract	COVID 19 is the disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2; SC2) which has caused a world-wide pandemic with striking morbidity and mortality. Evaluation of early SC2 strains suggested limited viral genetic diversity. However, genetic and epidemiologic investigations in the interim have revealed impressive genetic variability. Many of these viral variants are now defined as variants of concern (VOC) based on genetic alterations in their spike (S) and other proteins that cause enhanced transmissibility, decreased susceptibility to antibody neutralization or therapeutics and or their ability to induce severe disease. The delta δ and omicron (o) variants are particularly problematic based on their impressive and unprecedented transmissibility and ability to cause break through infections. The delta variant also accumulates at high concentrations in host tissues and has caused waves of lethal disease. SC2 infection is mediated by S protein binding to cellular ACE2 receptors and subsequent S protein protease processing. Because studies from our laboratory have demonstrated that chitinase 3-like-1 (CHI3L1) stimulates ACE2 and S priming proteases, studies were undertaken to determine if interventions that target CHI3L1 are effective inhibitors of SC2 viral variant infection. Here we demonstrate that CHI3L1 augments epithelial cell infection by pseudoviruses that express the alpha, beta, gamma, delta or omicron S proteins and that the CHI3L1 inhibitors anti-CHI3L1 and kasugamycin inhibit epithelial cell infection by these VOC pseudovirus moieties. Thus, CHI3L1 is a universal, VOC-independent therapeutic target in COVID 19.
Keywords	covid19
Language	English
Publishing date	2022-01-24
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2022.01.21.477274
Database	COVID19

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Article ; Online: Correction: Chitinase 1 regulates pulmonary fibrosis by modulating TGF-β/SMAD7 pathway via TGFBRAP1 and FOXO3.

Lee, Chang-Min / He, Chuan-Hua / Park, Jin Wook / Lee, Jae Hyun / Kamle, Suchitra / Ma, Bing / Akosman, Bedia / Cotez, Roberto / Chen, Emily / Zhou, Yang / Herzog, Erica L / Ryu, Changwan / Peng, Xueyan / Rosas, Ivan O / Poli, Sergio / Bostwick, Carol Feghali / Choi, Augustine M / Elias, Jack A / Lee, Chun Geun

Life science alliance

2023 Volume 6, Issue 5

Language	English
Publishing date	2023-04-10
Publishing country	United States
Document type	Journal Article ; Published Erratum
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202302065
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Article ; Online: CHI3L1 regulates PD-L1 and anti-CHI3L1-PD-1 antibody elicits synergistic antitumor responses.

Ma, Bing / Akosman, Bedia / Kamle, Suchitra / Lee, Chang-Min / He, Chuan Hua / Koo, Ja Seok / Lee, Chun Geun / Elias, Jack A

The Journal of clinical investigation

2021 Volume 131, Issue 21

Abstract: Evasion of the immune response is a hallmark of cancer, and programmed cell death 1 (PD-1) and PD-1 ligand 1 (PD-L1) are major mediators of this immunosuppression. Chitinase 3-like 1 (CHI3L1) is induced in many cancers, where it portends a poor prognosis ...

Abstract	Evasion of the immune response is a hallmark of cancer, and programmed cell death 1 (PD-1) and PD-1 ligand 1 (PD-L1) are major mediators of this immunosuppression. Chitinase 3-like 1 (CHI3L1) is induced in many cancers, where it portends a poor prognosis and contributes to tumor metastasis and spread. However, the mechanism(s) that CHI3L1 uses in metastasis have not been defined. Here we demonstrate that CHI3L1 regulates the expression of PD-L1, PD-L2, PD-1, LAG3, and TIM3 and plays a critical role in melanoma progression and lymphatic spread. CHI3L1 also contributed to IFN-γ-stimulated macrophage PD-L1 expression, and RIG-like helicase innate immunity suppressed CHI3L1, PD-L1, and melanoma progression. Individual antibodies against CHI3L1 or PD-1 had discrete antitumor effects and additive antitumor responses in metastasis models and T cell-tumor cell cocultures when administered simultaneously. Synergistic cytotoxic tumor cell death was seen in T cell-tumor cell cocultures, and significantly enhanced antitumor responses were seen in in vivo tumor models treated with bispecific antibodies that simultaneously target CHI3L1 and PD-1. CHI3L1 contributes to tumor progression by stimulating the PD-1/PD-L1 axis and other checkpoint molecules. The simultaneous targeting of CHI3L1 and the PD-1/PD-L1 axis with individual and, more powerfully, with bispecific antibodies represents a promising therapy for pulmonary metastasis and progression.
MeSH term(s)	Animals ; Antibodies, Bispecific/immunology ; Antibodies, Bispecific/pharmacology ; Antibodies, Neoplasm/immunology ; Antibodies, Neoplasm/pharmacology ; B7-H1 Antigen/antagonists & inhibitors ; B7-H1 Antigen/immunology ; Chitinase-3-Like Protein 1/antagonists & inhibitors ; Chitinase-3-Like Protein 1/immunology ; Lung Neoplasms/immunology ; Lung Neoplasms/pathology ; Lung Neoplasms/prevention & control ; Lung Neoplasms/secondary ; Melanoma, Experimental/drug therapy ; Melanoma, Experimental/immunology ; Melanoma, Experimental/pathology ; Mice ; Mice, Knockout ; Neoplasm Metastasis ; Neoplasm Proteins/antagonists & inhibitors ; Neoplasm Proteins/immunology
Chemical Substances	Antibodies, Bispecific ; Antibodies, Neoplasm ; B7-H1 Antigen ; Cd274 protein, mouse ; Chil1 protein, mouse ; Chitinase-3-Like Protein 1 ; Neoplasm Proteins
Language	English
Publishing date	2021-10-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Video-Audio Media
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI137750
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