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Article ; Online: IL-12p40 Monomer: A Potential Player in Macrophage Regulation.

Jeong, Brian / Pahan, Kalipada

Immuno

2024 Volume 4, Issue 1, Page(s) 77–90

Abstract: Macrophages are myeloid phagocytic leukocytes whose functions are to protect against infections, mediate T-cell responses, and maintain tissue homeostasis. IL-12p40 monomer is a cytokine that is largely produced by macrophages, and it has, for the ... ...

Abstract	Macrophages are myeloid phagocytic leukocytes whose functions are to protect against infections, mediate T-cell responses, and maintain tissue homeostasis. IL-12p40 monomer is a cytokine that is largely produced by macrophages, and it has, for the longest time, been considered a largely non-functional cytokine of the IL-12 family. However, new research has emerged that demonstrates that this p40 monomer may play a bigger role in shaping immune environments. To shed light on the specific effects of p40 monomer on macrophages and their surrounding environment, we showed, through cell culture studies, qPCR, ELISA, and immunofluorescence analyses, that the direct administration of recombinant p40 monomer to RAW 264.7 cells and primary lung macrophages stimulated the production of both pro-inflammatory (TNFα) and anti-inflammatory (IL-10) signals. Accordingly, p40 monomer prevented the full pro-inflammatory effects of LPS, and the neutralization of p40 monomer by mAb a3-3a stimulated the pro-inflammatory effects of LPS. Furthermore, we demonstrated that the intranasal administration of p40 monomer upregulated TNFα
Language	English
Publishing date	2024-02-23
Publishing country	Switzerland
Document type	Journal Article
ISSN	2673-5601
ISSN (online)	2673-5601
DOI	10.3390/immuno4010005
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Article: Cinnamein Inhibits the Induction of Nitric Oxide and Proinflammatory Cytokines in Macrophages, Microglia and Astrocytes.

Pahan, Swarupa / Raha, Sumita / Dasarathi, Sridevi / Pahan, Kalipada

Journal of clinical & experimental immunology

2023 Volume 8, Issue 1, Page(s) 520–529

Abstract: Chronic inflammation driven by proinflammatory cytokines (TNFα, IL-1β, IL-6, etc.), and nitric oxide (NO) plays an important role in the pathogenesis of several autoimmune, inflammatory as well as neurodegenerative disorders like rheumatoid arthritis, ... ...

Abstract	Chronic inflammation driven by proinflammatory cytokines (TNFα, IL-1β, IL-6, etc.), and nitric oxide (NO) plays an important role in the pathogenesis of several autoimmune, inflammatory as well as neurodegenerative disorders like rheumatoid arthritis, multiple sclerosis, Alzheimer's disease, Parkinson's disease, Huntington's disease, etc. Therefore, identification of nontoxic anti-inflammatory drugs may be beneficial for these autoimmune, inflammatory and neurodegenerative disorders. Cinnamein, an ester derivative of cinnamic acid and benzyl alcohol, is used as a flavoring agent and for its antifungal and antibacterial properties. This study underlines the importance of cinnamein in inhibiting the induction of proinflammatory molecules in RAW 264.7 macrophages and primary mouse microglia and astrocytes. Stimulation of RAW 264.7 macrophages with lipopolysaccharide (LPS) and interferon γ (IFNγ) led to marked production of NO. However, cinnamein pretreatment significantly inhibited LPS- and IFNγ-induced production of NO in RAW 264.7 macrophages. Cinnamein also reduced the mRNA expression of inducible nitric oxide synthase (iNOS) and TNFα in RAW cells. Accordingly, LPS and viral double-stranded RNA mimic polyinosinic: polycytidylic acid (polyIC) stimulated the production of TNFα, IL-1β and IL-6 in primary mouse microglia, which was inhibited by cinnamein pretreatment. Similarly, cinnamein also inhibited polyIC-induced production of TNFα and IL-6 in primary mouse astrocytes. These results suggest that cinnamein may be used to control inflammation in different autoimmune, inflammatory and neurodegenerative disorders.
Language	English
Publishing date	2023-01-31
Publishing country	United States
Document type	Journal Article
DOI	10.33140/jcei.08.01.01
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Article ; Online: A Broad Application of CRISPR Cas9 in Infectious, Inflammatory and Neurodegenerative Diseases.

