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Article ; Online: RIPosomes are targets of IRGM-SQSTM1-dependent autophagy.

Mehto, Subhash / Kundu, Soumya / Chauhan, Swati / Chauhan, Santosh

2023 Volume 19, Issue 3, Page(s) 1045–1047

Abstract: The NOD1-NOD2-RIPK2-NFKB/NF-κB pro-inflammatory axis plays a significant role in regulating the immune response to bacterial infection. However, an excess of NFKB-dependent cytokine response can be detrimental and, thus, should be kept under control to ... ...

Abstract	The NOD1-NOD2-RIPK2-NFKB/NF-κB pro-inflammatory axis plays a significant role in regulating the immune response to bacterial infection. However, an excess of NFKB-dependent cytokine response can be detrimental and, thus, should be kept under control to maintain the innate immune balance. In our recent study, first, we showed that bacterial infection induces the biogenesis of RIPK2 oligomers (RIPosomes) that are recruited around the bacteria to enhance an NFKB-dependent pro-inflammatory response. Next, we showed that SQSTM1- and IRGM-dependent selective macroautophagy/autophagy degrades RIPosomes and their components to limit NOD1-NOD2-RIPK2-NFKB pro-inflammatory signaling. Consistently, depletion of IRGM results in an augmented RIPK2-dependent pro-inflammatory cytokine response induced by
MeSH term(s)	Animals ; Mice ; Autophagy ; Inflammation/metabolism ; NF-kappa B/metabolism ; Nod2 Signaling Adaptor Protein/metabolism ; Sequestosome-1 Protein/metabolism ; Signal Transduction
Chemical Substances	NF-kappa B ; Nod2 Signaling Adaptor Protein ; Sequestosome-1 Protein ; Sqstm1 protein, mouse ; Ifi1 protein, mouse
Language	English
Publishing date	2023-01-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2023.2166724
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Article ; Online: Recent Advances Towards Diagnosis and Therapeutic Fingerprinting for Alzheimer's Disease.

Pradhan, Lilesh Kumar / Sahoo, Pradyumna Kumar / Chauhan, Santosh / Das, Saroj Kumar

Journal of molecular neuroscience : MN

2022 Volume 72, Issue 6, Page(s) 1143–1165

Abstract: Since the report of "a peculiar severe disease process of the cerebral cortex" by Alois Alzheimer in 1906, it was considered to be a rare condition characterized by loss of cognition, memory impairment, and pathological markers such as senile plaques or ... ...

Abstract	Since the report of "a peculiar severe disease process of the cerebral cortex" by Alois Alzheimer in 1906, it was considered to be a rare condition characterized by loss of cognition, memory impairment, and pathological markers such as senile plaques or neurofibrillary tangles (NFTs). Later on, the report was published in the textbook "Psychiatrie" and the disease was named as Alzheimer's disease (AD) and was known to be the consequences of aging; however, owing to its complex etiology, there is no cure for the progressive neurodegenerative disorder. Our current understanding of the mechanisms involved in the pathogenesis of AD is still at the mechanistic level. The treatment strategies applied currently only alleviate the symptoms and co-morbidities. For instance, the available treatments such as the usage of acetylcholinesterase inhibitors and N-methyl D-aspartate antagonists have minimal impact on the disease progression and target the later aspects of the disease. The recent advancements in the last two decades have made us more clearly understand the pathophysiology of the disease which has led to the development of novel therapeutic strategies. This review gives a brief idea about the various facets of AD pathophysiology and its management through modern investigational therapies to give a new direction for development of targeted therapeutic measures.
MeSH term(s)	Acetylcholinesterase ; Alzheimer Disease/diagnosis ; Alzheimer Disease/drug therapy ; Amyloid beta-Peptides ; Humans ; Neurofibrillary Tangles/pathology ; Plaque, Amyloid/therapy ; tau Proteins
Chemical Substances	Amyloid beta-Peptides ; tau Proteins ; Acetylcholinesterase (EC 3.1.1.7)
Language	English
Publishing date	2022-05-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1043392-2
ISSN	1559-1166 ; 0895-8696
ISSN (online)	1559-1166
ISSN	0895-8696
DOI	10.1007/s12031-022-02009-7
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Article: Editorial: The Dynamics of Stress Granules.

Mehto, Subhash / Liu, Beidong / Hu, Ronggui / Chauhan, Santosh

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 789678

Language	English
Publishing date	2021-11-16
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.789678
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Article: An Unusual Case of Symptomatic Isolated Lingual Cysticercosis: Clinical Suspicion Helped Prevent Disseminated Disease.

