scholarly journals PERAN SISTEM IMUN TERHADAP TERJADINYA PNEUMONIA TERKAIT STROKE

Author(s):  
Al Rasyid

THE ROLE OF IMMUNE SYSTEM ON THE OCCURRENCE OF STROKE- ASSOCIATED PNEUMONIAABSTRACTStroke associated pneumonia (SAP) is one of the medical complication which associated with high mortality rate. Several studies conclude two factors involve significantly in pathophysiology of SAP, one of which is immunodepression state. Immunodepression occurs by 3 main pathways, symphathetic system activation, parasymphathetic system activation, and HPA (hypothalamus-pituitary-adrenal)  axis activation. Simultaneously, they induce proinflammatory response suppression and immune cells alternation, which lead to an infection like pneumonia. Therefore, establishing an effective immunomodulation therapy could be one of the main focus in comprehensive stroke management’s future studies.Keywords: Immunodepression, stroke-associated pneumoniaABSTRAKKomplikasi pneumonia terkait stroke menjadi salah satu faktor penyebab mortalitas tertinggi. Studi-studi menyimpulkan bahwa ada dua faktor yang berperan pada patofisiologi pneumonia, salah satunya adalah imunodepresi terkait stroke. Imunodepresi terjadi melalui 3 jaras, yaitu aktivitas simpatis, aktivitas parasimpatis, dan aksis hipotalamus- pituitari-adrenal. Secara simultan, ketiganya menekan respons proinflamasi dan mengubah sel-sel imun sehingga pneumonia dapat mudah terjadi. Pembuatan terapi imunomodulasi yang dapat mencegah infeksi namun tidak memperburuk kondisi iskemia dapat menjadi fokus studi penanganan stroke komprehensif di masa datang.Kata kunci: Imunodepresi, pneumonia terkait stroke  

2021 ◽  
Vol 12 ◽  
Author(s):  
Alecia M. Blaszczak ◽  
Anahita Jalilvand ◽  
Willa A. Hsueh

The role of adipose tissue (AT) inflammation in obesity and its multiple related-complications is a rapidly expanding area of scientific interest. Within the last 30 years, the role of the adipocyte as an endocrine and immunologic cell has been progressively established. Like the macrophage, the adipocyte is capable of linking the innate and adaptive immune system through the secretion of adipokines and cytokines; exosome release of lipids, hormones, and microRNAs; and contact interaction with other immune cells. Key innate immune cells in AT include adipocytes, macrophages, neutrophils, and innate lymphoid cells type 2 (ILC2s). The role of the innate immune system in promoting adipose tissue inflammation in obesity will be highlighted in this review. T cells and B cells also play important roles in contributing to AT inflammation and are discussed in this series in the chapter on adaptive immunity.


2021 ◽  
Vol 12 ◽  
Author(s):  
Chiel van Geffen ◽  
Astrid Deißler ◽  
Markus Quante ◽  
Harald Renz ◽  
Dominik Hartl ◽  
...  

The immune system is receiving increasing attention for interstitial lung diseases, as knowledge on its role in fibrosis development and response to therapies is expanding. Uncontrolled immune responses and unbalanced injury-inflammation-repair processes drive the initiation and progression of idiopathic pulmonary fibrosis. The regulatory immune system plays important roles in controlling pathogenic immune responses, regulating inflammation and modulating the transition of inflammation to fibrosis. This review aims to summarize and critically discuss the current knowledge on the potential role of regulatory immune cells, including mesenchymal stromal/stem cells, regulatory T cells, regulatory B cells, macrophages, dendritic cells and myeloid-derived suppressor cells in idiopathic pulmonary fibrosis. Furthermore, we review the emerging role of regulatory immune cells in anti-fibrotic therapy and lung transplantation. A comprehensive understanding of immune regulation could pave the way towards new therapeutic or preventive approaches in idiopathic pulmonary fibrosis.


Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Sterling C Kneedler ◽  
Lauren Phillips ◽  
Kayla R Hudson ◽  
Katharine M Beckman ◽  
Alan R Parrish ◽  
...  

