Showing posts with label H1N1. Show all posts
Showing posts with label H1N1. Show all posts

Thursday, December 31, 2009

Cigarette Smoking and Invasive Pneumococcal Disease - Implications for Severity of H1N1

Cigarette smoking is the strongest risk factor for pneumococcal disease among immunocompetant non-elderly people. (Nuorti) As we have noted, cigarette also disrupts the major antioxidant system Nrf2. A recent report has shown that pneumococcal disease makes complications from H1N1 much more severe. Because of the relationship of Nrf2 and its important influence on modulation of inflammatory processes. It is worth suggesting that the dysruption of Nrf2 may contribute to H1N1 infection complications and because there have been polymorphs in Nrf2 identified - these polymorphs may make a person either more at risk or less at risk for complications related to H1N1. The implications of this includes that unless a person understands these risk factors related to their own genetic makeup it is advisable to take a physician's advice that is based on recent knowledge and understanding instead of those who claim to be "experts" in environmental disease.


CiteULike: Cigarette Smoking and Invasive Pneumococcal Disease: "Nuorti, J. P., Butler, J. C., Farley, M. M., Harrison, L. H., McGeer, A., Kolczak, M. S., Breiman, R. F., and Team, T. A. B. C. S. (2000). Cigarette smoking and invasive pneumococcal disease. N Engl J Med, 342(10):681-689."


Tokairin, Y., Shibata, Y., Sata, M., Abe, S., Takabatake, N., Igarashi, A., Ishikawa, T., Inoue, S., and Kubota, I. (2008). Enhanced immediate inflammatory response to streptococcus pneumoniae in the lungs of mice with pulmonary emphysema. Respirology (Carlton, Vic.), 13(3):324-332. http://www.citeulike.org/user/HEIRS/article/2651950

Nuorti, J. P., Butler, J. C., Farley, M. M., Harrison, L. H., McGeer, A., Kolczak, M. S., Breiman, R. F., and Team, T. A. B. C. S. (2000). Cigarette smoking and invasive pneumococcal disease. N Engl J Med, 342(10):681-689. http://www.citeulike.org/user/HEIRS/article/6462894

Reddy, N. M., Suryanarayana, V., Kalvakolanu, D. V., Yamamoto, M., Kensler, T. W., Hassoun, P. M., Kleeberger, S. R., and Reddy, S. P. (2009). Innate immunity against bacterial infection following hyperoxia exposure is impaired in nrf2-deficient mice. J Immunol, 183(7):4601-4608.

Severity of H1N1 influenza linked to presence of Streptococcus pneumoniae. EurekAlert. December 31, 2009. http://www.eurekalert.org/pub_releases/2009-12/cums-soh123009.php

Thursday, December 17, 2009

First immunological clue to why some H1N1 patients get very ill or die

First immunological clue to why some H1N1 patients get very ill or die: "URL: First immunological clue to why some H1N1 patients get very ill or die


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Wednesday, November 4, 2009

Cat catches swine flu

Cat catches swine flu

Wednesday, September 9, 2009

The AhR and Diseases of the Lung!

Nrf2 is a modulator of inflammatory mediators as well as, interacts with the aryl hydrocarbon (AhR). Neff-Layford suggests that activation of the AhR by pollutants dysregulates IFN-gamma through an iNOS pathway which may lead to a difference in the severity of infection. The author explains further that overproduction of IFN-gamma leads to hyperinflammation in lungs of humans and animals and the levels of IFN-gamma and iNOS correlates with severity of those with acute respiratory distress syndrome. She points out that both influenza and activation of the AhR have been implicated as increasing the severity of these diseases. She concludes that inappropriate activation of the AhR contributes to the severity and complexity of diseases of the lung.

Neff-LaFord, H., Teske, S., Bushnell, T. P., and Lawrence, B. P. (2007). Aryl hydrocarbon receptor activation during influenza virus infection unveils a novel pathway of ifn- production by phagocytic cells1. The Journal of Immunology, 179:247-255 http://www.citeulike.org/user/HEIRS/article/5759129