Pahan, Kalipada

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2019 Volume 14, Issue 4, Page(s) 534–536

Abstract: Being the most important immune-responsive cell type of the CNS, microglia always glorify the so-called crossroad of Neurology, Immunology and Pharmacology. As microglial activation is a hallmark of different neurodegenerative disorders including ... ...

Abstract	Being the most important immune-responsive cell type of the CNS, microglia always glorify the so-called crossroad of Neurology, Immunology and Pharmacology. As microglial activation is a hallmark of different neurodegenerative disorders including Alzheimer's disease (AD), Parkinson's disease (PD), HIV-associated neurocognitive disorders (HAND), Amyotrophic lateral sclerosis (ALS), etc., selective targeting of microglial cell signaling may be a valid option to control these neurodegenerative disorders with lesser side effects. This is particularly important as no effective therapies are available against these diseases and available neuroimmune modulators are known to target multiple cell types in a non-cell-specific manner. How we can achieve such specificity? A newly-developed cutting-edge molecular biology tool is rocking biomedical research in recent years so much so that it has already come under major lawsuits between the University of California Berkeley and the MIT-Harvard Broad Institute regarding its ownership rights, probably halting the Nobel committee to announce the most coveted prize to its owners. It is none other than Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR). In nutshell, the Cas9 enzyme has been paired with the bacterial immune system, CRISPR, to ultimately turn CRISPR/Cas9 as an effective genome editor. Therefore, this special issue has been devoted to highlight some of the recent discoveries on CRISPR/Cas9 in neurodegenerative disorders and explain these discoveries in the light of neuroimmune pharmacology.
MeSH term(s)	Animals ; CRISPR-Associated Protein 9/genetics ; CRISPR-Associated Protein 9/immunology ; CRISPR-Cas Systems/genetics ; CRISPR-Cas Systems/immunology ; Gene Editing/methods ; Gene Editing/trends ; HIV Infections/genetics ; HIV Infections/immunology ; HIV Infections/therapy ; Humans ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/therapy ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/immunology ; Neurodegenerative Diseases/therapy
Chemical Substances	CRISPR-Associated Protein 9 (EC 3.1.-)
Language	English
Publishing date	2019-11-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-019-09889-4
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Article ; Online: Therapeutic efficacy of cinnamein, a component of balsam of Tolu/Peru, in controlled cortical impact mouse model of TBI.

Poddar, Jit / Rangasamy, Suresh B / Pahan, Kalipada

Neurochemistry international

2024 Volume 176, Page(s) 105742

Abstract: Traumatic brain injury (TBI) remains a major health concern which causes long-term neurological disability particularly in war veterans, athletes and young adults. In spite of intense clinical and research investigations, there is no effective therapy to ...