Hypertension is associated with immune system activation and inflammation. Renal infiltration of both innate and adaptive immune cells contributes to injury, dysfunction, and increased blood pressure. Activated immune cells that exit blood vessels into the interstitium then travel through lymphatic vessels to draining lymph nodes where they signal to other immune cells to increase the immune response. It is unknown how renal lymphatic vessels change in the context of hypertension, immune system activation, inflammation, and injury. We hypothesized that renal macrophage infiltration, inflammation, and injury would significantly increase lymphangiogenesis in various strains of rats. SHR rats that exhibit hypertension and renal injury (SHR-A3 strain) had significantly increased numbers of renal lymphatic vessels at 40 weeks of age compared to WKY controls (total of 3 fields of view: 52 ± 1 vs. 28 ± 1; p<0.05). This was associated with increased renal macrophage infiltration. SHR rats that exhibit hypertension but minimal renal injury (SHR-B2 strain) had significantly less renal lymphatic vessel numbers compared to WKY controls (25 ± 2 vs. 28 ± 1; p<0.05) and normal levels of macrophages. The signals for lymphangiogenesis, VEGF-C and its receptor VEGF-R3, were both increased significantly at the protein level in the kidneys of SHR-A3 rats at 18 weeks but not different in the kidneys of SHR-B2 rats compared to WKY controls. To test whether the increased lymphangiogensis is due to hypertension and/or renal inflammation and injury, we obtained kidneys from Fischer 344 rats that exhibit normal blood pressure but develop renal inflammation and injury as they age. Compared to kidneys from control 4-month old Fischer rats, kidneys from 20-month and 24-month old Fischer rats had significantly increased numbers of lymphatic vessels (32 ± 3 vs. 74 ± 1 vs. 110 ± 6, respectively; p<0.05) and this was also associated with increased macrophage infiltration. Protein levels of VEGF-C and VEGF-R3 were increased significantly in 20-month old Fischer rats compared to 4-month old controls. These data together demonstrate that renal immune cell infiltration, inflammation, and injury increases lymphangiogenesis.


2019 ◽  
Vol 11 ◽  
pp. 251584141986812
Author(s):  
Tanima Bose

Pemphigoid disease is classified according to the phenotypical location of the disease and the presence of different types of antibodies. The ocular distribution of pemphigoid mainly occurs in patients with bullous pemphigoid and mucous membrane pemphigoid. Several immune cells, including the cells of the innate immune system (neutrophils and γδ T cells) and the adaptive immune system (T and B cells), are involved in pemphigoid disease. The treatment of pemphigoid is still wide-ranging, and the most utilized treatment is the use of immunosuppressants and corticosteroids. In this scenario, it is absolutely important to screen the immune cells that are involved in this group of diseases and to determine if a targeted treatment approach is plausible. In conclusion, this review will identify some newer treatment possibilities for the whole spectrum of pemphigoid diseases.


1998 ◽  
Vol 30 (6) ◽  
pp. 863-868 ◽  
Author(s):  
J. M. DAVIS ◽  
J. A. WEAVER ◽  
M. L. KOHUT ◽  
L. H. COLBERT ◽  
A. GHAFFAR ◽  
...  

2010 ◽  
Vol 1 (4) ◽  
pp. 229-234 ◽  
Author(s):  
Taraneh Moini Zanjani ◽  
Masoumeh Sabetkasaei ◽  
Behnaz Karimian ◽  
Farzaneh Labibi ◽  
Babak Farokhi ◽  
...  

