scholarly journals Traumatic Brain Injury Alters Dendritic Cell Differentiation and Distribution in Lymphoid and Non-Lymphoid Organs

Author(s):  
Orest Tsymbalyuk ◽  
Volodymyr Gerzanich ◽  
Marc Simard ◽  
Chozha Rathinam

Abstract Pathophysiological consequences of traumatic brain injury (TBI) mediated secondary injury remain incompletely understood. In particular, the impact of TBI on the differentiation and maintenance of dendritic cells (DCs), remains completely unknown. Here, we report that DC- differentiation, maintenance and functions are altered at both early and late phases of TBI. Our studies identify that; 1. frequencies and absolute numbers of DCs in the spleen and BM are altered at both acute and late phases of TBI; 2. surface expression of key molecules involved in antigen presentation of DCs were affected both at early and late phases of TBI; 3. distribution and functions of tissue-specific DC subsets of both circulatory and lymphatic systems were imbalanced following TBI; 4. early differentiation program of DCs, especially the commitment of hematopoietic stem cells to common DC progenitors, were deregulated after TBI; and 5. intracellular ROS levels were reduced in DC progenitors and differentiated DCs at both early and late phases of TBI. Our data demonstrate, for the first time, that TBI affects the distribution pattern of DCs and induces an imbalance among DC subsets in both lymphoid and non-lymphoid organs. In addition, the current study demonstrates that TBI results in reduced levels of ROS in DCs at both early and late phases of TBI, which may explain altered DC differentiation paradigm following TBI. A deeper understanding on the molecular mechanisms that contribute to DC defects following TBI would be essential and beneficial in treating infections in patients with acute central nervous system (CNS) injuries.

2021 ◽  
Author(s):  
Orest Tsymbalyuk ◽  
Volodymyr Gerzanich ◽  
Marc Simard ◽  
Chozha Rathinam

Abstract Pathophysiological consequences of traumatic brain injury (TBI) mediated secondary injury remain incompletely understood. In particular, the impact of TBI on the differentiation and maintenance of dendritic cells (DCs), remains completely unknown. Here, we report that DC- differentiation, maintenance and functions are altered at both early and late phases of TBI. Our studies identify that; 1. frequencies and absolute numbers of DCs in the spleen and BM are altered at both acute and late phases of TBI; 2. surface expression of key molecules involved in antigen presentation of DCs were affected both at early and late phases of TBI; 3. distribution and functions of tissue-specific DC subsets of both circulatory and lymphatic systems were imbalanced following TBI; 4. early differentiation program of DCs, especially the commitment of hematopoietic stem cells to common DC progenitors, were deregulated after TBI; and 5. intracellular ROS levels were reduced in DC progenitors and differentiated DCs at both early and late phases of TBI. Our data demonstrate, for the first time, that TBI affects the distribution pattern of DCs and induces an imbalance among DC subsets in both lymphoid and non-lymphoid organs. In addition, the current study demonstrates that TBI results in reduced levels of ROS in DCs at both early and late phases of TBI, which may explain altered DC differentiation paradigm following TBI. A deeper understanding on the molecular mechanisms that contribute to DC defects following TBI would be essential and beneficial in treating infections in patients with acute central nervous system (CNS) injuries.


2021 ◽  
Author(s):  
Orest Tsymbalyuk ◽  
Volodymyr Gerzanich ◽  
Marc Simard ◽  
Chozha Vendan Rathinam

Pathophysiological consequences of traumatic brain injury (TBI) mediated secondary injury remain incompletely understood. In particular, the impact of TBI on the differentiation and maintenance of dendritic cells (DCs), remains completely unknown. Here, we report that DC- differentiation, maintenance and functions are altered at both early and late phases of TBI. Our studies identify that; 1. frequencies and absolute numbers of DCs in the spleen and BM are altered at both acute and late phases of TBI; 2. surface expression of key molecules involved in antigen presentation of DCs were affected both at early and late phases of TBI; 3. distribution and functions of tissue-specific DC subsets of both circulatory and lymphatic systems were imbalanced following TBI; 4. early differentiation program of DCs, especially the commitment of hematopoietic stem cells to common DC progenitors, were deregulated after TBI; and 5. intracellular ROS levels were reduced in DC progenitors and differentiated DCs at both early and late phases of TBI. Our data demonstrate, for the first time, that TBI affects the distribution pattern of DCs and induces an imbalance among DC subsets in both lymphoid and non-lymphoid organs. In addition, the current study demonstrates that TBI results in reduced levels of ROS in DCs at both early and late phases of TBI, which may explain altered DC differentiation paradigm following TBI. A deeper understanding on the molecular mechanisms that contribute to DC defects following TBI would be essential and beneficial in treating infections in patients with acute central nervous system (CNS) injuries.


