Leukotrienes
According to the study of Prostaglandins and leukotrienes as inflammatory mediators by John A Salmon and Gerald A Higgs(a), Leukotrienes
is produced in leukocytes as a result of oxidative metabolism of
arachidonic acid by the enzyme arachidonate 5-lipoxygenase, belonging to
the family of eicosanoid inflammatory mediators(a). Its production is
usually accompanied by the production of histamine and prostaglandins.
11. Bradykinin, prostaglandins and leukotrienes and Osteoarthritis
Osteoarthritis (OA) of the knee and hip is among
the most frequent and debilitating arthritic conditions. According to
the study by the McMaster University Faculty of Health Sciences, despite
the central involvement of hyaline cartilage in OA pathogenesis, the
source of pain likely stems from the richly innervated synovium,
subchondral bone and periosteum components of the joint. Tissue damage
during joint degeneration generates nociceptive stimuli. The presence of
inflammatory mediators, including bradykinin, prostaglandins and leukotrienes,
lowers the threshold of the Aδ and C pain fibres, resulting in a
heightened response to painful stimuli. it is important to base and
centre the management of OA patients on the severity of
patient-important outcomes, rather than purely an assessment of damage
to the joint. The joint damage, as interpreted from radiographs, is not
necessarily representative of the symptoms experienced(11).
12. Leukotriene B4 receptors BLT1 and BLT2 in inflammatory arthritis
Lipid mediators derived from arachidonic acid
through the cyclooxygenase and lipoxygenase pathways are known to be
important mediators of inflammation. According to the study by the
James Graham Brown Cancer Center, Louisville, in
the study of study of developed mice deficient in BLT2 by targeted
disruption, indicated that the BLT2(-/-) mice developed normally, and
analysis of immune cells showed that disruption of BLT2 did not alter
BLT1 expression or function. Mast cells from the C57BL/6 mice but not
from the BLT2(-/-) mice showed intracellular calcium mobilization in
response to 12(S)-hydroxyheptadeca-5Z, 8E, 10E-trienoic acid. In an
autoantibody-induced inflammatory arthritis model, the BLT2(-/-) mice
showed reduced incidence and severity of disease, including protection
from bone and cartilage loss. Reciprocal bone marrow transplant
experiments identified that loss of BLT2 expression on a bone
marrow-derived cell lineage offers protection against severe
disease(12).
13. Excessive synthesis of leukotrienes in the pathogenesis of systemic sclerosis
Systemic sclerosis (SSc, scleroderma) is an autoimmune disease
characterized by widespread vascular injury and progressive fibrosis of
the skin and internal organs. SSc-related involvement of the lungs,
heart, kidneys and/or the gastrointestinal system accounts for the increased mortality of scleroderma patients. According to the Medical University of Bialystok, Leukotrienes
play an important role in the regulation of all the processes vital to
the pathogenesis of SSc, namely inflammation, vascular function and
connective tissue remodeling. The available data suggests that an
excessive synthesis of leukotrienes may contribute to the development and progression of SSc. Accordingly, blockade of leukotriene pathways appears to be a new, promising target for the treatment of SSc(13).
14. Inhibition of leukotriene D4 and eosinophilic gastroenteritis
Eosinophilic Gastroenteritis (EG) is a rare condition, caused by eosinophilic inflammatory infiltrates in the gastrointestinal tract.
It is usually treated successfully with systemic glucocorticoids.
According to the study by the Department of internal medicine, UZ
Leuven, montelukast, a leukotriene receptor antagonist inhibits leukotriene
D4, an important cytokine in the inflammatory cascade. Although
montelukast could not replace steroid therapy, it acted as a steroid
sparing agent in our patient(14).
15. Churg-Strauss and the Inhibition of leukotriene D4
Churg-Strauss syndrome (CSS) is a systemic small vessel vasculitis involving lungs, skin, heart, gastrointestinal tract
and peripheral nerves. According to the study lead by Carlesimo M,
there is a report of a 36-year-old woman with a necrotic lesion on the
left foot of two months duration, associated with hypereosinophilia,
patchy lung infiltrates, cardiac damage and a mononeuritis. The personal
history was remarkable only for an asthma, treated with Montelukast, a leukotriene
receptor antagonist (LRA). Clinical symptoms, laboratory exams and
instrumental examinations led us to the diagnosis of CSS. In recent
years several studies have reported the possible relationship between
use of leukotriene receptor antagonist (LRA) and CSS expression(15).
16. Treatment of asthma with antileukotrienes and Churg-Strauss syndrome
Since antileukotriene treatment for asthma was introduced, there has
been debate about whether such therapy can lead to Churg-Strauss
Syndrome (CSS). According to Hospital Central de Asturias, Oviedo,
Hospital Puerta de Hierro, there is a report of which suspected CSS in a
patient with bronchopulmonary, cutaneous and analytical signs and whom
we treated with oral steroids. After clinical improvement, one year
later, steroids were replaced by antileukotrienes, after which the same
clinical picture developed. The vasculitis characteristic of CSS was
confirmed pathologically(16).