Chauhan, Anindita / Sharma, Kush / Sharma, Preeti / Sharma, Rishabh / Chauhan, Madan Singh / Chauhan, Santosh / Wadhwan, Vijay

Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India

2023 Volume 76, Issue 2, Page(s) 2127–2130

Abstract: Intraorally, cysticercosis is regarded as uncommon and a diagnostic challenge. Here, we report a diagnostic conundrum of an unusual case of innocuous appearing lesion on the tongue presenting as moderately tender swelling finally diagnosed as lingual ... ...

Abstract	Intraorally, cysticercosis is regarded as uncommon and a diagnostic challenge. Here, we report a diagnostic conundrum of an unusual case of innocuous appearing lesion on the tongue presenting as moderately tender swelling finally diagnosed as lingual cysticercosis, based on USG (Ultrasound), CT (Computed Tomography) findings and characteristic histopathologic features.
Language	English
Publishing date	2023-12-28
Publishing country	India
Document type	Journal Article
ZDB-ID	1471137-0
ISSN	0973-7707 ; 2231-3796 ; 0019-5421
ISSN (online)	0973-7707
ISSN	2231-3796 ; 0019-5421
DOI	10.1007/s12070-023-04449-y
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Article: Innate immunity and inflammophagy: balancing the defence and immune homeostasis

Chauhan, Swati / Jena, Kautilya Kumar / Mehto, Subhash / Chauhan, Nishant Ranjan / Sahu, Rinku / Dhar, Kollori / Yadav, Rina / Krishna, Sivaram / Jaiswal, Pundrik / Chauhan, Santosh

FEBS journal. 2022 July, v. 289, no. 14

2022

Abstract: Extensive crosstalk exists between autophagy and innate immune signalling pathways. The stimuli that induce pattern recognition receptor (PRR)‐mediated innate immune signalling pathways, also upregulate autophagy. The purpose of this increased autophagy ... ...

Abstract	Extensive crosstalk exists between autophagy and innate immune signalling pathways. The stimuli that induce pattern recognition receptor (PRR)‐mediated innate immune signalling pathways, also upregulate autophagy. The purpose of this increased autophagy is to eliminate the stimuli and/or suppress the inflammatory pathways by targeted degradation of PRRs or intermediary proteins (termed ‘inflammophagy’). By executing these functions, autophagy dampens excess inflammation triggered by the innate immune signalling pathways. Thus, autophagy helps in the maintenance of the body's innate immune homeostasis to protect from inflammatory and autoimmune diseases. Many autophagy‐dependent mechanisms that could control innate immune signalling have been studied over the last few years. However, still, the understanding is incomplete, and studies that are more systematic should be undertaken to delineate the mechanisms of inflammophagy. Here, we discuss the available knowledge of crosstalk between autophagy and PRR signalling pathways.
Keywords	autophagy ; homeostasis ; inflammation ; innate immunity
Language	English
Dates of publication	2022-07
Size	p. 4112-4131.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	REVIEW
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16298
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Article ; Online: Unravelling the potential of gut microbiota in sustaining brain health and their current prospective towards development of neurotherapeutics.

Banerjee, Ankita / Pradhan, Lilesh Kumar / Sahoo, Pradyumna Kumar / Jena, Kautilya Kumar / Chauhan, Nishant Ranjan / Chauhan, Santosh / Das, Saroj Kumar

Archives of microbiology

2021 Volume 203, Issue 6, Page(s) 2895–2910

Abstract: Increasing incidences of neurological disorders, such as Parkinson's disease (PD), multiple sclerosis (MS), Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS) are being reported, but an insight into their pathology remains elusive. Findings ...

Abstract	Increasing incidences of neurological disorders, such as Parkinson's disease (PD), multiple sclerosis (MS), Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS) are being reported, but an insight into their pathology remains elusive. Findings have suggested that gut microbiota play a major role in regulating brain functions through the gut-brain axis. A unique bidirectional communication between gut microbiota and maintenance of brain health could play a pivotal role in regulating incidences of neurodegenerative diseases. Contrarily, the present life style with changing food habits and disturbed circadian rhythm may contribute to gut homeostatic imbalance and dysbiosis leading to progression of several neurological disorders. Therefore, dysbiosis, as a primary factor behind intestinal disorders, may also augment inflammation, intestinal and blood-brain barrier permeability through microbiota-gut-brain axis. This review primarily focuses on the gut-brain axis functions, specific gut microbial population, metabolites produced by gut microbiota, their role in regulating various metabolic processes and role of gut microbiota towards development of neurodegenerative diseases. However, several studies have reported a decrease in abundance of a specific gut microbial population and a corresponding increase in other microbial family, with few findings revealing some contradictions. Reports also showed that colonization of gut microbiota isolated from patients suffering from neurodegenerative disease leads to the development of enhance pathological outcomes in animal models. Hence, a systematic understanding of the dominant role of specific gut microbiome towards development of different neurodegenerative diseases could possibly provide novel insight into the use of probiotics and microbial transplantation as a substitute approach for treating/preventing such health maladies.
MeSH term(s)	Animals ; Brain/physiology ; Gastrointestinal Microbiome/physiology ; Humans ; Neurodegenerative Diseases/etiology
Language	English
Publishing date	2021-03-24
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	124824-8
ISSN	1432-072X ; 0302-8933
ISSN (online)	1432-072X
ISSN	0302-8933
DOI	10.1007/s00203-021-02276-9
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Article: Unravelling the potential of gut microbiota in sustaining brain health and their current prospective towards development of neurotherapeutics