AbstractBackgroundEvidence for a role of immune system in hyperalgesic pain states is increasing. Recent work in neuroimmunology suggests that the immune system does more than simply perform its well known functions of recognizing and removing invading pathogens and tumors. Interest in neuroinflammation and neuroimmune activation has grown rapidly in recent years with the recognition of the role of central nervous system inflammatiom and immune responses in the aetiology of pain states. Among various theories, the role of inflammatory responses of the injured nerve has recently received attention. Cytokines are heterogenous group of polypeptides that activate the immune system and mediate inflammatory responses, acting on a variety of tissue, including the peripheral and central nervous system. Interleukin-6 (IL-6) a pro-inflammatory cytokine, is potentially important in pain aetiology, have pronociceptive actions. Neuropathic pain may be due to a primary insult to the peripheral or central nervous system. Substances released during inflammation from immune cells play an important role in the development and maintenance of chronic pain. Nimesulide, a highly selective cox-2 inhibitor, effectively reduces hyperalgesia due to peripherally administration of inflammatory agents like formalin. The safety of nimesulide was reported for some conditions in which other NSAIDs are contraindicated. Here we have determined the effect of nimesulide on pain behaviour and serum IL-6 level in chronic constriction injury (CCI) model of neuropathic pain.MethodsExperiments were carried out on male Wistar rats, (weight 150–200 g, n = 8). Rats were divided into 3 different groups: 1-CCI + saline 0.9% 2Sham + saline 0.9% (control) 3CCI + drug. Nimesulide (1.25, 2.5, 5 mg/kg, i.p.) was injected 1h before surgery and continued daily to day 14 post-ligation. 42 °C water for thermal hyperalgesia, von Frey filaments for mechanical allodynia, acetone test for cool allodynia and 10 °C water for cold hyperalgesia were respectively used as pain behavioural tests. Behavioural tests were recorded before surgery and on postoperative days 1, 3, 5, 7, 10, 14 and the serum concentration of IL-6 was determined at the day 14.ResultsThe results of this study showed a decrease in hyperalgesia and allodynia following nimesulide administration.ConclusionsIt appears that nimesulide was able to reduce pain behaviour due to nerve inflammation and a parallel decrease in the serum IL-6 concentration was observed.ImplicationsThe immune system is an important mediator in the cascade of events that ultimately results in hyperalgesia. Cytokines contribute to the patheogenesis of neuropathic pain, therefore drugs that inhibit cytokine release from immune cells may reduce inflammatory pain states.


F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 2141
Author(s):  
Katie Alexander ◽  
Charles O. Elson

Bacteria and mammals have co-evolved with one another over millennia, and it has become impossible to interpret mucosal immunity without taking the microbiota into consideration. In fact, the primary role of the mucosal immune system is regulating homeostasis and the host relationship with the microbiota. Bacteria are no longer seen as simply invading pathogens, but rather a necessary component to one’s own immune response. On the one hand, the microbiota is a vital educator of immune cells and initiator of beneficial responses; but, on the other, dysbiosis of microbiota constituents are associated with inflammation and autoimmune disorders. In this review, we will consider recent advances in the understanding of how the microbiota influences host mucosal immunity, particularly the initial development of the immune response and its implications.


2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Anna Cláudia Calvielli Castelo Branco ◽  
Fábio Seiti Yamada Yoshikawa ◽  
Anna Julia Pietrobon ◽  
Maria Notomi Sato

Inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, and leukotrienes, impact the immune system, usually as proinflammatory factors. Other mediators act as regulatory components to establish homeostasis after injury or prevent the inflammatory process. Histamine, a biogenic vasoactive amine, causes symptoms such as allergies and has a pleiotropic effect that is dependent on its interaction with its four histamine receptors. In this review, we discuss the dualistic effects of histamine: how histamine affects inflammation of the immune system through the activation of intracellular pathways that induce the production of inflammatory mediators and cytokines in different immune cells and how histamine exerts regulatory functions in innate and adaptive immune responses. We also evaluate the interactions between these effects.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jin-Wei Xin ◽  
Zhi-Xin Chai ◽  
Cheng-Fu Zhang ◽  
Qiang Zhang ◽  
Yong Zhu ◽  
...  

Abstract The yak, Bos grunniens, is the only large mammal in the Qinghai-Tibet Plateau and has been bred to provide meat, milk, and transportation. Previous studies indicate that the immune system contributes to the yak’s adaptation to high-altitude environments. In order to further investigate changes in immune function during yak development, we compared the transcriptome profiles of gluteus and lung tissues among yaks at 6, 30, 60, and 90 months of age. Analyses of significantly differentially expressed genes (DEGs) in lung tissues revealed that immune function was more activated at 6-months and less activated at 90-months than in the 30 and 60-month-old animals. DEG exploration in gluteal tissues revealed that immune functions were more highly activated at both 6 and 90-months, compared with 30 and 60-months. Immune system activation in the muscle and lung tissues of 30-month-old yaks may increase their resistance to infections, while decreased may be due to aging. Furthermore, the higher immune activation status in the gluteal tissues in 90-month-old yaks could be due to muscle injury and subsequent regeneration, which is supported by the fact that 5 unigenes related with muscle injury and 3 related to muscle regeneration displayed greater expression levels at 90-months than at 30 and 60-months. Overall, the present study highlights the important role of the immune system in yak development, which will facilitate future investigations.


Sign in / Sign up

Export Citation Format

Share Document