17. Leukotrienes: the immune-modulating lipid mediators of disease
The leukotrienes are important lipid
mediators with immune modulatory and proinflammatory properties. When
formed in excess, these compounds play a pathogenic role in several
acute and chronic inflammatory diseases, such as asthma, rheumatoid
arthritis, and inflammatory bowel disease. According to the study by the
Department of Medical Biochemistry and Biophysics, Division of
Chemistry 2, Karolinska Institutet, Classical bioactions of leukotrienes
include chemotaxis, endothelial adherence, and activation of
leukocytes, chemokine production, as well as contraction of smooth
muscles in the microcirculation and respiratory tract. Recent genetic, morphological, and biochemical approaches, have pointed to the involvement of leukotrienes
in cardiovascular diseases including atherosclerosis, myocardial
infarction, stroke, and abdominal aortic aneurysm. Moreover, new
insights have changed our previous notion of leukotrienes as mediators of inflammatory reactions to molecules that can fine-tune the innate and adaptive immune response(17).
18. Trihydroxyflavones and the inflammatory processes
In the study to evaluate the anti-inflammatory potential of a series of
trihydroxyflavones by testing their ability to scavenge reactive oxygen
species (ROS) and reactive nitrogen species (RNS) in cells and cell-free
systems and to inhibit the
proinflammatory pathways mediated by the enzymes cyclooxygenase (COX)
and 5-lipoxygenase (5-LOX), in which reactive species have a proven
involvement, showed that The tested trihydroxyflavones proved to be
effective inhibitors of neutrophils' oxidative burst and were shown to
scavenge different ROS and RNS in cell-free systems.
The most active compound in the majority of the assays was
3,3',4'-trihydroxyflavone, which was somehow expected due to the
presence of the ortho-dihydroxy in the B-ring, an important structural
feature in terms of free radical scavenging activity and the compounds
were able to inhibit the production of leukotriene B(4) by 5-LOX in
activated neutrophils. 3,5,7-Trihydroxyflavone was able to inhibit both
COX-1 and COX-2, which makes it a dual inhibitor of COX and 5-LOX
pathways and, therefore, a promising candidate for a new therapeutic
option in the treatment of inflammatory processes(18).
19. Leukotrienes and neuropathic/inflammatory pain
In the study to summarize the recent studies examining the expression of leukotrienes (LTs) and their receptors in nociceptive pathways, and their crucial roles in pathological pain conditions, by examininf of whether LTs were implicated in neuropathic pain
following peripheral nerve injury. Using the SNI model in
rats, investigating the expression of LT synthases and receptors mRNAs
in the spinal cord and the roles on the pain
behaviors, showed that the increase of LT synthesis in spinal microglia
produced via p38 mitogen-activated protein kinase (MAPK) plays a role
in the generation of neuropathic pain. We also examined the expression and roles on pain
behaviors of LT receptors in the dorsal root ganglion (DRG) using a
peripheral inflammation model. The data indicate CysLT2 expressed in DRG
neurons may play a role as a modulator of P2X3, and contribute to the
potentiation of the neuronal activity following peripheral
inflammation(19).
20. Lukotrienes in the pathogenesis of dysmenorrhea in adolescent girls
In the study to determine the role of prostaglandins and leukotrienes
in the pathogenesis of dysmenorrhea in a data of Twenty patients with
dysmenorrhea aged 16.2+/-1.2 years and 20 healthy age-matched controls
with eumenorrhea (absence of pain during menstruation) showed that there is a distinct pattern of leukotriene
production during the menstrual cycle, but the changes in the systemic
level are not responsible for their role in the pathogenesis of
dysmenorrhea. Further studies at the local level in the target organ are necessary to elucidate the role of the lipid mediators in the pathogenesis of dysmenorrhea(20).
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Sources
(11) http://www.ncbi.nlm.nih.gov/pubmed/22471357
(12) http://www.ncbi.nlm.nih.gov/pubmed/20656922
(13) http://www.ncbi.nlm.nih.gov/pubmed/22763975
(14) http://www.ncbi.nlm.nih.gov/pubmed/22319970
(15) http://www.ncbi.nlm.nih.gov/pubmed/22230414
(16) http://www.ncbi.nlm.nih.gov/pubmed/11181230
(17) http://www.ncbi.nlm.nih.gov/pubmed/23063073
(18) http://www.ncbi.nlm.nih.gov/pubmed/22806885
(19) http://www.ncbi.nlm.nih.gov/pubmed/21804200
(20) http://www.ncbi.nlm.nih.gov/pubmed/19227413
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