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Anti- inflammatory effects of nicotine in obesity and ulcerative colitis . Chronic low- grade inflammation is a key feature of obesity, which is characterized by the elevated production of pro- inflammatory cytokines by the adipose tissue itself . Chronic and relapsing inflammation is at the core of inflammatory bowel disease (IBD), which is characterized by activation of the pro- inflammatory transcription factor nuclear factor- .
Nicotine has been proven effective in reducing obesity- related inflammation and insulin resistance . In fact, ulcerative colitis patients with a history of smoking usually acquire their disease after they have stopped smoking . Patients who smoke intermittently often experience an improvement in their colitis symptoms during the periods when they smoke .
A patch of cecal inflammation around the appendiceal orifice can occasionally be seen in patients with left-sided UC. The clinical implication of cecal patch is not clear, and a recent controlled study revealed that UC patients. We performed a literature review comparing two main approaches - right hemicolectomy and primary closure with omental patch. World Journal of Emergency Surgery 2011 6:36 DOI: 10.1186/1749-7922-6-36 Because inflammation in ulcerative colitis typically does not extend into the small intestine and occurs in proximity to the epithelium.
Therefore the development of drugs designed to suppress the aberrant inflammatory response in obesity and ulcerative colitis may be of significant help in giving relief to patients. Recent studies suggest that the parasympathetic nervous system, in particular the efferent vagus nerve, regulates immune responses via the peripheral release of acetylcholine (ACh) .
Thus, the cholinergic anti- inflammatory pathway could be exploited to suppress inflammation in obesity and gastrointestinal (GI) dysfunction. This article will discuss recent advances in understanding the anti- inflammatory effects of nicotine in obesity and gut dysfunction, including ulcerative colitis. Nicotine suppresses the production of pro- inflammatory cytokines. There is no doubt that the net effect of cigarette smoking is pro- inflammatory primarily as a result of increased oxidative stress, which occurs when the amount of reactive oxygen species (ROS) generated in cells exceeds the capacity of normal detoxification systems .
Oxidative stress is one potential explanation for the enhanced DNA breaks in smokers . Thus, it has implications for understanding the mechanisms by which smoking induces organ damage. There is overwhelming medical and scientific consensus that cigarette smoking causes lung cancer, heart disease, emphysema, and other serious diseases in smokers. Cigarette smoke contains molecules that act as potent carcinogens (e.
Inflammation in ulcerative colitis is characteristically restricted to the mucosal surface. However, some patients with proctitis or left-sided colitis have a cecal patch of inflammation, 68 x 68 D'Haens, G, Geboes, K, Peeters, M, Baert, F P. Cecal patch (cecal involvement without pancolitis). Patchy involvement Esp. Fenoglio, CM.; Haggitt, RC.; Ahren, C.; Correa, P. Ulcerative Colitis Ulcerative colitis is an inflammatory bowel disease characterized by inflammation of the inner lining of the intestines. The disease usually starts in the rectum and sigmoid colon and ascends toward the cecum; it rarely affects the small intestine.
However, nicotine, while being the addictive agent, is often viewed as the least harmful of these compounds. In fact, nicotine exhibits anti- inflammatory properties in many systems . The vagus nerve can restrain serum TNF levels, and prevents septic shock and organ damage . Since ACh is the principal neurotransmitter of the vagus nerve, preliminary studies analyzed the potential of cholinergic agonists to prevent TNF production in immune cells . These studies collectively defined an interaction described as the . As defined in these studies, the anti- inflammatory properties of nicotine are generally restricted to . In general, cytokines can be divided into those with predominantly pro- inflammatory actions and those with anti- inflammatory actions.
Pro- inflammatory cytokines include TNF- . In addition, it has been strongly implicated as a mediator of sepsis and studies of sepsis have shown elevated circulating levels of this cytokine .
Anti- inflammatory cytokines include IL1 receptor antagonist, IL- 1. IL- 1. 3, and TNF- binding proteins 1 and 2 (for review see . Both the vagus nerve and nicotine exert their inhibitory effects through the activation of Jak. STAT3 . Since an excess of TNF- . Interestingly, TTP- knockout mice develop severe inflammatory arthritis, autoimmune dysfunction, and myeloid hyperplasia, demonstrating the importance of TTP in limiting the inflammatory response . HMGB1, a nucleosome protein that acts as a pro- inflammatory cytokine, stimulates other pro- inflammatory cytokines (TNF- .
Treatment with nicotine attenuated serum HMGB1 levels, decreased the clinical signs of sepsis, provided significant protection against death and improved survival in . Additionally, nicotine treatment was not started until 2.
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However, non- neuronal cells, including immune cells throughout the body also express n. ACh. Rs where they contribute to diverse physiological processes including immunomodulation . Confocal image of a whole mount preparation of the myenteric plexus of the stomach stained using monoclonal antibody m.
