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Article ; Online: Immune drivers of physiological and pathological pain.

Jain, Aakanksha / Hakim, Sara / Woolf, Clifford J

2024 Volume 221, Issue 5

Abstract: Physiological pain serves as a warning of exposure to danger and prompts us to withdraw from noxious stimuli to prevent tissue damage. Pain can also alert us of an infection or organ dysfunction and aids in locating such malfunction. However, there are ... ...

Abstract	Physiological pain serves as a warning of exposure to danger and prompts us to withdraw from noxious stimuli to prevent tissue damage. Pain can also alert us of an infection or organ dysfunction and aids in locating such malfunction. However, there are instances where pain is purely pathological, such as unresolved pain following an inflammation or injury to the nervous system, and this can be debilitating and persistent. We now appreciate that immune cells are integral to both physiological and pathological pain, and that pain, in consequence, is not strictly a neuronal phenomenon. Here, we discuss recent findings on how immune cells in the skin, nerve, dorsal root ganglia, and spinal cord interact with somatosensory neurons to mediate pain. We also discuss how both innate and adaptive immune cells, by releasing various ligands and mediators, contribute to the initiation, modulation, persistence, or resolution of various modalities of pain. Finally, we propose that the neuroimmune axis is an attractive target for pain treatment, but the challenges in objectively quantifying pain preclinically, variable sex differences in pain presentation, as well as adverse outcomes associated with immune system modulation, all need to be considered in the development of immunotherapies against pain.
MeSH term(s)	Female ; Male ; Humans ; Pain ; Neurons ; Cognition ; Ganglia, Spinal ; Immunotherapy
Language	English
Publishing date	2024-04-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20221687
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Article ; Online: Role of macrophage autophagy in postoperative pain and inflammation in mice.

Mitsui, Kazuha / Hishiyama, Sohei / Jain, Aakanksha / Kotoda, Yumi / Abe, Masako / Matsukawa, Takashi / Kotoda, Masakazu

Journal of neuroinflammation

2023 Volume 20, Issue 1, Page(s) 102

Abstract: Background: Postoperative pain and inflammation are significant complications following surgery. Strategies that aim to prevent excessive inflammation without hampering natural wound-healing are required for the management of postoperative pain and ... ...

Abstract	Background: Postoperative pain and inflammation are significant complications following surgery. Strategies that aim to prevent excessive inflammation without hampering natural wound-healing are required for the management of postoperative pain and inflammation. However, the knowledge of the mechanisms and target pathways involved in these processes is lacking. Recent studies have revealed that autophagy in macrophages sequesters pro-inflammatory mediators, and it is therefore being recognized as a crucial process involved in regulating inflammation. In this study, we tested the hypothesis that autophagy in macrophages plays protective roles against postoperative pain and inflammation and investigated the underlying mechanisms. Methods: Postoperative pain was induced by plantar incision under isoflurane anesthesia in mice lacking macrophage autophagy (Atg5flox/flox LysMCre +) and their control littermates (Atg5flox/flox). Mechanical and thermal pain sensitivity, changes in weight distribution, spontaneous locomotor activity, tissue inflammation, and body weight were assessed at baseline and 1, 3, and 7 days after surgery. Monocyte/macrophage infiltration at the surgical site and inflammatory mediator expression levels were evaluated. Results: Atg5flox/flox LysMCre + mice compared with the control mice exhibited lower mechanical and thermal pain thresholds and surgical/non-surgical hindlimb weight-bearing ratios. The augmented neurobehavioral symptoms observed in the Atg5flox/flox LysMCre + mice were associated with more severe paw inflammation, higher pro-inflammatory mediator mRNA expression, and more monocytes/macrophages at the surgical site. Conclusion: The lack of macrophage autophagy augmented postoperative pain and inflammation, which were accompanied by enhanced pro-inflammatory cytokine secretion and surgical-site monocyte/macrophage infiltration. Macrophage autophagy plays a protective role in postoperative pain and inflammation and can be a novel therapeutic target.
MeSH term(s)	Mice ; Animals ; Macrophages/metabolism ; Inflammation/metabolism ; Pain, Postoperative/drug therapy ; Autophagy ; Pain Threshold
Language	English
Publishing date	2023-05-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-023-02795-w
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Article ; Online: Unraveling the Plastic Peripheral Neuroimmune Interactome.

