Lung inflammation

Many types of lung cells produce chemokines in vitro, but the requirements for stimulation vary in important ways. The alveolar macrophage is the sentinel cell in the normal alveolar spaces and is the predominant cell that produces chemokines in the lungs. Alveolar macrophages bear pattern recognition receptors on their surface that recognize common pathogen-associated microbial patterns 

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Chemokines also are produced by nonmyeloid cells in the lungs, including type II pneumocytes, fibroblasts, pleural mesothelial cells, and endothelial cells. In general, these parenchymal cells do not respond directly to LPS, but produce IL-8 and MCP-1 in response to the acute pro-inflammatory cytokines TNFa and IL-ip (49-54). Endothelial cells respond to LPS when it is presented in combination with soluble CD14 in plasma (55). In this sense, TNFa and IL-ip serve to amplify chemokine production in the lungs by linking cytokine production by myeloid and nonmyeloid cells. 

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Mild exposure to HF via inhalation can irritate the nose, throat, and respiratory system. The onset of symptoms may be delayed for several hours. Severe exposure via inhalation can cause nose and throat bums, lung inflammation, and pulmonary edema, and can also result in other systemic effects including hypocalcemia (depletion of body calcium levels), which if not promptly treated can be fatal. Permissible air concentrations are (42) OSHA PEL, 3 ppm (2.0 mg/m ) as E OSHA STEL, 6 ppm (5.2 mg/m ) as E and ACGIH TLV, 3 ppm (2.6 mg/m ) as E. Ingestion can cause severe mouth, throat, and stomach bums, and maybe fatal. Hypocalcemia is possible even if exposure consists of small amounts or dilute solutions of HE. 

These elements produce nasty burns that are slow to heal. The mucous membranes are attacked especially, and chlorine poisoning" is really a lung inflammation. Under no circumstances should inexperienced people handle these substances without close guidance. 

Rola-Pleszczynski, M., Gouin, S. and Begin, R. (1984). Asbestos-induced lung inflammation. Inflammation 8, 53-62. 

Gonzalo JA, Pan Y, Lloyd CM, et al. Mouse monocyte-derived chemokine is involved in airway hyperreactivity and lung inflammation. J Immunol 1999 163(1) 403 111. 

Lukacs NW, Berlin A, Schols D, Skerlj RT, Bridger GJ. AMD3100, a CxCR4 antagonist, attenuates allergic lung inflammation and airway hyperreactivity. Am J Pathol 2002 160(4) 1353-1360. 

Pulmonary hbrosis is a potentially fatal condition that is the end result of persistent lung inflammation and can occur in a variety of clinical settings (1,8,65). It can be a manifestation of environmental or occupational exposure,... 

D Ambrosio D, Mariani M, Panina-Bordignon P, Sinigaglia F. Chemokines and their receptors guiding T lymphocyte recruitment in lung inflammation. Am J Respir Crit Care Med 2001 164(7) 1266-1275. 

Controversial results were reported by Warheit et al. in two studies [57, 65] in which rats were exposed to raw SWNTs. Cell proliferation and cytotoxicity indices indicated that exposure to SWNTs produced only transient inflammation. Histological examination of exposed animals, however, identified the development of granulomas, which were non-dose dependent, nonuniform in distribution and not progressive after 1 month. The presence of granulomas was considered inconsistent with the lack of severe lung inflammation. These two reports highlighted the need for more research on the potential pulmonary toxicity of CNTs, shifting the scientific focus towards this aim. 

Recently, it has been shown that inhalation of MWNTs caused suppression of the systemic immunity without resulting in significant lung inflammation or tissue damage [82,83]. Inhaled MWNTs in fact modified the functionality of spleen cells in exposed mice [82]. Notably, the activity of cyclooxygenase (COX) enzymes in spleen was affected as a response to a cytokine (TGF(5) released from the lungs. This cytokine activated the COX pathway in the spleen, triggering T-cell dysfunction and systemic immunosuppression [83]. 

Nemmar, A. et al. (2007) Enhanced peripheral fhrombogenidty after lung inflammation is mediated by platelet-leukocyte activation role of P-selectin. Journal of Thrombosis and Haemostasis,... 

Single injection of ultrafine particles of nickel metal (20 nm diameter) at 5 mg Severe lung inflammation, cytotoxicity, and increased epithelial permeability 42... 

Azadniv, M. et al., Neutrophils in lung inflammation which reactive oxygen species are being measured , Inhal. Toxicol., 13, 485, 2001. 

Beisswenger, C. and Bals, R., Antimicrobial peptides in lung inflammation, Chem. Immunol. Allergy. 86, 55, 2005. 

Caution Ricin is extremely toxic to cells and acts by inhibiting protein synthesis. After aerosol exposure, signs and symptoms would depend on the dose inhaled. Humans can be expected to develop severe lung inflammation with progressive cough, dyspnea, cyanosis, and pulmonary edema. 

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