Abstract	Traumatic brain injury (TBI) remains a major health concern which causes long-term neurological disability particularly in war veterans, athletes and young adults. In spite of intense clinical and research investigations, there is no effective therapy to cease the pathogenesis of the disease. It is believed that axonal injury during TBI is potentiated by neuroinflammation and demyelination and/or failure to remyelination. This study highlights the use of naturally available cinnamein, also chemically known as benzyl cinnamate, in inhibiting neuroinflammation, promoting remyelination and combating the disease process of controlled cortical impact (CCI)-induced TBI in mice. Oral delivery of cinnamein through gavage brought down the activation of microglia and astrocytes to decrease the expression of inducible nitric oxide synthase (iNOS), glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1 (Iba1) in hippocampus and cortex of TBI mice. Cinnamein treatment also stimulated remyelination in TBI mice as revealed by PLP and A2B5 double-labeling, luxol fast blue (LFB) staining and axonal double-labeling for neurofilament and MBP. Furthermore, oral cinnamein reduced the size of lesion cavity in the brain, improved locomotor functions and restored memory and learning in TBI mice. These results suggest a new neuroprotective property of cinnamein that may be valuable in the treatment of TBI.
Language	English
Publishing date	2024-04-17
Publishing country	England
Document type	Journal Article
ZDB-ID	283190-9
ISSN	1872-9754 ; 0197-0186
ISSN (online)	1872-9754
ISSN	0197-0186
DOI	10.1016/j.neuint.2024.105742
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Zs.A 1610: Show issues

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Article ; Online: Smooth or Risky Revisit of an Old Malaria Drug for COVID-19?

Pahan, Priyanka / Pahan, Kalipada

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2020 Volume 15, Issue 2, Page(s) 174–180

Abstract: Hydroxychloroquine (HCQ) is an old medication for malaria. In addition to handling this parasitic disease, HCQ is also used to treat a number of autoimmune disorders including rheumatoid arthritis and systemic lupus erythematosus when other medications ... ...

Abstract	Hydroxychloroquine (HCQ) is an old medication for malaria. In addition to handling this parasitic disease, HCQ is also used to treat a number of autoimmune disorders including rheumatoid arthritis and systemic lupus erythematosus when other medications are not effective. Recently a new viral infection (COVID-19) is rocking the entire world so much that it has already taken more than 200,000 lives throughout the world within the last two months and the World Health Organization was forced to declare it as a pandemic on March 11, 2020. Interestingly, some reports indicate that this wonder drug may be also beneficial for COVID-19 and accordingly, many clinical trials have begun. Here, we discuss different modes of action (anti-inflammatory, antioxidant, inhibition of endosomal acidification, suppression of angiotensin-converting enzyme 2 or ACE2 glycosylation, etc.) of HCQ that might be responsible for its possible anti-COVID-19 effect. On the other hand, this review also makes an honest attempt to delineate mechanisms (increase in vasoconstriction, inhibition of autophagy, depletion of T cells, etc.) indicating how it may aggravate certain conditions and why caution should be taken before granting widespread repurposing of HCQ for COVID-19. Graphical Abstract.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Antimalarials/pharmacology ; Betacoronavirus/drug effects ; COVID-19 ; Coronavirus Infections/drug therapy ; Drug Repositioning ; Humans ; Hydroxychloroquine/pharmacology ; Pandemics ; Pneumonia, Viral/drug therapy ; SARS-CoV-2
Chemical Substances	Anti-Inflammatory Agents ; Antimalarials ; Hydroxychloroquine (4QWG6N8QKH)
Keywords	covid19
Language	English
Publishing date	2020-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-020-09923-w
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Article: Can cinnamon spice down autoimmune diseases?

Pahan, Swarupa / Pahan, Kalipada

Journal of clinical & experimental immunology

2020 Volume 5, Issue 6, Page(s) 252–258

Abstract: Autoimmune diseases are one of the dreadful group of human diseases that have always been of keen interest to researchers. Due to complex and broad-spectrum nature, scientists are not yet able to pinpoint the pathogenesis of and delineate effective ... ...

Abstract	Autoimmune diseases are one of the dreadful group of human diseases that have always been of keen interest to researchers. Due to complex and broad-spectrum nature, scientists are not yet able to pinpoint the pathogenesis of and delineate effective therapy against this group of diseases. However, it is becoming clear that a decrease in number and function of T regulatory cells (Treg), an increase in autoreactive Th1/Th17 cells and associated immunomodulation and inflammation participate in the pathogenesis of many autoimmune diseases. Cinnamon (
Language	English
Publishing date	2020-11-23
Publishing country	United States
Document type	Journal Article
DOI	10.33140/jcei.05.06.01
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Article ; Online: Cinnamic acid, a natural plant compound, exhibits neuroprotection in a mouse model of Sandhoff disease via PPARα.