Jain, Aakanksha / Hakim, Sara / Woolf, Clifford J

Journal of immunology (Baltimore, Md. : 1950)

2020 Volume 204, Issue 2, Page(s) 257–263

Abstract: Sensory neurons and immune cells share a common microenvironmental niche for surveying tissue integrity. The immune and nervous systems both sense deviations in homeostasis and initiate protective responses and, upon malfunction, also jointly contribute ... ...

Abstract	Sensory neurons and immune cells share a common microenvironmental niche for surveying tissue integrity. The immune and nervous systems both sense deviations in homeostasis and initiate protective responses and, upon malfunction, also jointly contribute to disease. Barrier tissues are heavily innervated by nociceptors, the sensory neurons that detect noxious stimuli, leading to pain and itch. The same tissues are also home to diverse immune cells that respond to infections and injury. The physical proximity of nociceptors and immune cells allows for direct local interactions between the two, independent of the CNS. We discuss in this study their ligand-receptor-based interactions and propose the need to shift from studying individual neuroimmune interactions to exploring the reciprocal neuroimmune interaction network in its entirety: the "neuroimmune interactome." Identification of the nature of the interactome in health and its plasticity in disease will unravel the functional consequences of interactions between nociceptors and immune cells.
MeSH term(s)	Animals ; Humans ; Neuroimmunomodulation/immunology ; Neuronal Plasticity/physiology ; Sensory Receptor Cells/physiology
Language	English
Publishing date	2020-01-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1900818
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Article ; Online: Innate Control of Adaptive Immunity: Beyond the Three-Signal Paradigm.

Jain, Aakanksha / Pasare, Chandrashekhar

Journal of immunology (Baltimore, Md. : 1950)

2017 Volume 198, Issue 10, Page(s) 3791–3800

Abstract: Activation of cells in the adaptive immune system is a highly orchestrated process dictated by multiples cues from the innate immune system. Although the fundamental principles of innate control of adaptive immunity are well established, it is not fully ... ...

Abstract	Activation of cells in the adaptive immune system is a highly orchestrated process dictated by multiples cues from the innate immune system. Although the fundamental principles of innate control of adaptive immunity are well established, it is not fully understood how innate cells integrate qualitative pathogenic information to generate tailored protective adaptive immune responses. In this review, we discuss complexities involved in the innate control of adaptive immunity that extend beyond TCR engagement, costimulation, and priming cytokine production but are critical for the generation of protective T cell immunity.
MeSH term(s)	Adaptive Immunity ; Animals ; Cytokines/immunology ; Humans ; Immunity, Innate ; Mice ; Receptors, Antigen, T-Cell/immunology ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocytes/immunology
Chemical Substances	Cytokines ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2017-05-08
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1602000
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Article: Macrophages protect against sensory axon degeneration in diabetic neuropathy.

Hakim, Sara / Jain, Aakanksha / Petrova, Veselina / Indajang, Jonathan / Kawaguchi, Riki / Wang, Qing / Duran, Elif Sude / Nelson, Drew / Adamson, Stuart S / Greene, Caitlin / Woolf, Clifford J

bioRxiv : the preprint server for biology

2024

Abstract: Diabetic peripheral neuropathy (DPN) is a common complication of diabetes, causing sensory loss and debilitating neuropathic ... ...

Abstract	Diabetic peripheral neuropathy (DPN) is a common complication of diabetes, causing sensory loss and debilitating neuropathic pain
Language	English
Publishing date	2024-01-30
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.30.577801
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Article: A Retrospective Observational Study to Determine the Early Predictors of In-hospital Mortality at Admission with COVID-19.

Jain, Aakanksha Chawla / Kansal, Sudha / Sardana, Raman / Bali, Roseleen K / Kar, Sujoy / Chawla, Rajesh

Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine

2021 Volume 24, Issue 12, Page(s) 1174–1179

Abstract: Introduction: Coronavirus disease-2019 (COVID-19) systemic illness caused by a novel coronavirus severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) has been spreading across the world. The objective of this study is to identify the clinical ... ...

