Inflammatory states

Asthma is an extremely complex condition characterized by variable and reversible airways obstmction combiaed with nonspecific bronchial hypersensitivity (1 3). The cause of asthma, which is not always readily diagnosed (4), remains unknown. Days, if not weeks, ate needed to document the spontaneous reversal of the airways obstmction ia some patients. Asthmatics experience both an immediate hypersensitivity response and a delayed late-phase reaction, each mediated by a different pathway. Chronic asthma has come to be viewed as an inflammatory disease (5). The late-phase reaction plays a key role ia iaduciag and maintaining the inflammatory state which ia turn is thought to iaduce the bronchial hyperresponsiveness (6). The airways obstmction results from both contraction of airways smooth muscle and excessive bronchial edema. Edema, a characteristic of inflammatory states, is accompanied, ia this case, by the formation of a viscous mucus which can completely block the small airways. 

An important component of the inflammatory state in adipose tissue in obesity comes from the infiltration of the tissue by macrophages. These are likely to be attracted through the secretion by adipocytes of MCP-1 and MEF. The macrophages in turn secrete factors which both directly add to the total production of inflammatory agents by adipose tissue and also catalyse the production of such agents from adipocytes - and perhaps preadipocytes as well. 

An acute-phase reactant protein, the plasma concentration of which increases in inflammatory states. 

Once formed, collagen is relatively metabolically stable. However, its breakdown is increased during starvation and various inflammatory states. Excessive production of collagen occurs in a number of conditions, eg, hepatic cirrhosis. 

F. The Levels of Certain Proteins in Plasma Increase During Acute Inflammatory States or Secondary TO Certain Types of Tissue Damage... 

These proteins are called acute phase proteins (or reactants) and include C-reactive protein (CRP, so-named because it reacts with the C polysaccharide of pneumococci), ai-antitrypsin, haptoglobin, aj-acid glycoprotein, and fibrinogen. The elevations of the levels of these proteins vary from as little as 50% to as much as 1000-fold in the case of CRP. Their levels are also usually elevated during chronic inflammatory states and in patients with cancer. These proteins are believed to play a role in the body s response to inflammation. For example, C-reactive protein can stimulate the classic complement pathway, and ai-antitrypsin can neutralize certain proteases released during the acute inflammatory state. CRP is used as a marker of tissue injury, infection, and inflammation, and there is considerable interest in its use as a predictor of certain types of cardiovascular conditions secondary to atherosclerosis. Interleukin-1 (IL-1), a polypeptide released from mononuclear phagocytic cells, is the principal—but not the sole—stimulator of the synthesis of the majority of acute phase reactants by hepatocytes. Additional molecules such as IL-6 are involved, and they as well as IL-1 appear to work at the level of gene transcription. 

Association of Pain, neuropathic pain is defined as pain initiated or caused by a primary lesion, dysfunction in the nervous system". Neuropathy can be divided broadly into peripheral and central neuropathic pain, depending on whether the primary lesion or dysfunction is situated in the peripheral or central nervous system. In the periphery, neuropathic pain can result from disease or inflammatory states that affect peripheral nerves (e.g. diabetes mellitus, herpes zoster, HIV) or alternatively due to neuroma formation (amputation, nerve transection), nerve compression (e.g. tumours, entrapment) or other injuries (e.g. nerve crush, trauma). Central pain syndromes, on the other hand, result from alterations in different regions of the brain or the spinal cord. Examples include tumour or trauma affecting particular CNS structures (e.g. brainstem and thalamus) or spinal cord injury. Both the symptoms and origins of neuropathic pain are extremely diverse. Due to this variability, neuropathic pain syndromes are often difficult to treat. Some of the clinical symptoms associated with this condition include spontaneous pain, tactile allodynia (touch-evoked pain), hyperalgesia (enhanced responses to a painful stimulus) and sensory deficits. 

Tea extracts have been demonstrated to inhibit a wide range of inflammatory responses and may be useful in treating chronic inflammatory states. For example, rheumatoid arthritis is an inflammatory disease that causes pain, swelling, stiffness and loss of function in the joints. The antioxidants in green tea may prevent or reduce the severity of these symptoms by reducing inflammation and slowing cartilage breakdown (Adcocks et al, 2002 Haqqi et al, 1999). 

We have prepared pure dog Hp by our method for human Hp type 1-1. Rabbit-antidog Hp serum was easily obtained. It was found to cross-react with human Hp. The Hp-level in dog plasma increases after injection of endotoxin or turpentine (G7), and, as in humans, it increases after surgical trauma (A9) and disappears after Hb injection (VI). In rats, guinea pigs, and rabbits the plasma Hp level rises markedly after induction of different types of inflammatory states (II, M5, R3), but the absolute values never reach the high level seen in pathological conditions in man. 

The putative role of angiogenesis in chronic inflammatory diseases is the maintenance of the inflammatory state by allowing ongoing recruitment of inflammatory cells and by supplying nutrients and oxygen to proliferating inflamed tissue. The increased endothelial surface creates an enormous capacity for the production of cytokines, adhesion molecules, and other inflammatory stimuli [35]. 

Increased numbers, particularly of neutrophils, characterize many inflammatory states. This is a physiologically appropriate response and no treatment is necessary. Conversely, there may be elevations due to underlying haematological malignancies or seen in acute or chronic leukaemia. Once such a suspicion arises the patient should immediately be referred to a clinical haematologist. Specialist investigation and management falls outside the ambit of this chapter. 

Sinus problems, hay fever, bronchial asthma, hives, eczema, contact dermatitis, food allergies, and reactions to drugs are all allergic reactions associated with the release of histamine and other autocoids, such as serotonin, leukotrienes, and prostaglandins. Histamine release is frequently associated with various inflammatory states and may be increased in urticarial reactions, mastocytosis, and basophilia. Histamine also acts as a neurotransmitter in the central nervous system (CNS). Upon release from its storage sites, histamine exerts effects ranging from mild irritation and itching to anaphylactic shock and eventual death. 

PMN-elastase is not an acute-phase protein, but as an enzyme from activated neutrophils, it is a sensitive and specific marker of the inflammatory state with a diagnostic value similar to or even higher than that of CRP. Its increase occurs earlier and is characterized by a higher dynamism of changes, which correlates with the clinical course of the disease (D9, D10,12, Ml, Ul). 

Neopterin. Neopterin is a low-molecular-weight substance derived from guanosine triphosphate (GTP) via the enzyme GTP-cyclohydrolase 1. Numerous investigators have demonstrated that neopterin, a product of human macrophages stimulated by y interferon and other cytokines, is a useful in vivo marker of the activation of cellular immunity (U4, Wl). Increased values of neopterin in body fluids have been reported in patients with malignancy, infections, and several inflammatory states. 

The greatest problem connected to gluten protein immunoreactivity as well as with peptides which are responsible for inflammatory states in celiac disease is the presence of peptides containing proline that are resistant to proteolysis. The group of specific enzymes is required for hydrolysis of peptide bonds in which proline residue is present (Hausch et al., 2003). 

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