Raha, Sumita / Paidi, Ramesh K / Dutta, Debashis / Pahan, Kalipada

NeuroImmune pharmacology and therapeutics

2024 Volume 3, Issue 1, Page(s) 17–32

Abstract: Tay-Sachs disease (TSD) and its severe form Sandhoff disease (SD) are autosomal recessive lysosomal storage metabolic disorders, which often result into excessive GM2 ganglioside accumulation predominantly in lysosomes of nerve cells. Although patients ... ...

Abstract	Tay-Sachs disease (TSD) and its severe form Sandhoff disease (SD) are autosomal recessive lysosomal storage metabolic disorders, which often result into excessive GM2 ganglioside accumulation predominantly in lysosomes of nerve cells. Although patients with these diseases appear normal at birth, the progressive accumulation of undegraded GM2 gangliosides in neurons leads to early death accompanied by manifestation of motor difficulties and gradual loss of behavioral skills. Unfortunately, there is still no effective treatment available for TSD/SD. The present study highlights the importance of cinnamic acid (CA), a naturally occurring aromatic fatty acid present in a number of plants, in inhibiting the disease process in a transgenic mouse model of SD. Oral administration of CA significantly attenuated glial activation and inflammation and reduced the accumulation of GM2 gangliosides/glycoconjugates in the cerebral cortex of Sandhoff mice. Besides, oral CA also improved behavioral performance and increased the survival of Sandhoff mice. While assessing the mechanism, we found that oral administration of CA increased the level of peroxisome proliferator-activated receptor α (PPARα) in the brain of Sandhoff mice and that oral CA remained unable to reduce glycoconjugates, improve behavior and increase survival in Sandhoff mice lacking PPARα. Our results indicate a beneficial function of CA that utilizes a PPARα-dependent mechanism to halt the progression of SD and thereby increase the longevity of Sandhoff mice.
Language	English
Publishing date	2024-03-15
Publishing country	Germany
Document type	Journal Article
ISSN	2750-6665
ISSN (online)	2750-6665
DOI	10.1515/nipt-2023-0027
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Article ; Online: Corrigendum to "Upregulation of tripeptidyl-peptidase 1 by 3-hydroxy-(2,2)-dimethyl butyrate, a brain endogenous ligand of PPARα: Implications for late-infantile Batten disease therapy" [Neurobiology of Disease 127 (2019) 362-373].

Chakrabarti, Sudipta / Chandra, Sujyoti / Roy, Avik / Kundu, Madhuchhanda / Pahan, Kalipada

Neurobiology of disease

2024 Volume 194, Page(s) 106479

Language	English
Publishing date	2024-03-27
Publishing country	United States
Document type	Published Erratum
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2024.106479
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Article ; Online: Mode of Action of Aspirin in Experimental Autoimmune Encephalomyelitis.

Pahan, Swarupa / Pahan, Kalipada

DNA and cell biology

2019 Volume 38, Issue 7, Page(s) 593–596

Abstract: Multiple sclerosis (MS) is a chronic and debilitating autoimmune disorder of the central nervous system in which the autoimmune T cells destroy myelin, thus causing lesion, damage, and neuronal dysfunction. Experimental autoimmune encephalomyelitis (EAE) ...