Abstract	Introduction: Coronavirus disease-2019 (COVID-19) systemic illness caused by a novel coronavirus severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) has been spreading across the world. The objective of this study is to identify the clinical and laboratory variables as predictors of in-hospital death at the time of admission in a tertiary care hospital in India. Materials and methods: Demographic profile, clinical, and laboratory variables of 425 patients admitted from April to June 2020 with symptoms and laboratory-confirmed diagnosis through real-time polymerase chain reaction (RT-PCR) were studied. Descriptive statistics, an association of these variables, logistic regression, and CART models were developed to identify early predictors of in-hospital death. Results: Twenty-two patients (5.17%) had expired in course of their hospital stay. The median age [interquartile range (IQR)] of the patients admitted was 49 years (21-77 years). Gender distribution was male - 73.38% (mortality rate 5.83%) and female-26.62% (mortality rate 3.34%). The study shows higher association for age (>47 years) [odds ratio (OR) 4.52], male gender (OR 1.78), shortness of breath (OR 2.02), oxygen saturation <93% (OR 9.32), respiratory rate >24 (OR 5.31), comorbidities like diabetes (OR 2.70), hypertension (OR 2.12), and coronary artery disease (OR 3.18) toward overall mortality. The significant associations in laboratory variables include lymphopenia (<12%) (OR 8.74), C-reactive protein (CRP) (OR 1.99), ferritin (OR 3.18), and lactate dehydrogenase (LDH) (OR 3.37). Using this statistically significant 16 clinical and laboratory variables, the logistic regression model had an area under receiver operating characteristic (ROC) curve of 0.86 (train) and 0.75 (test). Conclusion: Age above 47 years, associated with comorbidities like hypertension and diabetes, with oxygen saturation below 93%, tachycardia, and deranged laboratory variables like lymphopenia and raised CRP, LDH, and ferritin are important predictors of in-hospital mortality. How to cite this article: Jain AC, Kansal S, Sardana R, Bali RK, Kar S, Chawla R. A Retrospective Observational Study to Determine the Early Predictors of In-hospital Mortality at Admission with COVID-19. Indian J Crit Care Med 2020;24(12):1174-1179.
Language	English
Publishing date	2021-01-14
Publishing country	India
Document type	Journal Article
ZDB-ID	2121263-6
ISSN	1998-359X ; 0972-5229
ISSN (online)	1998-359X
ISSN	0972-5229
DOI	10.5005/jp-journals-10071-23683
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Article ; Online: The secondary somatosensory cortex gates mechanical and heat sensitivity.

Taub, Daniel G / Jiang, Qiufen / Pietrafesa, Francesca / Su, Junfeng / Carroll, Aloe / Greene, Caitlin / Blanchard, Michael R / Jain, Aakanksha / El-Rifai, Mahmoud / Callen, Alexis / Yager, Katherine / Chung, Clara / He, Zhigang / Chen, Chinfei / Woolf, Clifford J

Nature communications

2024 Volume 15, Issue 1, Page(s) 1289

Abstract: The cerebral cortex is vital for the processing and perception of sensory stimuli. In the somatosensory axis, information is received primarily by two distinct regions, the primary (S1) and secondary (S2) somatosensory cortices. Top-down circuits ... ...

Abstract	The cerebral cortex is vital for the processing and perception of sensory stimuli. In the somatosensory axis, information is received primarily by two distinct regions, the primary (S1) and secondary (S2) somatosensory cortices. Top-down circuits stemming from S1 can modulate mechanical and cooling but not heat stimuli such that circuit inhibition causes blunted perception. This suggests that responsiveness to particular somatosensory stimuli occurs in a modality specific fashion and we sought to determine additional cortical substrates. In this work, we identify in a mouse model that inhibition of S2 output increases mechanical and heat, but not cooling sensitivity, in contrast to S1. Combining 2-photon anatomical reconstruction with chemogenetic inhibition of specific S2 circuits, we discover that S2 projections to the secondary motor cortex (M2) govern mechanical and heat sensitivity without affecting motor performance or anxiety. Taken together, we show that S2 is an essential cortical structure that governs mechanical and heat sensitivity.
MeSH term(s)	Mice ; Animals ; Somatosensory Cortex/physiology ; Hot Temperature ; Cerebral Cortex
Language	English
Publishing date	2024-02-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-45729-7
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Article: Nociceptor neuroimmune interactomes reveal cell type- and injury-specific inflammatory pain pathways.

Jain, Aakanksha / Gyori, Benjamin M / Hakim, Sara / Bunga, Samuel / Taub, Daniel G / Ruiz-Cantero, Mari Carmen / Tong-Li, Candace / Andrews, Nicholas / Sorger, Peter K / Woolf, Clifford J

bioRxiv : the preprint server for biology

2023

Abstract: Inflammatory pain associated with tissue injury and infections, results from the heightened sensitivity of the peripheral terminals of nociceptor sensory neurons in response to exposure to inflammatory mediators. Targeting immune-derived inflammatory ... ...

