Immunoinflammatory responses in gastrointestinal tract injury and recovery.

Abstract

Inflammation is a non-specific immune response to infection, irritation or other injury, the key features being redness, warmth, swelling and pain. A number of mediators are released which alter the resistance of mucosa to injury induced by noxious substances. Oxidative stress is a unifying mechanism of injury in many types of disease processes, including gastrointestinal diseases. It has been defined as an imbalance in the activity of pro and antioxidants. Pro-oxidants favour free radical formation while antioxidants inhibit or retard the same. A number of markers of oxidative stress have been identified. This review provides an overview of various mediators of inflammation and oxidative stress, and diverse approaches for prevention and treatment of gastrointestinal inflammation.

Autistic Children Exhibit Decreased Levels of Essential Fatty Acids in Red Blood Cells

“…We also cannot assume that our observations of both decreased PUFA levels and increased PGE2 levels in autistic individuals represent a cause-effect relationship, as PGE2 levels can be influenced by other factors such as diet [ 35 , 36 ]. For example, many children with autism suffer from gastrointestinal issues, including inflammation [ 42 ], which may involve increased production of pro-inflammatory prostaglandins such as PGE2 [ 43 ]. Larger studies are necessary to test multiple n-6 and n-3 markers of the PUFA metabolism pathway in order to better elucidate whether abnormal metabolism is responsible for the decreased PUFA levels and increased PGE2 levels in autistic individuals, or if dietary factors play a role in these findings.…”

Antioxidant and anti-inflammatory activities contribute to the prophylactic effect of semi-purified fractions obtained from the crude methanol extract of Muntingia calabura leaves against gastric ulceration in rats

“…The mucosal surface is protected by a unique barrier mechanism. Specific immune responses to these antigens challenge the mucosal immune system to maintain homeostasis of the gastrointestinal functions and structure (Verma et al, 2013). The failure of the endogenous mucosal defense mechanisms such as bicarbonate secretion, mucus-bicarbonate barrier, surface active phospholipids, prostaglandins (PGs), mucosal blood flow, cell renewal and migration, non-enzymatic and enzymatic antioxidants and some growth factors to sufficiently counteract with the aggressive factors that includes acid and pepsin secretion, Helicobacter pylori, refluxed bile, release of leukotrienes and reactive oxygen species (ROS) results in gastric damage (Mota et al, 2009).…”

Trehalase as a possible marker of intestinal ischemia--reperfusion injury.

“…According to our previous experimental study, the major source of intestinal graft damage in the early stages was preservation injury (ischemia) (37.98%), reperfusion (53.91%) and the minor part was due to mechanical manipulation (8.11%) (Varga et al, 2009). It is clear that splanchnic hypoperfusion involves reduction in intestinal motility and enzymatic activities, immunoinflammatory responses (Verma et al, 2013) and causes morphological as well as functional changes (Morini et al, 2010). The nonspecific signs and symptoms of mesenteric vascular disease can significantly delay diagnosis (Sandeep & Shashank, 2009).…”