Author(s):  
Fleur Lorton ◽  
Jeanne Simon-Pimmel ◽  
Damien Masson ◽  
Elise Launay ◽  
Christèle Gras-Le Guen ◽  
...  

AbstractObjectivesTo evaluate the impact of implementing a modified Pediatric Emergency Care Applied Research Network (PECARN) rule including the S100B protein assay for managing mild traumatic brain injury (mTBI) in children.MethodsA before-and-after study was conducted in a paediatric emergency department of a French University Hospital from 2013 to 2015. We retrospectively included all consecutive children aged 4 months to 15 years who presented mTBI and were at intermediate risk for clinically important traumatic brain injury (ciTBI). We compared the proportions of CT scans performed and of in-hospital observations before (2013–2014) and after (2014–2015) implementation of a modified PECARN rule including the S100B protein assay.ResultsWe included 1,062 children with mTBI (median age 4.5 years, sex ratio [F/M] 0.73) who were at intermediate risk for ciTBI: 494 (46.5%) during 2013–2014 and 568 (53.5%) during 2014–2015. During 2014–2015, S100B protein was measured in 451 (79.4%) children within 6 h after mTBI. The proportion of CT scans and in-hospital observations significantly decreased between the two periods, from 14.4 to 9.5% (p=0.02) and 73.9–40.5% (p<0.01), respectively. The number of CT scans performed to identify a single ciTBI was reduced by two-thirds, from 18 to 6 CT scans, between 2013–2014 and 2014–2015. All children with ciTBI were identified by the rules.ConclusionsThe implementation of a modified PECARN rule including the S100B protein assay significantly decreased the proportion of CT scans and in-hospital observations for children with mTBI who were at intermediate risk for ciTBI.


2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Lauren Alexis De Crescenzo ◽  
Barbara Alison Gabella ◽  
Jewell Johnson

Abstract Background The transition in 2015 to the Tenth Revision of the International Classification of Disease, Clinical Modification (ICD-10-CM) in the US led the Centers for Disease Control and Prevention (CDC) to propose a surveillance definition of traumatic brain injury (TBI) utilizing ICD-10-CM codes. The CDC’s proposed surveillance definition excludes “unspecified injury of the head,” previously included in the ICD-9-CM TBI surveillance definition. The study purpose was to evaluate the impact of the TBI surveillance definition change on monthly rates of TBI-related emergency department (ED) visits in Colorado from 2012 to 2017. Results The monthly rate of TBI-related ED visits was 55.6 visits per 100,000 persons in January 2012. This rate in the transition month to ICD-10-CM (October 2015) decreased by 41 visits per 100,000 persons (p-value < 0.0001), compared to September 2015, and remained low through December 2017, due to the exclusion of “unspecified injury of head” (ICD-10-CM code S09.90) in the proposed TBI definition. The average increase in the rate was 0.33 visits per month (p < 0.01) prior to October 2015, and 0.04 visits after. When S09.90 was included in the model, the monthly TBI rate in Colorado remained smooth from ICD-9-CM to ICD-10-CM and the transition was no longer significant (p = 0.97). Conclusion The reduction in the monthly TBI-related ED visit rate resulted from the CDC TBI surveillance definition excluding unspecified head injury, not necessarily the coding transition itself. Public health practitioners should be aware that the definition change could lead to a drastic reduction in the magnitude and trend of TBI-related ED visits, which could affect decisions regarding the allocation of TBI resources. This study highlights a challenge in creating a standardized set of TBI ICD-10-CM codes for public health surveillance that provides comparable yet clinically relevant estimates that span the ICD transition.


2015 ◽  
Vol 105 ◽  
pp. 20-28 ◽  
Author(s):  
Linda Isaac ◽  
Keith L. Main ◽  
Salil Soman ◽  
Ian H. Gotlib ◽  
Ansgar J. Furst ◽  
...  

2014 ◽  
Vol 31 (8) ◽  
pp. 713-721 ◽  
Author(s):  
Janine M. Cooper ◽  
Cathy Catroppa ◽  
Miriam H. Beauchamp ◽  
Serem Eren ◽  
Celia Godfrey ◽  
...  

Brain Injury ◽  
2009 ◽  
Vol 23 (7-8) ◽  
pp. 639-648 ◽  
Author(s):  
Lakshmi Srinivasan ◽  
Brian Roberts ◽  
Tamara Bushnik ◽  
Jeffrey Englander ◽  
David A. Spain ◽  
...  

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