Abstract	Multiple sclerosis (MS) is a chronic and debilitating autoimmune disorder of the central nervous system in which the autoimmune T cells destroy myelin, thus causing lesion, damage, and neuronal dysfunction. Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS that is particularly useful for testing new therapeutic approaches against MS. Aspirin (acetyl salicylic acid) is one of the oldest and widely used medicines in the world, and recently it has been shown that low-dose aspirin is capable of suppressing the disease process of EAE in mice. One of the root causes of this autoimmune disease process is the decrease and/or suppression of Foxp3-expressing anti-autoimmune regulatory T cells (Tregs) and associated increase in autoimmune T-helper 1 (Th1) and Th17 cells. Aspirin upregulates Tregs and decreases Th1 and Th17 responses. Accordingly, the suppression of Tregs abrogates the protective effect of aspirin on EAE, indicating that aspirin protects EAE via Tregs. While there are several mechanisms for the maintenance of Tregs under immune insults, aspirin increases the level of interleukin-11 (IL-11), an immunomodulatory cytokine, and IL-11 alone is sufficient to protect Tregs. Being a multifunctional molecule, aspirin stimulates the activation of cAMP-response element-binding (CREB) to promote the recruitment of CREB to the
MeSH term(s)	Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Aspirin/pharmacology ; Aspirin/therapeutic use ; Cyclic AMP Response Element-Binding Protein/metabolism ; Encephalomyelitis, Autoimmune, Experimental/drug therapy ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Immunosuppressive Agents/pharmacology ; Immunosuppressive Agents/therapeutic use ; Interleukins/genetics ; Interleukins/metabolism ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Cyclic AMP Response Element-Binding Protein ; Immunosuppressive Agents ; Interleukins ; Aspirin (R16CO5Y76E)
Language	English
Publishing date	2019-05-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1024454-2
ISSN	1557-7430 ; 0198-0238 ; 1044-5498
ISSN (online)	1557-7430
ISSN	0198-0238 ; 1044-5498
DOI	10.1089/dna.2019.4814
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Zs.A 2061: Show issues

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Article: Glyceryl tribenzoate: A food additive with unique properties to be a substitute for cinnamon.

Pahan, Swarupa / Dasarathi, Sridevi / Pahan, Kalipada

Journal of clinical & experimental immunology

2021 Volume 6, Issue 5, Page(s) 367–372

Abstract: Cinnamon is a regularly used natural seasoning and flavoring material throughout the world for eras. Recent laboratory studies have demonstrated that oral cinnamon may be beneficial for different neuroinflammatory and neurodegenerative disorders such as ... ...

Abstract	Cinnamon is a regularly used natural seasoning and flavoring material throughout the world for eras. Recent laboratory studies have demonstrated that oral cinnamon may be beneficial for different neuroinflammatory and neurodegenerative disorders such as multiple sclerosis (MS), Parkinson's disease (PD), Alzheimer's disease (AD), and Lewy body diseases (LBD). However, cinnamon's certain limitations (e.g. unavailability of true Ceylon cinnamon throughout the world, impurities in ground cinnamon, etc.) have initiated an interest among researchers to find an alternate of cinnamon that can potentially deliver the same efficacy in the diseases mentioned above. Glyceryl tribenzoate (GTB) is a U.S. Food and Drug Administration (FDA)-approved flavoring ingredient that is used in food and food packaging industries. It has been found that similar to cinnamon, oral GTB is capable of upregulating regulatory T cells and suppressing the autoimmune disease process of experimental autoimmune encephalomyelitis, an animal model of MS. Moreover, both GTB and cinnamon metabolite sodium benzoate (NaB) have the potency to attenuate neurodegenerative pathology in a mouse model of Huntington disease (HD). Here, we have also demonstrated anti-inflammatory property of GTB in astrocytes and macrophages, a property that is also seen with cinnamon and its metabolite sodium benzoate (NaB). Therefore, here, we have made a sincere attempt to discuss the similarities and dissimilarities between cinnamon and GTB with a focus whether GTB has the potential to be considered as a substitute of cinnamon for neuroinflammatory and neurodegenerative disorders.
Language	English
Publishing date	2021-10-20
Publishing country	United States
Document type	Journal Article
DOI	10.33140/jcei.06.05.04
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