Banerjee, Ankita / Pradhan, Lilesh Kumar / Sahoo, Pradyumna Kumar / Jena, Kautilya Kumar / Chauhan, Nishant Ranjan / Chauhan, Santosh / Das, Saroj Kumar

Archives of microbiology. 2021 Aug., v. 203, no. 6

2021

Abstract: Increasing incidences of neurological disorders, such as Parkinson’s disease (PD), multiple sclerosis (MS), Alzheimer’s disease (AD) and amyotrophic lateral sclerosis (ALS) are being reported, but an insight into their pathology remains elusive. Findings ...

Abstract	Increasing incidences of neurological disorders, such as Parkinson’s disease (PD), multiple sclerosis (MS), Alzheimer’s disease (AD) and amyotrophic lateral sclerosis (ALS) are being reported, but an insight into their pathology remains elusive. Findings have suggested that gut microbiota play a major role in regulating brain functions through the gut–brain axis. A unique bidirectional communication between gut microbiota and maintenance of brain health could play a pivotal role in regulating incidences of neurodegenerative diseases. Contrarily, the present life style with changing food habits and disturbed circadian rhythm may contribute to gut homeostatic imbalance and dysbiosis leading to progression of several neurological disorders. Therefore, dysbiosis, as a primary factor behind intestinal disorders, may also augment inflammation, intestinal and blood–brain barrier permeability through microbiota–gut–brain axis. This review primarily focuses on the gut–brain axis functions, specific gut microbial population, metabolites produced by gut microbiota, their role in regulating various metabolic processes and role of gut microbiota towards development of neurodegenerative diseases. However, several studies have reported a decrease in abundance of a specific gut microbial population and a corresponding increase in other microbial family, with few findings revealing some contradictions. Reports also showed that colonization of gut microbiota isolated from patients suffering from neurodegenerative disease leads to the development of enhance pathological outcomes in animal models. Hence, a systematic understanding of the dominant role of specific gut microbiome towards development of different neurodegenerative diseases could possibly provide novel insight into the use of probiotics and microbial transplantation as a substitute approach for treating/preventing such health maladies.
Keywords	amyotrophic lateral sclerosis ; animals ; blood-brain barrier ; brain ; circadian rhythm ; dysbiosis ; inflammation ; intestinal microorganisms ; intestines ; lifestyle ; metabolites ; permeability ; probiotics ; sclerosis
Language	English
Dates of publication	2021-08
Size	p. 2895-2910.
Publishing place	Springer Berlin Heidelberg
Document type	Article
ZDB-ID	124824-8
ISSN	1432-072X ; 0302-8933
ISSN (online)	1432-072X
ISSN	0302-8933
DOI	10.1007/s00203-021-02276-9
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Article ; Online: SMARCD1 negatively regulates myeloid differentiation of leukemic cells via epigenetic mechanisms.

Saha, Subha / Samal, Priyanka / Madhulika, Swati / Murmu, Krushna Chandra / Chakraborty, Sohini / Basu, Jhinuk / Barik, Subhabrata / Jena, Kautilya Kumar / Das, Asima / Chauhan, Santosh / Prasad, Punit

Blood advances

2022 Volume 6, Issue 10, Page(s) 3106–3113

MeSH term(s)	Epigenesis, Genetic ; Hematopoiesis
Language	English
Publishing date	2022-01-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2021006235
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Article ; Online: IRGM governs the core autophagy machinery to conduct antimicrobial defense.

Chauhan, Santosh / Mandell, Michael A / Deretic, Vojo

Molecular cell

2015 Volume 58, Issue 3, Page(s) 507–521

Abstract: IRGM, encoded by a uniquely human gene conferring risk for inflammatory diseases, affects autophagy through an unknown mechanism. Here, we show how IRGM controls autophagy. IRGM interacts with ULK1 and Beclin 1 and promotes their co-assembly thus ... ...

