Bronchial inflammation

Ravensberg AJ, Ricciardolo EL, van Schadewijk A, et al. Eotaxin-2 and eotaxin-3 expression is associated with persistent eosinophilic bronchial inflammation in patients with asthma after allergen challenge. J Allergy Clin Immunol 2005 115(4) 779-785. 

Lukacs, N.W., Glovsky, M.M., and Ward, P.A., Complement-dependent immune complex-induced bronchial inflammation and hyperreactivity, Am. J. Physiol. Lung Cell Mol. Physiol. 280, 3, L512, 2001. 

Treatment with omalizumab, the monoclonal humanized anti-IgE antibody, is reserved for patients with chronic severe asthma inadequately controlled by high-dose inhaled corticosteroid plus long-acting B-agonist combination treatment (eg, fluticasone 500 meg plus salmeterol 50 meg inhaled twice daily). This treatment reduces lymphocytic, eosinophilic bronchial inflammation and effectively reduces the frequency and severity of exacerbations. It is reserved for patients with demonstrated IgE-mediated sensitivity (by positive skin test or radioallergosorbent test [RAST] to common allergens) and an IgE level within a range that can be reduced sufficiently by twice-weekly subcutaneous injections. 

A very old woman accidentally ingested a formulation containing zinc and copper sulphate (20). At 90 minutes after ingestion, the peak plasma concentrations were 20 mg/ml for zinc and 2 pg/ml for copper. The major complications were gastric and bronchial inflammation, due to the corrosive properties of these compounds. There were also systemic manifestations, with cardiovascular failure and renal insufficiency, but the patient made a complete recovery. 

Bonnans C, Chanez P, Chavis C (2004) Lipoxins in asthma potential therapeutic mediators on bronchial inflammation Allergy 59 1027-1041... 

We took advantage of a mouse model of allergic asthma to study the effects of nasal or bronchial applications of SEB on the development of allergic asthma in previously sensitized mice [53], Male BALB/c mice were kept under conventional pathogen-free conditions and were actively sensitized by 7 intraperitoneal injections of 10 xg ovalbumin (OVA) on alternate days from days 1 till 13 as described earlier [54], Mice were then exposed daily for 5 min to nebulized OVA (OVA mice) or saline (SAL mice) from days 33 till 37. This protocol resulted in OVA-challenged mice in the induction of bronchial eosinophilia, Th2 cytokine production, bronchial hyperresponsiveness and elevated OVA-specific IgE titers in serum as previously published [55], whereas SAL mice did not show any bronchial inflammation. One hour prior to the latter airway challenge on days 33, 35 and 37, the nose and bronchi were exposed to 10 xl of saline with or without SEB at 500 ng. 

In SAL mice, nasal application of SEB resulted in a significant increase in the total cell counts in BAL fluid. Compared to nasal application of SEB, endobronchial application of SEB induced a stronger bronchial inflammatory response in SAL mice. Similar observations were made when evaluating bronchial inflammation on histologic sections and by measuring the mean thickness of peribronchial inflammation. 

Repeated exposure of sensitized mice to nebulized OVA (OVA mice) without SEB contact induced bronchial inflammation characterized by mainly eosinophils in the BAL fluid and influx of inflammatory cells in bronchial tissue, as illustrated on hematoxylin-and-eosin-stained sections. When SEB was administered onto the nasal mucosa during the development of bronchial allergic inflammation in response to OVA inhalation, bronchial inflammation was clearly aggravated. Compared to nasal application of SEB in OVA mice, bronchial administration of SEB in OVA mice equally aggravated the inflammatory response in the lower airways. Thus, in bronchial tissue of OVA mice, the inflammatory response was aggravated by SEB contact via the nose and the bronchi. 

Although complementary mechanisms may exist, it is apparent that the accumulation of eosinophils is an important event in the development of chronic bronchial inflammation and asthma. While IL-5 is undoubtedly a key cytokine in this process, others such as IL-3 and GM-CSF may also play a role (Humbert,... 

Irritant is a non-corrosive substance which can cause skin (dermatitic) or lung (bronchial) inflammation after repeated contact. People who react in this way to a particular substance are sensitized or allergic to that substance. In most cases, it is likely that the concentration of the irritant may be more significant than the exposure time. Many household substances, such as wood preservatives, bleaches and glues are irritants. Many chemicals used as solvents are also irritants (white spirit, toluene and acetone). Formaldehyde and ozone are other examples of irritants. 

Watanabe and Ackman 1974), manage bronchial inflammation (Holmer 1989), and arthritis (Shahidi 2007). In regards to phospholipid-bound omega-3 fatty acids, a clinical study with 90 patients has shown that krill oil inhibits inflammation and reduces arthritic symptoms within a short period of treatment (Deutsch 2007). 

Lehtimaki L, Kankaanranta H, Saarelainen S, et al. Extended exhaled NO measurement differentiates between alveolar and bronchial inflammation. Am J Respir Crit Care Med 2001 163(7) 1557-1561. 

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