Abstract	Inflammatory pain associated with tissue injury and infections, results from the heightened sensitivity of the peripheral terminals of nociceptor sensory neurons in response to exposure to inflammatory mediators. Targeting immune-derived inflammatory ligands, like prostaglandin E2, has been effective in alleviating inflammatory pain. However, the diversity of immune cells and the vast array of ligands they produce make it challenging to systematically map all neuroimmune pathways that contribute to inflammatory pain. Here, we constructed a comprehensive and updatable database of receptor-ligand pairs and complemented it with single-cell transcriptomics of immune cells and sensory neurons in three distinct inflammatory pain conditions, to generate injury-specific neuroimmune interactomes. We identified cell-type-specific neuroimmune axes that are common, as well as unique, to different injury types. This approach successfully predicts neuroimmune pathways with established roles in inflammatory pain as well as ones not previously described. We found that thrombospondin-1 produced by myeloid cells in all three conditions, is a negative regulator of nociceptor sensitization, revealing a non-canonical role of immune ligands as an endogenous reducer of peripheral sensitization. This computational platform lays the groundwork to identify novel mechanisms of immune-mediated peripheral sensitization and the specific disease contexts in which they act.
Language	English
Publishing date	2023-02-03
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.02.01.526526
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Article: The Secondary Somatosensory Cortex Gates Mechanical and Thermal Sensitivity.

Taub, Daniel G / Jiang, Qiufen / Pietrafesa, Francesca / Su, Junfeng / Greene, Caitlin / Blanchard, Michael R / Jain, Aakanksha / El-Rifai, Mahmoud / Callen, Alexis / Yager, Katherine / Chung, Clara / He, Zhigang / Chen, Chinfei / Woolf, Clifford J

bioRxiv : the preprint server for biology

2023

Abstract: The cerebral cortex is vital for the perception and processing of sensory stimuli. In the somatosensory axis, information is received by two distinct regions, the primary (S1) and secondary (S2) somatosensory cortices. Top-down circuits stemming from S1 ... ...

Abstract	The cerebral cortex is vital for the perception and processing of sensory stimuli. In the somatosensory axis, information is received by two distinct regions, the primary (S1) and secondary (S2) somatosensory cortices. Top-down circuits stemming from S1 can modulate mechanical and cooling but not heat stimuli such that circuit inhibition causes blunted mechanical and cooling perception. Using optogenetics and chemogenetics, we find that in contrast to S1, an inhibition of S2 output increases mechanical and heat, but not cooling sensitivity. Combining 2-photon anatomical reconstruction with chemogenetic inhibition of specific S2 circuits, we discover that S2 projections to the secondary motor cortex (M2) govern mechanical and thermal sensitivity without affecting motor or cognitive function. This suggests that while S2, like S1, encodes specific sensory information, that S2 operates through quite distinct neural substrates to modulate responsiveness to particular somatosensory stimuli and that somatosensory cortical encoding occurs in a largely parallel fashion.
Language	English
Publishing date	2023-05-22
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.19.541449
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Article: The Secondary Somatosensory Cortex Gates Mechanical and Thermal Sensitivity.

Research square

2023

Abstract	The cerebral cortex is vital for the perception and processing of sensory stimuli. In the somatosensory axis, information is received by two distinct regions, the primary (S1) and secondary (S2) somatosensory cortices. Top-down circuits stemming from S1 can modulate mechanical and cooling but not heat stimuli such that circuit inhibition causes blunted mechanical and cooling perception. Using optogenetics and chemogenetics, we find that in contrast to S1, an inhibition of S2 output increases mechanical and heat, but not cooling sensitivity. Combining 2-photon anatomical reconstruction with chemogenetic inhibition of specific S2 circuits, we discover that S2 projections to the secondary motor cortex (M2) govern mechanical and thermal sensitivity without affecting motor or cognitive function. This suggests that while S2, like S1, encodes specific sensory information, that S2 operates through quite distinct neural substrates to modulate responsiveness to particular somatosensory stimuli and that somatosensory cortical encoding occurs in a largely parallel fashion.
Language	English
Publishing date	2023-06-28
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-2976953/v1
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