Abstract	IRGM, encoded by a uniquely human gene conferring risk for inflammatory diseases, affects autophagy through an unknown mechanism. Here, we show how IRGM controls autophagy. IRGM interacts with ULK1 and Beclin 1 and promotes their co-assembly thus governing the formation of autophagy initiation complexes. We further show that IRGM interacts with pattern recognition receptors including NOD2. IRGM, NOD2, and ATG16L1, all of which are Crohn's disease risk factors, form a molecular complex to modulate autophagic responses to microbial products. NOD2 enhances K63-linked polyubiquitination of IRGM, which is required for interactions of IRGM with the core autophagy factors and for microbial clearance. Thus, IRGM plays a direct role in organizing the core autophagy machinery to endow it with antimicrobial and anti-inflammatory functions.
MeSH term(s)	Anti-Infective Agents/metabolism ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Autophagy ; Autophagy-Related Protein-1 Homolog ; Autophagy-Related Proteins ; Beclin-1 ; Blotting, Western ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cell Line, Tumor ; Crohn Disease/genetics ; Crohn Disease/metabolism ; GTP-Binding Proteins/genetics ; GTP-Binding Proteins/metabolism ; Gene Expression ; HCT116 Cells ; HEK293 Cells ; HT29 Cells ; HeLa Cells ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Microscopy, Confocal ; Nod2 Signaling Adaptor Protein/genetics ; Nod2 Signaling Adaptor Protein/metabolism ; Protein Binding ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; RNA Interference ; Receptors, Pattern Recognition/genetics ; Receptors, Pattern Recognition/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; U937 Cells ; Ubiquitination
Chemical Substances	ATG16L1 protein, human ; Anti-Infective Agents ; Apoptosis Regulatory Proteins ; Autophagy-Related Proteins ; BECN1 protein, human ; Beclin-1 ; Carrier Proteins ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; NOD2 protein, human ; Nod2 Signaling Adaptor Protein ; Receptors, Pattern Recognition ; Autophagy-Related Protein-1 Homolog (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; ULK1 protein, human (EC 2.7.11.1) ; GTP-Binding Proteins (EC 3.6.1.-) ; IRGM protein, human (EC 3.6.1.-)
Language	English
Publishing date	2015-04-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2015.03.020
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Article ; Online: Mechanism of action of the tuberculosis and Crohn disease risk factor IRGM in autophagy.

Chauhan, Santosh / Mandell, Michael A / Deretic, Vojo

Autophagy

2015 Volume 12, Issue 2, Page(s) 429–431

Abstract: Polymorphisms in the IRGM gene, associated with Crohn disease (CD) and tuberculosis, are among the earliest identified examples documenting the role of autophagy in human disease. Functional studies have shown that IRGM protects against these diseases by ...

Abstract	Polymorphisms in the IRGM gene, associated with Crohn disease (CD) and tuberculosis, are among the earliest identified examples documenting the role of autophagy in human disease. Functional studies have shown that IRGM protects against these diseases by modulating autophagy, yet the exact molecular mechanism of IRGM's activity has remained unknown. We have recently elucidated IRGM's mechanism of action. IRGM functions as a platform for assembling, stabilizing, and activating the core autophagic machinery, while at the same time physically coupling it to conventional innate immunity receptors. Exposure to microbial products or bacterial invasion increases IRGM expression, which leads to stabilization of AMPK. Specific protein-protein interactions and post-translational modifications such as ubiquitination of IRGM, lead to a co-assembly with IRGM of the key autophagy regulators ULK1 and BECN1 in their activated forms. IRGM physically interacts with 2 other CD risk factors, ATG16L1 and NOD2, placing these 3 principal players in CD within the same molecular complex. This explains how polymorphisms altering expression or function of any of the 3 factors individually can affect the same process-autophagy. Furthermore, IRGM's interaction with NOD2, and additional pattern recognition receptors such as NOD1, RIG-I, and select TLRs, transduces microbial signals to the core autophagy apparatus. This work solves the long-standing enigma of how IRGM controls autophagy.
MeSH term(s)	Autophagy ; Crohn Disease/metabolism ; Crohn Disease/pathology ; GTP-Binding Proteins/metabolism ; HEK293 Cells ; Humans ; Models, Biological ; Risk Factors ; Tuberculosis/metabolism ; Tuberculosis/pathology
Chemical Substances	GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2015-08-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2015.1084457
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