Ab. 35, which recognizes alpha bungarotoxin- insensitive n. ACh. Rs. Note the punctate staining around neuronal cell bodies. Reprinted from Wiley- Liss, Inc: The Journal of Comparative Neurology 3. Copyright 1. 99. 8 . Neuronal n. ACh. Rs are composed of . The first type is composed of a heteromeric pentamer of . The second type is composed of a homomeric pentamer of .
Studies by Borovikova et al. Peritoneal and peripheral blood mononuclear cell- derived macrophages express .
Studies indicate that ACh post- transcriptionally suppresses TNF synthesis and inhibits the release of IL- 1. In addition, electrical vagal nerve stimulation has been shown to ameliorate disease in animal models of inflammatory conditions including sepsis . Thus, the production of pro- inflammatory cytokines from peripheral macrophages can be attenuated by vagal activity such that activation of this systemic . In contrast, chemical as well as surgical blockade of vagus nerve signaling significantly worsened colitis and enhanced colonic inflammatory mediators in two experimental models of colitis . In contrast, bilateral cervical vagotomy led to substantially increased serum and hepatic TNF- . Moreover, nicotine via its action on . Furthermore, nicotine reduced NF- .
Together, these results suggest a . In fact, splenectomy prevents the anti- inflammatory potential of the vagus nerve. Since the vagus nerve does not innervate the spleen but terminates in the celiac- mesenteric ganglia . Recent findings indicate that ACh released by the vagus nerve in the celiac- mesenteric ganglia activates postsynaptic . Splenic norepinephrine can inhibit cytokine production from macrophages via .
Thus, both the vagus nerve and . Moreover, both the parasympathetic vagus nerve and the sympathetic splenic nerve can team together and coordinate to control systemic inflammation in life threatening conditions such as sepsis. Cholinergic signaling to the spleen also plays an important role in modulating leukocyte migration during inflammation.
Endothelial cells express the . However, the endothelium is not directly innervated by the vagus nerve. Recent studies demonstrate that cholinergic signaling to the spleen regulates leukocyte migration to sites of tissue inflammation by reducing adhesion molecule expression . Thus, the spleen is a critical interface between the cholinergic anti- inflammatory pathway and the system regulation of immune cell trafficking and the cholinergic regulation of neutrophil migration is mediated, in part, through modulation of CD1. Vagus nerve stimulation significantly attenuates neutrophil surface CD1.
Activating this mechanism through direct stimulation of the endogenous vagus nerve pathway to the spleen (via splenic innervation) or through administration of pharmacological cholinergic agonists (which act through the spleen) may have important therapeutic potential to inhibit excessive and deleterious neutrophil migration into inflamed or infected tissues . The increase in obesity is associated with corresponding increases in type 2 diabetes, hypertension, cardiovascular disease and cancer . Obesity is also associated with an increased incidence of gastrointestinal (GI) disorders . A negative correlation among smoking, body weight, and caloric intake has been well demonstrated across species . Mice exposed to three cigarettes, three times a day for 4 days displayed a marked decrease in food intake and body weight . Animals exposed to 4 weeks of cigarette smoke had reduced food intake, body weight gain, fat mass, as well as plasma leptin concentration relative to control mice whereas equivalent food restriction only decreased body weight .
Moreover, potential weight gain on smoking cessation may deter people from quitting . Such individuals should be made aware that smoking is not an efficient way to control body weight. Although the mechanisms of appetite regulation by smoking are unknown, hypothalamic energy balance circuits were disturbed by cigarette smoke exposure as evidenced by the altered neuropeptide Y (NPY) concentration in the hypothalamic paraventricular nucleus, suggesting NPY signaling is involved in the appetite- suppressive effects of cigarette smoking .
Nicotine receptors are highly expressed in the hypothalamus and medulla, in nuclei that play a significant role in appetite regulation. Activation of hypothalamic .
Nicotine inhibited excitatory synaptic activity recorded in NPY, but not POMC neurons and also excited the arcuate nucleus hypocretin/orexin neurons that enhance cognitive arousal, but the responses were smaller than in POMC neurons . Increased NPY expression in food- restricted rats was inhibited by nicotine administration . Together, these findings indicate that nicotine has a number of actions on hypothalamic neurons that could contribute to the reduced food intake and weight loss associated with smoking. Low- grade inflammation is a key feature of obesity and links obesity to insulin resistance, impaired glucose tolerance and even diabetes.
Features of obesity- induced inflammation include increased production of pro- inflammatory cytokines, including TNF- . Furthermore, macrophage- specific disruption of the NF- . Ablation of JNK1 in hematopoietically- derived cells including macrophages also protected mice from diet- induced inflammation and insulin resistance without affecting adiposity . These data collectively demonstrate that macrophage inflammation is an important mediator of obesity- induced insulin resistance.
Interestingly, weight loss is associated with a reduction in the macrophage infiltration of WAT and an improvement of the inflammatory profile of gene expression.